Search Criteria: Research Area is "Sensorineural Research"
New Strains Awaiting Transfer from the Donor
Additional Register Interest Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. White belly spots, ranging in phenotype from a few white hairs to a defined spot are common in C3H/HeJ mice. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a ..... For more information please see the full phenotype on the strain data sheet | ||
| 001800 | FVB/NJ | Level 1 |
| FVB/NJ was inbred for the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ mice are commonly used for transgenic injection. Compared to many other inbred strains, FVB/NJ is highly susceptible to asthma-like airway responsiveness with significant generation of antigen-specific IgE. Despite having the H2q MHC haplotype, FVB/NJ are resistant to collagen-induced arthritis. This resistance stems from coding polymorphisms in Tcra-V11.1 and a genomic deletion of some Tcrb-V genes that includes Tcrb-V8.2. FVB/NJ have higher than average activity, anxiety, and basal body temperature, low stress-induced hyperthermia, and are homozygous for the Pde6brd1 allele, which results in early onset retinal degeneration. Although FVB/N typically do not develop spontaneous tumors, they are highly susceptible to chemic ..... For more information please see the full phenotype on the strain data sheet | ||
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997.
In response to challenge, 129X1/SvJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulo ..... | ||
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A/J inbred strain is widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, ..... | ||
| 000058 | B6(Cg)-Tyrc-2J/J | Level 2 |
| Mice homozygous for Tyrc-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyrc-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004). | ||
| 001026 | BALB/cByJ | Level 2 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000656 | CBA/J | Level 2 |
| CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965). The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al. 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al. 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter 1977, Leiter et al. 1977). | ||
| 000670 | DBA/1J | Level 2 |
| DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). There is high incidence of calcified lesions of the tongue with age. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975). | ||
| 000671 | DBA/2J | Level 2 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between three to four weeks of age) and becoming severe by two to three months of age. The age related hearing loss 8 mutation arose spontaneously in DBA/2J between 1951 and 1975. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroven ..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl ..... For more information please see the full phenotype on the strain data sheet | ||
| 000635 | C3H/HeOuJ | Level 3 |
| C3H/HeOuJ mice are used as a general purpose strain in a wide variety of research areas including cancer and sensorineural, research. C3H/HeOuJ mice and all other C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6brd1), causing blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. | ||
| 000658 | C3HeB/FeJ | Level 3 |
| This general purpose strain shares a common origin with C3H/HeJ and C3H/HeOuJ. Unlike C3H/HeJ, it carries a normal allele at the Tlr4 locus, but is homozygous for Pde6brd1, which causes retinal degeneration. | ||
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 3 |
| The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmdmdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmdmdx mutants do not express dystrophin and therefore have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997. | ||
| 003770 | B6.129X1-Trpv1tm1Jul/J | Level 4 |
| Mice that are homozygous targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in dorsal root ganglia. Cultured dorsal root ganglia neurons and skin preparations display no, or markedly attenuated, response to vanilloid compounds, acidified environments or heat (43 degrees C). In intact wild type mice, a subcutaneous injection of vanilloid compounds into the hind paw elicits a pain response with subsequent swelling. No pain response is observed in homozygotes and swelling is noticeably reduced. Also absent is the profound reduction in body temperature following a subcutaneous injection of capsaicin. Homozygotes appear to display robust deficits in thermally evoked pain-related behavior and do not display an aversion to ingesting capsaicin-supplemented drinking water. | ||
| 004326 | C3Bir.129P2(B6)-Il10tm1Cgn/Lt | Level 4 |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 005304 | C57BL/6NJ | Level 4 |
| This is an NIH subline of C57BL/6. It was separated from C57BL/6J in 1951. 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M (rs3709624) is C; 11-004367508-M (rs3659787) is A; 13-041017317-M (rs3722313) is C; 15-057561875-M (rs3702158) is G; 19-049914266-M (rs3724876) is T. C57BL/6J types as follows: 08-015199792-M is T; 11-004367508-M is G; 13-041017317-M is T; 15-057561875-M is A; 19-049914266-M is G (Petkov and Wiles 2005.) This strain does not have the deletion in the Nnt gene that has been found in the C57BL/6J strain (Stock No. 000664). | ||
| 000662 | C57BLKS/J | Level 4 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after eight weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background ..... For more information please see the full phenotype on the strain data sheet | ||
| 000668 | C57L/J | Level 4 |
| C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE) and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences. | ||
| 001140 | DBA/1LacJ | Level 4 |
| Historical reports indicate DBA/1J and DBA/1LacJ mice immunized with type II collagen develop a severe polyarthritis mediated by an autoimmune response. Recent in-house studies suggest that the response to collagen induction in the DBA/1LacJ strain is not as robust as indicated by earlier studies. Arthritis models such as B10.RIII-H2r H2-T18b/(71NS)SnJ (Stock No. 000457) and BUB/BnJ (Stock No. 000653) can be used as alternatives to DBA/1LacJ. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1 mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on a ..... For more information please see the full phenotype on the strain data sheet | ||
| 004104 | FVB.Cg-Mmp9tm1Tvu/J | Level 4 |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses. | ||
| 000676 | LP/J | Level 4 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 000486 | MRL/MpJ | Level 4 |
| The MRL/MpJ mice are large but docile to the point that males rarely fight. They are the parent and control strain for for MRL/MpJ-Faslpr (Stock Nos. 000485, 006825). Despite carrying the normal Fas gene, MRL/MpJ mice also exhibit autoimmune disorders, but symptoms are manifested much later in life compared to those the MRL/MpJ-Faslpr mice. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-Faslpr mouse but not in the wildtype control, MRL/MpJ. Also beginning at 3 months Faslpr mice exhibit very severe poliferative glomerulonephritis, whereas in the MRL/MpJ controls usually only mild glomerular lesions are detected. MRL/MpJ inbred female typically die at 73 weeks of age and males die at 93 weeks. This compares to a lifespan of 17 weeks in the female and 22 weeks for males in the mouse homozygous for Faslpr. See MRL/MpJ-Faslpr<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002423 | NON/ShiLtJ | Level 4 |
| Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, d ..... For more information please see the full phenotype on the strain data sheet | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/ShiLtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/ShiLtJ. | ||
| 000680 | PL/J | Level 4 |
| PL/J mice show a moderate susceptibility to experimental allergic encephalitis (EAE) with late onset and high mortality. Reports of leukemia incidence vary from 50% in females and 19% in males to 80-90%. In addition to a low threshold to electroconvulsive seizures, PL/J mice are susceptible to handling and rhythmic tossing-induced seizures (Kitami et al. 2004) and very highly responsive to phytohemagglutinin (Heiniger et al. 1975). | ||
| 000689 | SWR/J | Level 4 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l ..... For more information please see the full phenotype on the strain data sheet | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the ..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males ..... For more information please see the full phenotype on the strain data sheet | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 010635 | B6.129(FVB)-Alcamtm1Jawe/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Embryonic spinal motor nerve bundles exhibit modest defects in fasciculation and, in some cases, abnormal axon trajectories form bridges or turn at right angles to adjacent nerves. However, adult motor function appears grossly normal. A similar defect is observed in retinal ganglion cell axons of the optic fiber layer, in which axons appear fanned-out and defasciculated with wide bundles. Homozygotes exhibit two types of retinal dysplasias characterized by photoreceptor cell evaginations or protrusions from the outer nuclear layer and retinal folding (invagination) inside the orb. The donating investigator indicates that this phenotype is less commonly observed on the C57BL/6 background. ALCAM is also believed to be important for immune system functioning, including T cell activation, and is a marker of tumor progression in numerous ..... For more information please see the full phenotype on the strain data sheet | ||
| 012431 | B6.129-Adrbk2tm1Rjl/J | Repository- Live |
| Adrbk2 (adrenergic receptor kinase, beta 2; also called GRK3) is the major G protein-coupled receptor kinase family member in olfactory neurons, and mice lacking GRK3 exhibit a deficit in desensitization to olfactants. In homozygous mice, airway smooth muscle cells exhibit supersensitivity to muscarinic agents, and brain neurons exhibit altered kappa opioid receptor-dependent tolerance. Expression is eliminated in olfactory neuroepithelium, brain, and airway smooth muscle cells. | ||
| 016162 | B6.129-Gfi1tm2Tmo/J | Repository- Live |
| These mutant mice express EGFP (Enhanced Green Fluorescent Protein) from the endogenous Gfi1 locus. No endogenous gene product (protein) is detected in thymocytes from homozygotes, as detected by FACS analysis. Homozygotes exhibit neutropenia, decreased thymocyte number, and defective B cell and T cell differentiation. The Donating Investigator reports that homozygous mice must be maintained under spf conditions and have a lifespan of 1 year. GFP fluorescence expression mimics the expression pattern of the endogenous gene. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Almost all thymocytes from heterozygotes fluoresce. Fluorescence of thymocytes from homozygotes is more intense than fluorescence observed in heterozygotes. At embryonic day 17.5, homozygous embryos exhibit disorganized inner ear sensory epithelia, with abnormal outer hair cells morphology. Neonate ..... For more information please see the full phenotype on the strain data sheet | ||
| 016163 | B6.129-Gfi1tm3(Gfib1)Tmo/J | Repository- Live |
| These mutant mice express mouse Gfi1b (growth factor independent 1B) from the endogenous Gfi1 locus. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Higher expression levels of Gfi1b transcript is detected in inner ears as measured by RT-PCR analysis. The Gfi1b knock-in did not completely rescue the Gfi1 knock out phenotype (see STOCK No. 016161). Homozygotes have slightly fewer granulocytes in bone marrow, a small accumulation in bone marrow of immature myeloid cells and monocytes, and fewer mature circulating granulocytes when compared to wildtype controls. At 3 to 3.5 months in age, homozygotes are deaf, do not display a Preyer reflex, abnormal auditory brainstem response (over 100 dB at 8 kHz and over 90 dB at 16 and 32 kHz), and exhibit head bobbing and abnormal reaching response. In neonatal mutants, the cochlear inner hair cells are morphol ..... For more information please see the full phenotype on the strain data sheet | ||
| 010773 | B6.129-Trpv3tm1Apat/J | Repository- Live |
| Homozygous (TRPV3-/-) mice are viable and fertile, with deletion of Trpv3 (transient receptor potential cation channel, subfamily V, member 3) exons resulting in low levels of truncated TRPV3 transcript that does not encode the putative pore region or adjacent transmembrane domains five and six (essential domains of the ion channel). Homozygous mice lack functional TRPV3 with no abnormal affects on TRPV1/TRPV4 expression or overall dorsal root ganglia or skin anatomy. TRPV3-/- mice have strong deficits in responses to innocuous and noxious heat stimuli, but not in other sensory modalities, and retain a residual sensitivity to warm temperatures. Compared to wildtype mice, TRPV3-deficient mice are resistant to the anxiolytic-like and antidepressive-like behavioral effects (and concomitant changes in c-Fos activation in the brain) following treatment of the TRPV3 agonist, incensole acetate. Unlike wildtype keratinocytes, TRPV3-deficient keratinocytes are not a ..... For more information please see the full phenotype on the strain data sheet | ||
| 006084 | B6.129P2(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 002928 | B6.129P2-Cd40tm1Kik/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation. | ||
| 009132 | B6.129P2-P2ry2tm1Bhk/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of kidney tissue. Intracellular calcium ion levels in lung fibroblasts isolated from homozygotes fail to respond to nucleotide (UTP, ATP, ADP, UDP) challenge. Isolated airway epithelial cells have a loss of or diminished intracellular calcium response to nucleotide challenge. Unlike wild-type macrophages, macrophages derived from these animals fail to respond to extracellular stimulation with UTP. ATP- and adenosine 50[g-thio] triphosphate (ATPgS)-evoked aortic endothelium-dependent relaxation is reduced. Luminal nucleotide stimulated distal colonic ion transport is reduced. Homozygotes are more susceptible to lung infections of Pseudomonas aeruginosa, exhibit impaired neutrophil chemotaxis (loss in gradient sensing and migration distance), and loss of sensitivity to ..... For more information please see the full phenotype on the strain data sheet | ||
| 008198 | B6.129P2-Trpm8tm1Jul/J | Repository- Live |
| Mice homozygous for this TRPM8 targeted mutation are viable and fertile, with no differences in core body temperature compared to wildtype. Functional TRPM8 transcripts are absent in trigeminal ganglia from homozygous mutants however,a truncated, non-functional transcript is generated. Immunostaining of trigeminal ganglia, corneal afferents, and spinal cord dorsal horn reveals loss of TRPM8 expression in homozygous mutants. TRPM8-deficient mice exhibit behavioral deficits in their ability to discriminate between cold and warm surfaces, or to respond to evaporative cooling. Homozygous mice are not completely cold insensitive as they avoid contact with surfaces below 10 C (albeit with reduced efficiency). Cultured sensory neurons and intact sensory nerve fibers from TRPM8-deficient mice exhibit profoundly diminished responses to cold. These TRMP8 (transient receptor potential cation channel, subfamily M, member 8 (also called TRP melastatin 8 or cold and menthol receptor 1 (CMR1))) muta ..... For more information please see the full phenotype on the strain data sheet | ||
| 013787 | B6.129S1-Abcc6tm1Jfk/J | Repository- Live |
| Mice that are homozygous for this targeted mutation develop patchy, progressive mineralization of the dermis, kidneys, eyes, arteries, heart and subcutaneous tissues, mimicking the human disease symptoms of pseudoxanthoma elasticum. Mineralization of connective tissue capsule surrounding vibrissae is detectable at 5 weeks of age. Mineralization is associated with collagen fibrils and elastic fibers. Oxidative stress, as indicated by lipid peroxidation and protein oxidation, is higher in liver tissue and serum of mutant mice when compared to wildtype controls. Antioxidant diet reduces the oxidative stress levels in knock out mice, but does not prevent ectopic mineralization. The severity of mineralization can be altered by mineral intake as a diet with elevated magnesium levels prevents pathological connective tissue mineralization in mutants. Serum matrix gla protein (MGP) levels are reduced in homozygotes and the protein is under-carboxylated with diminished activity. Fetuin-A ..... For more information please see the full phenotype on the strain data sheet | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 010616 | B6.129S1-Jag1tm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of homozygous embryos, aged embryonic day 10. Homozygotes have an embryonic lethal phenotype, with defective vasculature formation in the embryo and yolk sac and widespread hemorrhaging at embryonic day 10.5. Heterozygotes exhibit iris coloboma, irregular/off center pupils and corneal opacity. | ||
| 010546 | B6.129S1-Jag2tm1Grid/J | Repository- Live |
| Mice that are homozygous for this targeted mutation have a perinatal lethal phenotype, dying shortly after birth due to craniofacial defects (cleft palate, due to fusion of unelevated palatal shelves with the tongue). Embryos homozygous for the mutation and aged embryonic day 10.5-11.5, display a hyperplastic thick apical ectodermal ridge of the limb buds. Homozygous neonates have bilateral cleft of the secondary palate and syndactyly (fused digits) of both forelimbs and hindlimbs, although the hindlimbs are more affected. The number of inner ear hair cells is increased in mutants. Histological analysis reveals an increased number of inner ear hair cells and disorganized stereocilia bundles in mutants. Homozygotes exhibit abnormal thymic morphology and decreased gamma-delta T cell number. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygotes have abnormal inner ear morphology (increased number of hair c ..... For more information please see the full phenotype on the strain data sheet | ||
| 010620 | B6.129S1-Notch2tm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Due to alternative splicing, 2 in-frame gene products (mRNA) are detected by RT-PCR analysis of homozygous embryos. The mutant transcripts would produce proteins with one or two EGF repeats deleted. Levels of the mutant transcripts are similar to the wildtype transcript level. This targeted allele is a hypomorph. Homozygotes are neonatal lethal due to developmental defects in the kidney, heart and eye vasculature. Homozygous neonates exhibit hypoplastic kidneys, with vasculature lesions at the cortical surface, and lack mature glomeruli. Bilateral microphthalmia, with retrolenticular hyperplasia, is observed in homozygotes. At age embryonic day 11.5, some homozygous embryos exhibit delayed growth, pericardial effusion and widespread hemorrhaging. Homozygous embryos that survive past embryonic day 11.5 display myocardial hy ..... For more information please see the full phenotype on the strain data sheet | ||
| 006228 | B6.129S1-Nox3het-3J/GrsrJ | Repository- Live |
| Homozygotes completely lack otoconia, both in the utricle and the saccule, as early as embryonic day 14 and this persists in the adult. However, the rest of the inner ear appears morphologically normal and hearing is normal. Otoconia appear to be normal in heterozygotes. Homozygotes can be identified by a significant sideways tilting of the head. When dropped 30cm to a soft surface homozygotes fail to land on their feet. They also fail to orient and swim in water, but instead rotate underwater and require rescue. | ||
| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. These mut ..... | ||
| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles ..... | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and ..... For more information please see the full phenotype on the strain data sheet | ||
| 002266 | B6.129S4-Bdnftm1Jae/J | Repository- Live |
| Mice heterozygous for the Bdnftm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Repository- Live |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by four months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a two- to three-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day three, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient ..... For more information please see the full phenotype on the strain data sheet | ||
| 016883 | B6.B10(D2)-Grm6nob3/Boc | Repository- Live |
| Although retinal sections are histologically normal, electroretinogram assessment of homozygotes shows near-normal a-wave but absent both scotopic and photopic b-waves. The contrast sensitivity and spatial frequency thresholds are reduced. Retinal ganglion cell ON responses have a longer latency than normal and fewer retinal ganglion cells respond to the bright phase of a full-field stimulus. There are fewer OFF-center retinal ganglion cells that have an ON response to a full-field stimulus, which is distinct from findings in mice homozygous for the no b-wave 4 (nob4) allele. | ||
| 000537 | B6.BR-Agtpbp1pcd/J | Repository- Live |
| Mice homozygous for the Purkinje cell degeneration spontaneous mutation (Agtpbp1pcd) show a moderate ataxia beginning at 3 to 4 weeks. Homozygous mutant mice are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic nuclei begin to appear in the photoreceptor cells between 18 and 25 days, and the outer rod segments become disorganized. Degeneration of the photor ..... For more information please see the full phenotype on the strain data sheet | ||
| 001809 | B6.Cg-Aw-J EdaTa-6J +/+ ArTfm/J | Repository- Live |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 000305 | B6.Cg-Fbn1Tsk +/+ Pldnpa/J | Repository- Live |
| Mice homozygous for the pallid spontaneous mutation Pldnpa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldnpa/Pldnpa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2p/Oca2p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi ..... For more information please see the full phenotype on the strain data sheet | ||
| 012910 | B6.Cg-Fxntm1Mkn Tg(FXN)YG22Pook/J | Repository- Live |
| The YG22 transgenic founder line carries a single copy of the human FXN gene with one GAA trinucleotide repeat sequence of 190 repeats. High levels of human FXN gene product (mRNA and protein) are detected by RT-PCR and Western blot analysis. 40-50% of the endogenous mouse Fxn gene product (protein) is detected by Western blot analysis in mice heterozygous for the targeted mutation alone. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology. The GAA triplet repeat exhibits intergenerational instability. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit progressive retinal degeneration, impaired and decreased locomotor activity and coordination, and an increase in body weight. At 9 months of age, muscle strength is decreased. Al ..... For more information please see the full phenotype on the strain data sheet | ||
| 016850 | B6.Cg-Pkd1l3tm1.1Abek/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. While no gene product (mRNA) is detected by in situ hybridization and RT-PCR analysis of taste buds of the circumvallate papillae with a probe specific for the transmembrane motif 9 to the C terminus, an incomplete gene product (mRNA) is detected by in situ hybridization analysis with a probe specific for transmembrane motif 2 to the C terminus. Apical localization of PKD2L1 protein is absent in the mutant taste buds. Recorded chorda tympani and glossopharyngeal nerve responses of homozygotes to taste stimuli is similar to wildtype controls. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background. No fluorescence from the GFP in the knock in construct has been observed in the mice.
When crossed to mice carrying a Pkd2l1tm1Hmat knockout mutation (Se ..... For more information please see the full phenotype on the strain data sheet | ||
| 016853 | B6.Cg-Pkd2l1tm1.1Yuni/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of taste buds of the circumvallate. Recorded chorda tympani nerve responses of homozygotes to sour and acid (HCl, acetic acid and citric) taste stimuli is reduced compared to wildtype controls. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background. No fluorescence from the mCherry in the knock in construct has been observed in the mice.
When crossed to mice carrying the Pkd1l3tm1Hmat targeted mutation (See Stock No. 016850), the double homozygous mutant mice exhibit reduced chorda tympani nerve responses to sour and acid taste stimuli. | ||
| 014545 | B6.Cg-Tg(Chat-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the ChAT-mhChR2-YFP BAC transgene (or ChAT-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to cholinergic neuronal populations by the mouse choline acetyltransferase (Chat or ChAT) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 014546 | B6.Cg-Tg(Chat-COP4*H134R/EYFP)6Gfng/J | Repository- Live |
| Mice hemizygous for the ChAT-mhChR2-YFP BAC transgene (or ChAT-ChR2-YFP BAC transgene) are viable and fertile (see note below), with expression of the mhChR2::YFP fusion protein directed to cholinergic neuronal populations by the mouse choline acetyltransferase (Chat or ChAT) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illum ..... For more information please see the full phenotype on the strain data sheet | ||
| 010536 | B6.Cg-Tg(Pcp2-cre)3555Jdhu/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse Purkinje cell protein (Pcp2). Cre recombinase expression is detected in Purkinje cells of the cerebellar folia and retinal bipolar cells. Expression was not found in spinal cord, heart, liver, kidney or cornea. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the offspring. This mutant mouse strain may be useful in studies of the nervous system, particularly Purkinje cells and retinal bipolar cells. | ||
| 014548 | B6.Cg-Tg(Slc32a1-COP4*H134R/EYFP)8Gfng/J | Repository- Live |
| Mice hemizygous for the VGAT-mhChR2-YFP BAC transgene (or VGAT-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to GABAergic interneuronal populations by the mouse vesicular GABA transporter (VGAT or Slc32a1) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mh ..... For more information please see the full phenotype on the strain data sheet | ||
| 014130 | B6.Cg-Tg(Thy1-YFP)GJrs/GfngJ | Repository- Live |
| These founder line G (or 17) transgenic mice express Yellow Fluorescent Protein gene under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter. Fluorescence is detected in all motor axons, many retinal ganglion cells, more than 80% of pre superior cervical ganglion neurons, less than 10% of post superior cervical ganglion neurons, neurons in cortical layers 2 through 6, and the cerebellar mossy fibers in the internal granule layer. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 007084 | B6.FVB(Cg)-Mmp9tm1Tvu/J | Repository- Live |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain de ..... | ||
| 011122 | B6;129-Mertktm1Grl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In response to endotoxin, homozygotes exhibit an increase in spleen size and a decrease in monocyte response. Retinal photoreceptor epithelial cells fail to phagocytose outer segment membranes resulting in complete photoreceptor degeneration and blindness.
When combined with the mutations Tyro3tm1Grl (Stock No. 007937) and Axltm1Grl (Stock No. 011121) mice exhibit a lymphoproliferative disorder, autoimmunity, increased apoptosis in multiple tissues, abnormal spermatogenesis and reduced (in females) fertility or infertility (in males). This mutant mouse strain may be useful in studies of autoimmunity, germ cell development homeostatic regulation and apoptosis. | ||
| 004293 | B6;129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet ..... | ||
| 013064 | B6;129-Tas1r1tm1Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas1r1 (taste receptor, type 1, member 1) gene which encodes a component of the heterodimeric G-protein coupled umami (monosodium L-glutamate, MSG) taste sensor. Homozygous mice lack expression of the gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. Although the mice show robust neural responses to sour (citric acid), salty (NaCl), bitter (6-n-propylthiouracil, PROP), and sweet (D-amino acids, sucrose, maltose, glucose, saccharin) tastants, responses to umami L-amino acid tastants are lost. This strain may be useful in studies of taste and nutrient sensing. | ||
| 013066 | B6;129-Tas1r3tm1Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas1r3 (taste receptor, type 1, member 3) gene which encodes a component of the heterodimeric G-protein coupled sweet receptor and umami (monosodium L-gluamate, MSG) sensor. Homozygous mice lack expression of the gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. Although the mice show robust neural responses to sour (citric acid), salty (NaCl), and bitter (6-n-propylthiouracil, PROP) tastants, umami (L-amino acid) taste responses are completely lost and sweet (D-amino acids, sucrose, maltose, glucose, saccharin) tastant responses are severely defective. This strain may be useful in studies of taste and nutrient sensing. | ||
| 013067 | B6;129-Tas2r105tm2Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas2r105 (taste receptor, type 2, member 105; also known as T2R5) gene which encodes a cycloheximide-specific G-protein coupled receptor associated with bitter taste sensing. Homozygotes selectively lack electrophysiological responses to the taste of cycloheximide, but not to other bitter substances tested. Responses to sweet, umami, salty and sour tastants are not affected. Homozygous mice lack expression of the targeted gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. This strain may be useful in studies of taste and chemosensation. | ||
| 013193 | B6;129S-Barhl1tm1Xia/J | Repository- Live |
| In this strain, the entire coding region of the endogenous BarH-like 1 (Barhl1) gene is replaced with a lacZ (β-galactosidase) reporter gene and a loxP-flanked neomycin resistance (neo) cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size, with β-gal staining in Barhl1 expressing tissues. LacZ expression in embryos and neonates is evident in all hair cells, but is more abundantly observed in the cochlear outer hair cells. LacZ expression in adults is strong in the outer hair cells, and weak in the inner and vestibular hair cells, with persistent expression in hair cells of the organ of Corti. These mice exhibit age-related progressive degeneration of both cochlear outer and cochlear inner hair cells in the organ of Corti, resulting in hearing loss. The progression is apical-to-basal for outer hair cell and basal-to-apical for inner hair cells. Barhl1-/- mice have elevated audit ..... For more information please see the full phenotype on the strain data sheet | ||
| 012355 | B6;SJL-Tg(Pvalb-COP4*H134R/EYFP)15Gfng/J | Repository- Live |
| Mice hemizygous for the Prv-mhChR2-YFP BAC transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neuronal populations by the mouse parvalbumin (Pvalb or Prv) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light (450-490 nm) leads to rapid ..... For more information please see the full phenotype on the strain data sheet | ||
| 012348 | B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012350 | B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-mhChR2-YFP transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 (optimized with an N-terminal beta2 nictinic acytlcholine receptor signal peptide and C-terminal ER-export and Golgi-export motifs) that harbors a gain-of-function H134R substitution fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light ..... For more information please see the full phenotype on the strain data sheet | ||
| 012332 | B6;SJL-Tg(Thy1-HOP/EYFP)2Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 2 exhibit high expression of EYFP in layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 2 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammalian systems ..... | ||
| 012334 | B6;SJL-Tg(Thy1-HOP/EYFP)4Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 4 exhibit high EGFP expression in layer 2/3 and layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 4 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammali ..... | ||
| 014555 | B6;SJL-Tg(Tph2-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the TpH2-mhChR2-YFP BAC transgene (or TpH2-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to serotonergic neuronal populations by the mouse tryptophan hydroxylase 2 (Tph2 or TpH2) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 001756 | B6C3Fe a/a-Cacng2stg/J | Repository- Live |
| Mice homozygous for the spontaneous mutation stargazer (Cacng2stg) are first recognizable at 14 days of age by their smaller body size and slightly ataxic gait. Female stargazer homozygous mutant mice are fertile, but most of the males are unable to breed. The mutation is named for the abnormal head movements resembling choreiform head tossing that is characteristic of these mice. The behavioral symptoms progressively worsen with age, but both males and females will live to over one year of age. Electrocorticographical recordings of stargazer mice reveal frequent, prolonged, generalized spike-wave cortical discharges with behavioral arrest. The abnormal brain wave patterns are similar to those seen in human beings with absence epilepsy. Waggler homozygotes (Cacng2stg-wag) manifest a less severe phenotype than stargazer homozygotes, but do display an ataxic gait and occasional seizures. In general, young stargazer mice are more healthy than waggler ho ..... For more information please see the full phenotype on the strain data sheet | ||
| 001022 | B6C3FeF1/J a/a | Repository- Live |
| 000314 | B6CBACa Aw-J/A-EdaTa/J-XO | Repository- Live |
| XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles. | ||
| 000501 | B6CBACa Aw-J/A-Aifm1Hq/J | Repository- Live |
| Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 ..... For more information please see the full phenotype on the strain data sheet | ||
| 000391 | B6EiC3Sn a/A-Pax6Sey-Dey/J | Repository- Live |
| Mice homozygous for the spontaneous semidominant Dickie's small eye mutation(Pax6Sey-Dey) die during embryogenesis. Heterozygous mutant mice are characterized by an overall small body size, small eyes with coloboma, small or lacking lens with cataract, abnormal folding of the retina and reduction of the pigment layer. The anterior chamber is usually missing. Mutations in the Pax6 gene lead to an impairment of axonal growth and differentiation, and delay migration of preneuronal cells. Optic nerve cross-sectional area and fiber count are decreased in these mutant mice, but probably indirectly as a consequence of reduced neural retina size. Formation of lens and of nasal cavity placodes are dependent on normal Pax6 expression. | ||
| 001923 | B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J | Repository- Live |
| The Tim mutation (translocation induced circling mutation) was induced by ethylene oxide in a mutagenesis experiment. The mutation was induced simultaneously with a reciprocal translocation between Chrs 4 and 17. Because the mutation has so far been inseparable from the translocation, it may be that one of the translocation breakpoints has disrupted a gene on Chr 4 or 17. Heterozygotes exhibit circling, head tossing, poor limb coordination, and corneal clouding. The affected mice are usually smaller than wildtype littermates. Inner ear studies have not been done. The mutants swim poorly but can orient themselves in the water. One mutated copy of the gene is dominant over two normal alleles because segmentally trisomic mice with two normal Chrs 4 and 17 and the small 417 translocation product have the behavioral abnormalitites. Breeding is generally poor. | ||
| 005252 | B6EiC3Sn.BLiA-Ts(1716)65Dn/DnJ | Repository- Live |
| Segmentally trisomic Ts(1716)65Dn mice provide a postnatal model for Down syndrome. Ts65Dn mice have three copies of most of the genes on mouse Chr 16 that are orthologous to human Chr 21 genes. These extra genes, along with the centromere and about 5% of proximal mouse Chr 17 are contained in a small extra chromosome derived from a reciprocal translocation. See FISH chromosome spreads. Trisomic mice with the wild-type allele of Pde6b, are similar to the B6EiC3Sn-a/A-Ts(1716)65Dn/J (Stock No. 001924) trisomic mice in that they display slightly shorter body length and lower body weight (see Ts65Dn mouse photograph), show reduced grip strength, nocturnal hyperactivity, and impaired performance in the Morris water maze. Any differences in the Morris water maze tests for the two genetic backgrou ..... For more information please see the full phenotype on the strain data sheet | ||
| 003647 | B6EiC3Sn.BLiAF1/J | Repository- Live |
| This F1 hybrid is made using a C3H parent that is congenic for the wild-type allele of Pde6b. Thus, this F1 hybrid is useful for maintaining fragile mutations on a mixed background without the confounding retinal degeneration that is normally found in C3H strains. | ||
| 003237 | BALB/cByJ-Agtpbp1pcd-3J/J | Repository- Live |
| Mice homozygous for the Purkinje cell degeneration 3 Jackson spontaneous mutation (pcd3J) have an external and histological phenotype that is very similar to the original Purkinje cell degeneration mutation (pcd). Homozygous pcd mutant mice show a moderate ataxia beginning at 3 to 4 weeks, are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic ..... For more information please see the full phenotype on the strain data sheet | ||
| 005412 | BALB/cByJ-Fgfr1Eask/GrsrJ | Repository- Live |
| The ear askew mutation is homozygous embryonic lethal. Heterozygotes have unilateral or bilateral low-set ears and malformed pinna. There is variable expressivity. Heterozygotes are viable and fertile, but auditory brainstem response assessment shows severe hearing loss at 6 months of age. | ||
| 000653 | BUB/BnJ | Repository- Live |
| BUB/BnJ mice carry a specific T cell receptor V beta mutation, making this strain highly susceptible to collagen-induced arthritis. This T cell receptor V beta restriction works in concert with other uncharacterized modifying genes present in BUB/BnJ mice. BUB/BnJ mice carry no detectable endogenous ecotropic MuLV DNA sequences. Mice are also reported to have high serum complement activity. In response to challenge, BUB/BnJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). BUB/BnJ mice are homozygous for the Mass1frings allele (monogenic, audiogenic seizure susceptibility 1) and are susceptible to audiogenic seizures prior to 25 days of age (Skradski, et al 2001). In addition, the Mass1frings allele acounts for early onset hearing impairment by 3-4 weeks of age (Johnson KR, et al 2005). | ||
| 000031 | BXD24/TyJ-Cep290rd16/J | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
In 2004, a spontaneous mutation, rd16, was discovered in this recombinant inbred line. Mice exhibit complete degeneration of retinal photoreceptors (Seecharan et al. 2003) resulting in blindness. | ||
| 002802 | C3.BLiA Pde6b+-Krd/J | Repository- Live |
| This is a semidominant, homozygous lethal mutation. | ||
| 000480 | C3.MRL-Faslpr/J | Repository- Live |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr> ..... For more information please see the full phenotype on the strain data sheet | ||
| 001428 | C3Fe.SWV-Mbpshi/J | Repository- Live |
| Mice homozygous for the shiverer spontaneous mutation (Mpbshi) show a generalized tremor during locomotion from 12 days of age. This shivering increases in severity with age, and there is incoordination of the hindlimbs. Post-weaning mice undergo seizure-like attacks during which they may lie rigid and motionless for many seconds. Homozygotes are noticeably smaller than their littermates by 4 weeks of age and their life span is shortened. They usually die between 50 and 100 days of age, often while undergoing an attack. They are fertile but do not breed well. There is a severe myelin deficiency throughout the CNS, and a moderate hypomyelination in the PNS. Occasional regions of normal appearing myelin are found throughout the CNS. Heterozygous mice behave normally and have structurally normal myelin but produce only half the normal amount of MBP in both CNS and PNS. Myelin deficient (Mbpshi-mld) homozygotes closely resemble shiverer mice in behavior, ..... For more information please see the full phenotype on the strain data sheet | ||
| 006038 | C3H/HeDiSn-Dscam2J/GrsrJ | Repository- Live |
| Mice homozygous for the Dscam2J mutation can be identified as early as 2 days of age resting on their backs instead of their stomachs and struggling to maintain balance. They develop overt thoracic kyphosis and a domed skull and appear to walk on their toes. Homozygotes fail swim tests wherein they are unable to swim in a straight line, curl up their bodies, and sink to the bottom. However, they have normal auditory brain stem responses indicative of normal cochlear hair cell function and connectivity. Degeneration of spinal joints, dystrophic axons in the lumbar spinal cord and small areas of degenerating epaxial skeletal muscle are found in aging homozygotes. On this background, in the presence of the Pde6brd1 mutation, the inner nuclear layer and retinal ganglion layer are disorganized, a phenotype beyond the retinal degeneration inherent in the background. Additionally, the dopaminergic amacrine cells have fasciculated neurites and are orga ..... For more information please see the full phenotype on the strain data sheet | ||
| 000661 | C3H/HeSnJ | Repository- Live |
| 008393 | C3H;101-Dync1h1Swl/PopJ | Repository- Live |
| Mice heterozygous for the radiation-induced Sprawling mutation of the cytoplasmic dynein heavy chain 1 gene (Dync1h1Swl) are viable and fertile (the donating investigator reports that less than 50% of males breed successfully). Heterozygous mice display an early-onset hereditary proprioceptive sensory neuropathy with muscle spindle deficiency. Mice are distinguishable around one week after birth by the presence of hindlimb flexion during tail suspension, and around three to four weeks of age develop a typical unsteady gait characterized by jerky and wobbly locomotion. At rest, the hindlimbs are splayed and flexed forward and hindpaws are incapable of gripping structures. Defective proprioception is suggested as proprioceptive sensory neurons are severely compromised in the lumbar dorsal root ganglia of newborns and the H reflex is defective despite normal motor nerve function in the hindlimbs. Homozygous mice die in utero before embryonic day (E)8.5, indicating ..... For more information please see the full phenotype on the strain data sheet | ||
| 003648 | C3Sn.BLiA-Pde6b+/DnJ | Repository- Live |
| One caveat to working with C3H inbred mice is the retinal degeneration caused by the Pde6brd1 mutation. This congenic has the wild-type allele of Pde6b from C57BL/LiA bred onto the C3H/HeSnJ background and thus offers most of the strain characteristics of the robust C3H background but without the early onset retinal degeneration. | ||
| 014165 | C57BL/6-Myo3atm1.1Mckg/J | Repository- Live |
| These Myo3aKI/KI mice contain the nonsense mutation TAT>TAG at codon 1041 of the myosin IIIA (Myo3a) gene. This mutation introduces a premature stop codon in exon 28, analogous to a Myo3a mutation found in humans with adult on-set hearing loss (DFNB30). Homozygotes are viable, fertile, and normal in size. DFNB30 is an inherited progressive hearing loss first identified in a Middle Eastern family, Family N. Myo3a is normally expressed in the vestibular hair cells of the inner ear. These mice exhibit significant hearing loss during the third month of life, beginning at high frequencies and eventually progressing to all frequencies. The inner and outer hair cells of these mice exhibit degeneration by 10 and 17 months of age, respectively, showing greater loss towards the base of the cochlea. These mice may be useful for studying adult on-set human hearing loss DFNB30. | ||
| 013148 | C57BL/6-Tg(Pdgfra-cre)1Clc/J | Repository- Live |
| Hemizygous Pdgfra-cre mice are viable and fertile, with cre expression directed to retinal Muller glial cells by the mouse Pdgfra (platelet derived growth factor receptor, alpha polypeptide) promoter. Expression is predominantly in the cell bodies of the inner nuclear layer (INL) of the retina, but some expression may be observed in the outer nuclear layer (ONL) and in the ganglion cell layer (GCL). The donating investigator indicates that although not examined, cre may also be active in many types of central nervous system glial cells. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. | ||
| 006912 | C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J | Repository- Live |
| Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4+ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco ..... For more information please see the full phenotype on the strain data sheet | ||
| 006926 | C57BL/6J-EgfrVel/J | Repository- Live |
| Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series. | ||
| 004391 | C57BL/6J-Chr 13A/J/NaJ | Repository- Live |
| A chromosome substitution or consomic strain is an inbred strain with one of its chromosomes replaced by the homologous chromosome of another inbred strain. The C57BL/6J and A/J strains in this set were chosen because they differ in their susceptibility to diseases such as arthritis, asthma, atherosclerosis, cancer, several infectious diseases, inflammatory responses, and physiological, behavioral and sensory phenotypes. Chromosome substitution strain nomenclature is designated as Host Strain - Chromosome #<Donor Strain>/Laboratory code. For example, C57BL/6J-Chr1A/NaJ carries chromosome 1 for strain A/J (A) on a C57BL/6J background, was constructed in the laboratory of Joseph Nadeau (Na) and is maintained at The Jackson Laboratory (J). Chromosome substitution strains or consomic strains can accelerate quantitative trait loci identification and mapping. | ||
| 004385 | C57BL/6J-Chr 7A/J/NaJ | Repository- Live |
| A chromosome substitution or consomic strain is an inbred strain with one of its chromosomes replaced by the homologous chromosome of another inbred strain. The C57BL/6J and A/J strains in this set were chosen because they differ in their susceptibility to diseases such as arthritis, asthma, atherosclerosis, cancer, several infectious diseases, inflammatory responses, and physiological, behavioral and sensory phenotypes. Chromosome substitution strain nomenclature is designated as Host Strain - Chromosome #<Donor Strain>/Laboratory code. For example, C57BL/6J-Chr1A/NaJ carries chromosome 1 for strain A/J (A) on a C57BL/6J background, was constructed in the laboratory of Joseph Nadeau (Na) and is maintained at The Jackson Laboratory (J). Chromosome substitution strains or consomic strains can accelerate quantitative trait loci identification and mapping. | ||
| 002623 | C57BL/6JSmn-Dstncorn1-2J/J | Repository- Live |
| Histological assessment of corneas from mice homozygous for the Dstn corn1-2J mutation reveals focal epithelial thickening and enlarged surface epithelial cells with degenerating nuclei. These mice lack the neovascularization found in mice homozygous for the Dstn corn1 mutation and have a more mild corneal epithelial phenotype. Preliminary assessment indicates that this variation in phenotype results from the distinct mutations in Dstn, not from differences in genetic background. In both mutants the corneal epithelial cells show increased levels and altered organizational patterns of filamentous actin. In the Dstncorn1 mutants this alteration to filamentous actin has been shown to result in accelerated proliferation of basal corneal epithelial cells. (Smith et al., 1996; Wang et al., 2001; Ikeda et al., 2003.) | ||
| 000667 | C57BR/cdJ | Repository- Live |
| C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD ..... For more information please see the full phenotype on the strain data sheet | ||
| 000669 | C58/J | Repository- Live |
| This strain was developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock. A mating of the same male but a different female gave rise to the commonly used C57BL group of strains. C58/J mice exhibit a high incidence of leukemia (>90% by one year of age). C58/J mice also exhibit an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). Bone marrow cells of C58/J mice (and mice of 9 other strains, excluding closely derived C57 strains) carry the interleukin 3 receptor, alpha chain; mutation 1 allele (Il3ram1) which confers non-responsiveness to Interleukin-3 (IL-3). IL-3 normally stimulates colony formation of multiple lineages of hematopoietic cells. Other characteristics include: low social prefere ..... For more information please see the full phenotype on the strain data sheet | ||
| 010822 | CByJ(Cg)-dde/GrsrJ | Repository- Live |
| dde homozygotes have disproportionate dwarfing evident at birth by shortened limbs, although the axial skeleton appears normal. The back feet have fused toes. Retinal dysplasia presents as white lines in the retina and electroretinaograms show abnormal rod and cone function. Males are sterile and females are poor breeders and poor mothers, often requiring foster mothers to rear the pups. The lifespan of homozygotes varies with some dying shortly after wean and others surviving to approximately one year of age. Ailments identified in homozygotes include emphysema, stomach polyp, apoptitic cells of the tesis, thyroid cysts, holes in the thoracid chord white matter, and holes in the skeletal muscle fibers in the leg. While it has been proposed that dde may offer a model for Walker-Wardburg syndrome, this has not yet been proven. | ||
| 014182 | CByJ.Cg-Fgfr3m1J/GrsrJ | Repository- Live |
| Mice homozygous for the recessive Fgfr3m1J allele have skeletal deformities that result in kyphosis, scoliosis, and a bent tail, which is often found to exit the pelvis at an abnormal angle. ABR threshold assessment shows hearing loss to the point of deafness at 3 to 4 weeks of age, the earliest age assessed. Male homozygotes display infertility, but females do breed and rear pups. Homozygotes have not been found to have a reduced lifespan, distinct from the reduced lifespan or prenatal lethality found in homozygotes for targeted deletions of this gene. | ||
| 004070 | CByJ.Cg-hml/GrsrJ | Repository- Live |
| Homozygotes have a faith-to-thrive phenotype such that they have a smaller body size and unbalanced gait detectable at 10 days of age. Those that survive to 2 months of age can generally live up to 18 months. The inner ear has extensive hypoplasia of the membranous labyrinth, a rudimentary tectorial membrane, and enlarged scala vestibuli and severe hearing loss or complete deafness are found at 19 days of age both by failed response to sounds and auditory brainstem response analysis. Homozygotes also fail to orient in water. | ||
| 000657 | CE/J | Repository- Live |
| CE/J mice are very responsive to phytohemagglutinin and resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breed ..... | ||
| 001998 | CFW-Em/J | Repository- Live |
| 007048 | DBA/2J-Gpnmb+/SjJ | Repository- Live |
| This coisogenic strain has a functional allele of Gpnmb. Homozygous mice do not develop elevated intraocular pressure or glaucoma, although they exhibit a mild iris stromal atrophy (ISA). This strain provides a genetically matched control for DBA/2J (Stock No. 000671). The inbred strain DBA/2J is homozygous for the glaucoma-related GpnmbR150X and Tyrp1isa mutations. | ||
| 004624 | FVB.129P2-Pde6b+ Tyrc-ch Fmr1tm1Cgr/J | Repository- Live |
| Hemizygous male and homozygous female mice for this knockout show many phenotypic characteristics of the Fragile X Syndrome in humans that lack the fragile X mental retardation protein (FMRP) as a result of a mutation in the FMR1 gene. FMRP is an RNA binding protein whose function is shown to be involved in translational regulation of specific dendritic mRNAs. Certain regions of the brain in these mice are characterized by the presence of long, thin dendritic spines on excitatory neurons. Behavioral traits include deficits in classical delay eye-blink conditioning, autistic-like core symptoms of altered social interaction and occurrence of repetitive behaviors with additional hyperactivity, reduced anxiety, and increased errors in a learning assay. Whole-cell patch-clamp recordings in the anterior cingulate cortex show that long-term potentiation is completely abolished. A similar decrease in long-term potentiation is found in the la ..... For more information please see the full phenotype on the strain data sheet | ||
| 004828 | FVB.129P2-Pde6b+ Tyrc-ch/AntJ | Repository- Live |
| These mice are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. Mice from the colony of FVB.129P2-Fmr1tm1Cgr/J, Stock No. 004624, that no longer carried the mutant allele for Fmr1 were used to establish this line. Mice are pigmented as a result of the homozygosity of the Tyrc-ch allele. This mutant mouse strain may be useful in studies where a sighted mouse on the FVB background is an appropriate control, such as behavioral studies. This strain serves as the control for the FVB.129P2-Fmr1tm1Cgr/J strain, Stock No. 004624 . | ||
| 003257 | FVB/N-Tg(GFAPGFP)14Mes/J | Repository- Live |
| Transgenic mice overexpress Green Fluorescent Protein under the control of the astrocyte-specific glial fibrillary acidic protein promoter. Bright fluorescence is observed in the cell bodies and processes of unfixed or fixed astrocyte preparations throughout the CNS of hemizygous mice. In addition retinal Mullers cells expressed the GFP transgene in response to degeneration of neighboring photoreceptors. These mice provide a method to follow changes in astrocyte morphology during development or disease processes. | ||
| 002374 | FVB/N-Tg(MMTV-PyVT)634Mul/J | Repository- Live |
| Mice carrying the (MMTV-PyVT) transgene are viable, but show loss of lactational ability coincident with transgene expression. Female carriers develop palpable mammary tumors as early as 5 weeks of age. Adenocarcinomas arise in virgin and breeder females as well as males, which are multifocal, highly fibrotic, and involve the entire mammary fat pad. Males also develop adenocarcinoma of the seminal vesicles and hemangiomas. Pulmonary metastases are observed in 80-94% of tumor-bearing female mice. Transgene expression is detected at high levels in male and female mammary glands. Lower levels are detected in salivary gland, seminal vesicles, ovaries, and lungs (believed to be the result of pulmonary metastases). | ||
| 002856 | FVB/N-Tg(TIE2-lacZ)182Sato/J | Repository- Live |
| Transgenic mice carry a beta-galactosidase reporter gene under the control of the murine Tek (Tie2) promoter. LacZ is expressed specifically in vascular endothelial cells in embryonic and adult mice. The transgenic line may be useful when crossed with tumor producing strains and the transgene used to visualize neovascularization during tumorigenesis. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002106 | KK/HlJ | Repository- Live |
| KK/HlJ male mice exhibit diabetic symptoms that includes hyperglycemia, hyperinsulinemia, and insulin resistance. This strains serves as a model of noninsulin dependent diabetes mellitus, type 2. | ||
| 000675 | LG/J | Repository- Live |
| LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis (Peng et al., 1996). LG/J was the predominant strain used to develop the MRL/LpJ (Stock No. 000486) inbred strain, a model for autoimmunity. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975). | ||
| 000677 | MA/MyJ | Repository- Live |
| A characteristic of MA/MyJ is the spontaneous mutation hf (hepatic fusion), which results in varying degrees of fusion in the hepatic lobes. | ||
| 000550 | MOLF/EiJ | Repository- Live |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of MOLF/EiJ (Wade et al. 1993, Capparelli et al. 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect gene expression. | ||
| 000679 | P/J | Repository- Live |
| P/J mice exhibit a high incidence of lymphatic leukaemia. They also show a high susceptibility to audiogenic and electroconvulsive seizures. P/J mice are also homozygous for a number of other mutations including nonagouti (a), brown (Tyrp1b), pink-eyed dilution (Oca2p), short ear (Bmp5se), dilute Myo5ad), and retinal degeneration 1 (Pdeb1rd1). | ||
| 000726 | RBF/DnJ | Repository- Live |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 000683 | RIIIS/J | Repository- Live |
| RIIIS/J mice have prolonged bleeding times with normal platelet activity and low levels of factor VIII:C and plasma von Willebrand factor antigen, making it a good animal model for human von Willebrand disease. This bleeding tendency is an incomplete dominant, autosomal trait. RIIIS/J mice also produce a low antibody response to several bacterial polysaccharide antigens and are reported to be resistant to collagen induced arthritis. Despite a B cell immunodeficiency, RIIS/J mice develop severe experimental autoimmune myasthenia gravis (EAMG) (Tuzun et al., 2004). RIII/J have a high incidence of mammary tumors and ovarian tumors. RIIIS/J mice carry Mtv8, and Mtv14, but high incidence of tumors has not been reported in these mice. In fact, some studies indicate a resistance to chemically induced tumors. RIIIS/J mice have been reported to develop far fewer lung tumors than A/J or SWR/J mice subsequent to Urethan treatment. BALB/c x RIII F1 males are also highly resistant to ..... | ||
| 003810 | STOCK Adrb1tm1Bkk Adrb2tm1Bkk/J | Repository- Live |
| Mice that are homozygous null for the Adrb1 and Adrb2 genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stimulation of beta adrenergic receptor function in these mice by agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity and metabolic rate. A severely attenuated chronotropic and hypotensive response is observed after administration of the non-selective beta adrenergic receptor agonist isoproterenol. An abnormal response to epinephrine is also seen, with bradycardia and a monophasic hypertensive blood pressure change being observed rather than the tachycardia and biphasic hypertensive/ hypotensive response seen in wildtype mice. When exercised, heart rates in null mice are lower than that of wild type mice. No difference is noted in the resting heart rate. | ||
| 004339 | STOCK Bdnftm3Jae/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this ..... | ||
| 013702 | STOCK Cep290tm1.1Jgg/J | Repository- Live |
| Homozygous Cep290 (centrosomal protein 290) targeted mutation neonates are runted and display retinal degeneration. Normal body weight is attained 1-2 months after birth. Both male and female homozygotes are sterile. This strain may be useful in studies of retinal degeneration, cilia/flagella development and fertility. | ||
| 003392 | STOCK Crb1rd8/J | Repository- Live |
| 005992 | STOCK Efna2tm1Jgf Efna5tm1Ddmo/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, and normal in size. While the donating investigator reports that 10-20% of females homozygous at both loci neglect their litters, no such neglect is reported in the colonies at The Jackson Laboratory (Aug 2009). Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci are reported to have greater reproductive performance compared to double homozygous mice. Furth ..... For more information please see the full phenotype on the strain data sheet | ||
| 017445 | STOCK Epha7tm1Ud/J | Repository- Live |
| In this strain, exon 1 of the Eph receptor A7 (Epha7) gene is deleted, abolishing gene expression. Homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. EPHA7 is a member of the Eph family of receptor tyrosine kinases and acts as a repellent during axonal growth, suppressing branching. EPHA7 is expressed as a gradient (anterior > posterior) in the superior colliculus (SC). Homozygous Epha7-/- mice exhibit some wiring defects in brain, where topographic mapping of both temporal and nasal axons is disturbed. These mice may be useful for studying the development of retinocollicular projection. | ||
| 010963 | STOCK Fxntm1Mkn Tg(FXN)YG22Pook/J | Repository- Live |
| The YG22 transgenic founder line carries a single copy of the human FXN gene with one GAA trinucleotide repeat sequence of 190 repeats. High levels of human FXN gene product (mRNA or protein) are detected by RT-PCR and Western blot analysis. 40-50% of the endogenous mouse Fxn gene product (protein) is detected by Western blot analysis in mice heterozygous for the targeted mutation alone. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology. The GAA triplet repeat exhibits intergenerational instability. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit progressive retinal degeneration, impaired and decreased locomotor activity and coordination, and an increase in body weight. At 9 months of age, muscle strength is decreased. Alt ..... For more information please see the full phenotype on the strain data sheet | ||
| 005051 | STOCK KitW-sh/HNihrJaeBsmJ | Repository- Live |
| Kit mutations affect melanogenesis, hematopoiesis and gametogenesis. The sash mutation affects melanoblast survival. Melanoblast density is severely reduced in homozygotes by E12 (Cable et al., 1995). Homozygote are white with black eyes and some pigment around the ears. Heterozygotes are black with a white sash at the midline. The KitW-sh mutation affects Kit expression in a tissue specific manner. Kit expression is abolished in mast cells and mutant mice have a mast cell deficit (Tono et al., 1992, Berrozpe et al., 1999). However, young animals (<4 weeks) have been reported to have mast cells in skin (Yamakazi et al., 1994). KitW-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the KitW and KitW-v mutations, KitW-sh germ cells and erythrocytes are not affected. Homozygtes have some ..... For more information please see the full phenotype on the strain data sheet | ||
| 013169 | STOCK Nphp1tm1Jgg/J | Repository- Live |
| Homozygous Nphp1 (nephronophthisis 1 (juvenile) homolog (human)) targeted mutation mice lack protein expression (examined in testes) and gradually develop a mild retinal degeneration that is slightly evident at 2 months of age. | ||
| 014581 | STOCK Trpm8tm1Apat/J | Repository- Live |
| These mutant mice express farnesylated enhanced GFP gene (EGFPf) from the endogenous Trpm8 locus. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No wildtype gene product (mRNA) is detected although low levels of a truncated mRNA splice variant is sometimes detected by RT-PCR analysis of total RNA derived from dorsal root ganglia (DRG) isolated from homozygotes. No Trpm8 locus mRNA is detected by in situ hybridization of DRG isolated from homozygotes. In thermotaxis assays performed in a cage equipped with surface temperature gradients, homozygous mice spend less time in the warmer area compared to wildtype controls. Homozygotes display diminished responses to application of acetone and injection of icilin. Noxious cold sensation of colder temperatures (sub zero) is normal. Mutant mice do not display cold-induced analgesia in response to pain. EGFPf-positive n ..... For more information please see the full phenotype on the strain data sheet | ||
| 014563 | STOCK Utrntm1Ked Dmdmdx/J | Repository- Live |
| Female mice that are homozygous for the Utrntm1Ked allele and the Dmdmdx allele, and male mice that are homozygous for the Utrntm1Ked allele and hemizygous for the Dmdmdx allele, exhibit a more severe phenotype than single Dmdmdx mutants: earlier onset of muscle dystrophy (degeneration, macrophage infiltration and necrosis), weight loss after weaning, joint contractures, kyphosis, dystrophy of extraocular muscles, abnormal electrocardiograms, infertility and premature death. Growth retardation onset is at weaning. By 4 of 6 weeks of age, the double mutants exhibit reduced body weight, reduced mobility, abnormal breathing pattern and slack posture. Muscle weakness and kyphosis (curvature of the spine) is progressive and the double mutant mice develop a waddling gait. Necrosis of the diaphragm muscle is observed in 6 day old double mutant mice. Muscle fibers with centralized nuclei are seen in ..... For more information please see the full phenotype on the strain data sheet | ||
| 001379 | STOCK In(4)56Rk Rd4/J | Repository- Live |
| 000729 | STOCK Rb(11.13)4Bnr/J | Repository- Live |
| 005965 | STOCK Tg(Pomc1-cre)16Lowl/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in brain area neurons involved in the control of food intake (arcuate nucleus (hypothalamus) and solitary tract nucleus (hindbrain)). When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in tissues that normally express Pomc1. The mice may be useful in studies of obesity, food intake, hunger, endocrine and exocrine function, and for tissue specific gene targeting.
View cre expression characterization. | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J-KitlSl/KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet | ||
| 017614 | B6(Cg)-Tyrc-2J Tg(UBC-mCherry)1Phbs/J | Under Development - Now Accepting Orders |
| These transgenic mice express monomeric red fluorescent protein (mCherry) under the direction of the human ubiqutin C promoter. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express mCherry in almost all tissues examined including pre- and post-implantation stage embryos, neonatal pups and adult mice. mCherry is strongly expressed in brain, testis, bladder, prostate and epipdymis and at lower levels in other tissues. No expression is detected in erythrocytes or thrombocytes. These mice may be useful as a bright and photostable means for visualizing morphogenesis and tissue rearrangements alone or in combination with mice expressing eGFP. | ||
| 013126 | B6.129-Accn1tm1Wsh/J | Under Development - Now Accepting Orders |
| Homozygous Accn1 (amiloride-sensitive cation channel 1, neuronal (degenerin)) targeted mutation mice display subtle alterations in mechanoreceptor and spiral ganglion function, and are more sensitive to light-induced retinal degeneration. Transcripts and protein are missing for both spliced forms of the gene, as determined by Western and Northern blot analysis of mouse brain. Homozygous mice show a reduced reproductive capacity that is reportedly 25% that of wildtype mice. This strain may be helpful in studies of touch sensation. | ||
| 017769 | B6.129-Trpv1tm1(cre)Bbm/J | Under Development - Now Accepting Orders |
| 017623 | B6.129-Trpv1tm2Bbm/J | Under Development - Now Accepting Orders |
| The TRVP1 nociceptor is primarily expressed in dorsal root ganglia and peripheral sensory nerve endings. It is also detected in the central nervous system and non-neuronal thermoregulatory tissues. In these knock-in mutant mice, beta-galactosidase (nlacZ) is detected in primary afferent neuron nuclei of the dorsal root ganglion (DRG) and trigeminal ganglia. More than 90% of capsaicin responsive cultured DRG neurons and more than 95% of TRPV1 immunoreactive neurons in DRG sections stain for beta-galactosidase. Beta-galactosidase activity is detected along the midline of the rostral midbrain and caudal hypothalamus. Alkaline phosphatase (ALPP) is detected in cell bodies and axonal processes of the dorsal root ganglion and spinal cord dorsal horn primary afferent terminals. If TRRVP1 nerve fibers are destroyed by capsaicin treatment, no ALPP histochemical staining is detected in the spinal cord. No ALPP staining is detected in the cell bodies of neurons in the brain. Beta-galactosid ..... For more information please see the full phenotype on the strain data sheet | ||
| 016896 | B6.129P2(Cg)-Cdc14btm1.2Pzg/J | Under Development - Now Accepting Orders |
| Cdc14b encodes a nuclear phosphatase that has been implicated in nuclear organization, centriole duplication, mitotic exit, cell cycle regulation, and DNA damage repair. Mice that are homozygous for this targeted mutation allele are viable, fertile, and normal in size. Truncated gene product (mRNA), that is not expected to produce functional protein, is detected by RT-PCR analysis of MEFs from homozygotes. Homozygotes develop cataracts and kyphosis much earlier than wildtype controls and exhibit impaired contextual fear conditioning. Homozygous females exhibit impaired fertility, with smaller litter sizes than wildtype controls. MEFs isolated from homozygotes display defective DNA damage repair and slowed growth rate in later-passages. | ||
| 017009 | B6.129X1-Nfe2l2tm1Ywk/J | Under Development - Now Accepting Orders |
| In this Nrf2 knockout strain, a β-galactosidase (lacZ) reporter followed by a neomycin resistance (neo) cassette replaces exon 5 and part of exon 4 encoding the nuclear factor, erythroid derived 2, like 2 (Nfe2l2) gene, abolishing gene function. Homozygotes are viable, fertile, and normal in size. NRF2, a member of the "cap 'n' collar" (CNC) subfamily of the basic region-leucine zipper transcription factors, is a regulator of endogenous antioxidant protection, microglial function, and chronic neuroinflammation. Inactivation of the CNC, DNA binding, and leucine zipper domains in Nrf2-/- mice results in age-related macular degeneration (AMD)-like retinal pathology, spontaneous choroidal neovascularization (CNV), increased sensitivity to toxins, impaired adipogenesis, abnormal mitochondria, and an increase in proinflammatory gene expression in microglia and astrocytes. These mice may be useful for studying oxidative stress in the pathogenesis ..... For more information please see the full phenotype on the strain data sheet | ||
| 016197 | B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J | Under Development - Now Accepting Orders |
| MCAT transgenic mice have a CMV enhancer/chicken beta-actin promoter (CAG; from the pCAGGS vector) driving the expression of a human Catalase (CAT) gene in mitochondria. Hemizygous MCAT mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Catalase is a an enzyme, normally expressed in peroxisomes, that reduces hydrogen peroxide (H2O2) to water and molecular oxygen, mitigating the potential for H2O2 to cause damage to molecules. Mitochondrial catalase expression in MCAT mice results in a 5.5-month increase in median life span for both males and females. Catalase activity is elevated in heart, skeletal muscle, and brain. Cardiac mitochondria have 50 times higher catalase activity than in wild-type littermates leading to a delay in cardiac pathology. They also display improved cardiac performance with age, reducing their susceptibility to cardiac hypertrophy a ..... For more information please see the full phenotype on the strain data sheet | ||
| 017754 | B6;129-Omptm1(tTA)Gogo/J | Under Development - Now Accepting Orders |
| An internal ribosome entry site (IRES) fused with a tetracycline-regulated transactivator (tTA) was inserted into the 3' untranslated region of the mouse olfactory marker protein (Omp) gene in these mice. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in the neurons of the olfactory bulb, and may be useful in studying the formation and organization of the olfactory and other sensory maps. For example, when mated to mice expressing the tetnus toxin light chain (TeTxLC) and β-galactosidase (lacZ) under the control of tetO, dox induction allows for visualization of ..... For more information please see the full phenotype on the strain data sheet | ||
| 017533 | B6N.129(Cg)-Sema5atm1.2Alk/J | Under Development - Now Accepting Orders |
| In this knockout strain, exon 6 of the semaphorin 5A (Sema5a) gene is excised (includes coding region), abolishing gene function. Sema5A is a transmembrane protein which acts as a repellant for axonal guidance during retinal neural development. Wildtype P0 and P3 mice express Sema5A in the outer neuroblastic layer, directly adjacent to the inner neuroblastic layer (INBL). At P7, P10, and P14, the expression is only observed in the middle to outer part of inner nuclear layer (INL), and transcripts are not detectable at P21, when retinal development is almost complete. Homozygotes are viable and fertile. When bred to mice lacking Sema5b (Stock No. 017534), SEMA5A/B double KO mice exhibit severe defects in retinal ganglion cells, amacrine cells, cholinergic amacrine cells, calretinin-positive amacrine cells, and calbindin-positive amacrine cells. The defects lead to neurite mistargeting within both the inner plexiform ..... For more information please see the full phenotype on the strain data sheet | ||
| 017557 | C57BL/6-Tg(BEST1-cre)1Jdun/J | Under Development - Now Accepting Orders |
| These mice express Cre recombinase under the control of the human bestrophin 1 (BEST) promoter. Mosaic Cre recombinase expression (mRNA) is seen in 50-90% of retinal pigment epithelium (RPE) cells, with some expression seen in the testis. When crossed with a strain containing a loxP site-flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in RPE cells. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating RPE specific-targeted mutants that would be useful in studies of human retinopathies.
For example, when bred to a strain expressing a floxed-Dicer1 gene (see Dicer1tm1Bdh Stock No. 006366 for example), this mutant mouse strain may be useful for studying age-related macular degeneration. | ||
| 017609 | FVB/N-Rr16Tn(sb-Tyr)1HCebOve/J | Under Development - Now Accepting Orders |
| These BART6-TP1H mice harbor a transposition-induced mutation near the bone morphogenetic protein 4 locus (Bmp4) on mouse chromosome 14.
The transposed integration site is reported to be at 46,829,514 [NCB137/mm9] on chromosome 14: this is ~150 kb away from Bmp4. The transposed integration site is tightly linked with the original integration site.
The donating investigator reports they have been unable to identify a transposon-induced deletion near Bmp4 and the mutation is not found within the BMP4 coding sequences. The mutation results in altered BMP4 expression (presumably via a transposition-induced inversion that leads to loss-of-function of an enhancer that is required for expression of BMP4 in the optic vesicle).
Heterozygous and homozygous mice from this line exhibit light grey/medium grey coat color. All homozygous mice exhibit congenital absence of both eyes (anophthalmia) due to defects in lens induction. Homozygous mice are fertile, although ~ ..... For more information please see the full phenotype on the strain data sheet | ||
| 014173 | STOCK Tyrc-2J Omptm1.1(COP4*/EYFP)Tboz/J | Under Development - Now Accepting Orders |
| These OMP-ChR2-YFP (OCY-58) mice express a ChR2(H134R)-EYFP fusion gene from the olfactory marker protein locus (Omp). Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. ChR2(H134R)-EYFP is expressed in all mature olfactory sensory neurons, rendering them light sensitive. Light directed at the olfactory epithelium or the glomeruli can elicit activity in mitral/tufted (M/T) cells of the olfactory bulb and can drive odor guided behavior. These mutant mice thus allow precise, timed delivery of stimuli input to the olfactory system. The Donating Investigator reports that this this targeted mutation creates a null allele. Due to possible olfactory deficits, analysis should be performed in heterozygous mice. The Donating Investigator recommends keeping the strain on the albino B6 background to avoid possible interference by pigmented melanocytes.
The ChR2(H134R)-EYFP fusio ..... | ||
| 016622 | STOCK Utrntm1Jrs Dmdmdx/J | Under Development - Now Accepting Orders |
| 004337 | 129(Cg)-Foxg1tm1(cre)Skm/J | Cryopreserved - Ready for recovery |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development. | ||
| 005987 | 129-Achetm1Loc/J | Cryopreserved - Ready for recovery |
| Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual ..... For more information please see the full phenotype on the strain data sheet | ||
| 002908 | 129-Col4a3tm1Dec/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Col4a3tm1Dec targeted mutation develop glomerulonephritis and die at about 8.5 weeks of age. Survival time of homozygous mutant mice is extended to about 14 weeks of age in mice maintained on a mixed genetic background. | ||
| 003486 | 129-Cstbtm1Rm/J | Cryopreserved - Ready for recovery |
| The progressive myoclonus epilepsies (PMEs) types are diseases characterized by tonic-clonic seizures, myoclonic seizures and progressive neurological dysfunction, including dementia and ataxia. Mice lacking cystatin B develop myoclonic seizures and ataxia, similar to symptoms seen in one of these human diseases. Specifically, this mouse is a model of Unverricht-Lundborg disease (EPM1).Strain background has an effect on phenotype. | ||
| 003009 | 129-Kcne1tm1Sfh/J | Cryopreserved - Ready for recovery |
| This strain is characterized by inner ear defects with a phenotype similar to shaker and waltzer. There is loss of hair cells and many supporting cells in the organ of Corti as well as in all vestibular end organs. The time course of hair cell degeneration is different for each portion of the inner ear. Heart abnormalities of homozygous mutant mice included a longer QT interval at slow heart rates, a paradoxical shorter QT interval at fast heart rates, and an overall exacerbated QT-heart rate adaptation compared with wild-type controls. This mutant serves as a model for Jervell and Lange-Nielsen disease in which patients suffer cardian arrhythmias and profound bilateral deafness. | ||
| 009091 | 129-Skitm1Cco/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. More than 80% of homozygotes on the 129 background exhibit exencephaly (severe neural tube closure defects) between embryonic day 15.5 (E15.5) and embryonic day 18.5 (E18.5). None exhibit facial clefting. The Donating Investigator reports that homozygotes display flattened or shorter snouts, iris malformation and polydactyly. The penetrance of the phenotype is highly background dependent. Heterozygotes are viable and fertile with timely cranial neural tube closure and, the Donating Investigator reports, no facial clefting. This mutant strain may be useful in studies of facial cleft formation, 1p36 deletion syndrome, oncogene function, apoptosis, and neural tube and skeletal muscle defects. | ||
| 001137 | 129P1/ReJ | Cryopreserved - Ready for recovery |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 002357 | 129P3/JEmsJ | Cryopreserved - Ready for recovery |
| 000212 | 129P4.Cg-Axin1Fu/J | Cryopreserved - Ready for recovery |
| The fused mutation is dominant and generally more severe in homozygotes, but has highly varying penetrance in both the heterozygote and homozygote, to the extent that some homozygotes do not have an abnormal phenotype. Phenotypic traits of mice carrying the Axin1Fu allele include shortened, bifurcated, or absent tails, kinked tails with fused vertebrae, other asymmetrical fusions of vertebrae, axial duplications, and ribs fused at the proximal ends. Imperforate anus, anemia at birth, waltzing movement, deafness, and missing or abnormal kidneys have also been reported. Both heterozygotes and homozygotes are generally fertile although female carriers transmit with a lower penetrance than males do. (Reed, 1936; Dunn and Gluecksohn-Waelsch, 1954; Theiler and Gluecksohn-Waelsch, 1956.) | ||
| 001198 | 129P4/RrRkJ | Cryopreserved - Ready for recovery |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 007965 | 129S-Dvl1tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders. | ||
| 009083 | 129S-Dvl3tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have a perinatal lethal phenotype. Neonates have breathing difficulties and are often cyanotic. Homozygous embryos exhibit cardiac conotruncal abnormalities such as persistent truncus arteriosis (PTA) and double outlet right ventricle (DORV), and cochlear defects (disoriented stereociliary bundles). This mutant mouse strain may be useful in studies of cardiac development, neural tube formation and development of the inner ear. | ||
| 006653 | 129S-Del(6)1Mom/MomJ | Cryopreserved - Ready for recovery |
| Using chromosome engineering technology, an approximately 600 kilobase genomic region was deleted that contains a cluster of 16 intact V1r vomeronasal receptor genes. The mutant mice display deficits in a subset of VNO-dependent behaviors: the expression of male sexual behavior and maternal aggression is substantially altered. Electrophysiologically, the epithelium of the VNO of such mice does not respond detectably to specific pheromonal ligands. | ||
| 010751 | 129S.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. | ||
| 010752 | 129S.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002323 | 129S4/SvJae-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 000385 | 129S;AKR-bs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spontaneous blind sterile mutation (bs) are characterized by bilateral nuclear cataracts, smaller than normal eyes, and glossy coats. Female mutant mice are fertile but males are sterile. Cataracts are visible in 16 day embryos and continue to adulthood. Adult male mice copulate normally but have smaller than normal testes. Defects in spermatogenesis lead to a reduced number of sperm and those that are formed completely lack acrosomes. | ||
| 009092 | A.129P-Skitm1Cco/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Homozygotes on the A/J background exhibit exencephaly (severe neural tube closure defects), with a higher embryonic lethality than homozygotes on the C56BL/6 or 129 backgrounds. None exhibit facial clefting. The Donating Investigator reports that homozygotes display flattened or shorter snouts, iris malformation and polydactyly. The penetrance of the phenotype is highly background dependent. Heterozygotes are viable and fertile with timely cranial neural tube closure, and a low incidence of facial clefting. The Donating Investigator reports some heterozygotes on the A/J background exhibit lateral facial clefting. This mutant strain may be useful in studies of facial cleft formation, 1p36 deletion syndrome, oncogene function, apoptosis, and neural tube and skeletal muscle defects. | ||
| 005445 | A.B6 Tyr+-Cybanmf333/J | Cryopreserved - Ready for recovery |
| These mutants were detected through routine inspections for overt abnormal behavior; head- and body tilt can be observed at approximately 4 weeks of age (average onset 4.6 +/- 0.6 weeks; n=15). Standard pathology work-up and a whole-mount ear exam on one mutant (56 days of age) revealed no abnormalities. Male or female mutants have been produced and the colony is maintained through regular breeding.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry. | ||
| 003906 | AK.B6-Cln8mnd/J | Cryopreserved - Ready for recovery |
| 000957 | AKXD28/TyJ | Cryopreserved - Ready for recovery |
| Similar to DBA/2J, AKXD28 mice develop an age-related glaucoma characterized by intraocular pressure elevation, retinal ganglion loss, and optic nerve excavation. Although both glaucoma related alleles, GpnmbR150X and Tyrp1isa, are present in AKXD28, the phenotype differs from DBA/2J. AKXD28 mice do not develop iris pigment dispersion (IPD) and develop a more severe retinal damage. | ||
| 000277 | ATEB/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the atrichosis spontaneous mutation (at) are characterized by sparsely distributed hair, especially on the trunk. The amount of hair varies, but affected mice can be easily recognized at 8 to 10 days old. Both sexes are sterile and have very small gonads with few germ cells. There is a great deficiency of primary spermatogonia in the testes. A quantitative study of maturation of ovarian oocytes showed that the proportion of resident oocytes recruited into the first wave of growth was much higher than in phenotypically normal heterozygous controls (J.J. Eppig, personal communication). This strain is also segregating for the eye blebs spontaneous mutation (Grip1eb). | ||
| 006446 | B10.Cg-H2h4 Sh3pxd2bnee/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the nose eyes ear mutation are runted, with proportionally smaller skeletons, shortened noses, shortened and domed skulls, reduced areal bone mineral density, diminished visceral and subcutaneous white adipose tissue, but not brown adipose tissue, and abnormal eyes and middle ears. The eyes have an enlarged anterior chamber, cloudy cornea, and severe peripheral anterior synechia of the irideocorneal angle. The middle ear shows inflammation as serous fluid with diffuse neutrophils with thickened epithelium. Elevated ABR thresholds are found in all homozygotes and homozygotes are infertile. | ||
| 000477 | B10.PA-Pldnpa H3e at/SnJ | Cryopreserved - Ready for recovery |
| This minor histocompatibility 3 (H3e) congenic strain is also carrying the closely linked pallid mutation (Pldnpa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga ..... For more information please see the full phenotype on the strain data sheet | ||
| 000497 | B6 x (B6xAKR-Frem1heb)F1/J | Cryopreserved - Ready for recovery |
| 000822 | B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J | Cryopreserved - Ready for recovery |
| 003483 | B6 x B10.D1-H2q/SgJ-Nox3het-2J/J | Cryopreserved - Ready for recovery |
| 000593 | B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the MitfMi spontaneous mutation are characterized by decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Cryopreserved - Ready for recovery |
| 004835 | B6 x B6JCu.Cg-wl/J | Cryopreserved - Ready for recovery |
| Homozygous wabbler-lethal mice are first recognizable at 12 days of age and usually die at about 4 weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. | ||
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 003602 | B6 x STOCK Cln6nclf-Edardl-3J/J | Cryopreserved - Ready for recovery |
| 000061 | B6 x STOCK Nox3het/J | Cryopreserved - Ready for recovery |
| Head tilt (Nox3het) is an autosomal recessive mutation that can cause abnormal circling behavior and hyperactivity in affected mice. Homozygotes also exhibit a subtle head tilt. Together, the abnormal behavioral phenotype is consistent with that of a vestibular disorder. Evoked auditory brainstem response profiles are normal indicating that the mutants are not deaf. Nox3het/Nox3het mutants are unable to sense orientation under water and therefore, cannot swim properly. If held by the tail, Nox3het/Nox3het mice retract, rather than extend, their limbs; they also flex ventrally, instead of dorsally as wild type mice do. When lowered quickly by the tail, Nox3het/Nox3het mice fail to extend their forelimbs in a normal manner and have difficulty righting themselves if dropped vertically from a short distance. Morphological assessment of the inner ear of homozygotes r ..... For more information please see the full phenotype on the strain data sheet | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil ..... | ||
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Cryopreserved - Ready for recovery |
| 005543 | B6(129)-Duox2thyd/J | Cryopreserved - Ready for recovery |
| 008617 | B6(A)-Tg(OPN1LW-DT)1Mame/J | Cryopreserved - Ready for recovery |
| Cone photoreceptors in these mice express a modified (DT176) diptheria toxin A chain (DTA) driven by the human red cone specific opsin promoter. This results in the ablation of the cone cells. These mice show no physical, behavioral, reproductive, or growth abnormalities, and the histologic appearance of their retinae remains unchanged over at least 8 months. This strain may be useful in studies of vision and signal processing within the central nervous system. | ||
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet | ||
| 002016 | B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ | Cryopreserved - Ready for recovery |
| 003916 | B6(Cg)-Col2a1sedc/J | Cryopreserved - Ready for recovery |
| Newborn homozygotes are smaller than normal, have a shortened trunk, and often display head bobbing. Decreased body weight persists into adulthood, and the noses, trunks, tails, skulls, and long bones of adults are shortened relative to those of normal siblings. Abnormal epiphyses, with dysplasia of the vertebrae, femora, and tibias are found. Although light microscopy failed to detect any abnormalities in the inner ear, the head bobbing characteristic accompanying this mutation is usually associated with inner ear defects. Auditory brainstem response threshold analysis of 10-15 week old homozygotes does show hearing impairment. Clefts develop between the inner and outer aspects of the inner nuclear layer of the retina (retinoschisis). | ||
| 008834 | B6(Cg)-Tmiesr-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spinner 2 Jackson mutation display head tilting and circling and are deaf. | ||
| 000562 | B6(Cg)-Tubtub/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p ..... For more information please see the full phenotype on the strain data sheet | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Cryopreserved - Ready for recovery |
| On the C57BL/6 background, homozygotes have a white coat color while heterozygotes have a black coat. Clinically, heterozygotes have variable amounts of pigment in the retina with a normal optic cup and retinal vessels. Homozygotes have an iris coloboma, a large optic cup and poor or no retinal vessels. Homozygotes show some pigment in the iris, which does not dilate. | ||
| 004640 | B6(MOR)-Lhfpl5hscy/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Lhfpl5hscy mutation circle rapidly, shake their heads from side to side, fail to swim, and are congenitally deaf. Although hair cells appear normal at birth, they degenerate. At 4 months of age, degeneration of the organ of Corti is also found, more pronounced in the basal region of the cochlea than the apex, with loss of inner and outer hair cells and decreased spiral ganglia (Longo-Guess et al., 2005). | ||
| 005624 | B6(V) Lepob-whe/GrsrJ | Cryopreserved - Ready for recovery |
| White eye homozygotes have partially or completely open eyelids at two days of age. Subsequently, likely as a consequence of infection, homozygotes develop a small white spot and atypical growth of blood vessels on the cornea of each eye, although occassionally only one eye is affected. | ||
| 002552 | B6(V)-Cdh23v-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the waltzer 2J spontaneous mutation (Cdh23v-2J) show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Homozygous mutant mice are very similar to the other waltzer mutants (Cdh23v and Cdh23v-J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (v/+ Myo7ash1/+) are deaf beginning at 3 to 6 months. Double heterozygotes have changes similar to those of the homozygotes in the organ of Corti, stria vascularis, and spiral ganglion, but less severe and with much later onset. Viability and breeding ability are somewhat reduced. | ||
| 009592 | B6.129(Cg)-Kcnn2tm1.1Jpad/J | Cryopreserved - Ready for recovery |
| Homozygous SK2-delta (SK2-null) mice are viable but subfertile (homozygous males exhibit poor reproductive success and homozygous females are nurturing but produce small, infrequent litters). No RNA or protein expression from the targeted allele is observed in brain tissues, and no EGFP expression is reported. Homozygous mice are smaller than wild-type until approximately 5 weeks of age. SK2-deficient mice exhibit whole body tremor beginning around 10 days of age, with ataxia and impaired righting reflex when placed on their back at young ages. Homozygotes also have inner ear abnormalities (impaired exocytotic response of immature inner hair cells and impaired function/long-term survival of olivocochlear fibers and efferent synapses on cochlear outer hair cells). These SK2-delta mice may be useful in studying the role of small-conductance calcium-activated potassium (SK) channels in after-hyperpolarization and action potentials of neuronal, inner ear (cochlea), and urinary bladder tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 013733 | B6.129-Accn2tm1Wsh/J | Cryopreserved - Ready for recovery |
| Homozygous Accn2 (amiloride-sensitive cation channel 2, neuronal; also called ASIC1a) targeted mutant mice display alterations in conditioned and unconditioned fear behaviors, eye blink conditioning, long term potentiation, learned helplessness, seizure termination, retinal function, pain perception, and neuronal death in several neurodegnerative disorders. Transcripts and protein are lacking in central and peripheral nervous system tissue. This strain may be useful in studies of synaptic transmission, synaptic plasticity, depression, fear, anxiety, learning and memory. | ||
| 013127 | B6.129-Accn3tm1Wsh/J | Cryopreserved - Ready for recovery |
| Homozygous Accn3 (amiloride-sensitive cation channel 3) targeted mutation mice display alterations in normal and pain-associated cutaneous mechanosensitivity and inflammatory pain sensation, visual loss associated with night blindness, and age-induced hearing loss. Mice show increased sensitivity of mechanoreceptors detecting light touch. Sensitivity of mechanoreceptors responding to noxious pinch is decreased as is the response of acid- and noxious heat-sensitive nociceptors. No mRNA is detectable by RT-PCR in the dorsal root ganglion. Protein is not found in trigeminal and dorsal root ganglion. This strain may be useful in further elucidating the role of this gene in mechanosensation. | ||
| 013168 | B6.129-Ahi1tm1Jgg/J | Cryopreserved - Ready for recovery |
| Homozygous Ahi1 (Abelson helper integration site 1) targeted mutation mice, completely lacking protein expression, are severely runted and frequently die during the neonatal period. Approximately 80% reportedly do not survive to adulthood. Surviving homozygotes exhibit retinal photoreceptor degeneration and also develop a mild, late-onset cystic kidney phenotype. By 5 months of age, the kidneys of homozygotes are smaller compared to littermate controls and show the characteristic histological triad of nephronophthisis: 1) tubular basement membrane abnormalities, including thickening and disintegration with tubular collapse; 2) interstitial cell infiltrate and fibrosis; 3) delayed appearance (1 year) of multiple microcysts and tubular dilation. This strain may be useful as a model of Joubert syndrome. | ||
| 012247 | B6.129-Aldh1a1tm1Gdu/J | Cryopreserved - Ready for recovery |
| This Aldh1a1 (aldehyde dehydrogenase family 1, subfamily A1) targeted mutant lacks exon 11 which encodes the substrate binding pocket and the tetramerization domain. Protein is not detected by Western blot analysis of liver, lung and testes. Protein is not detected by immunohistochemistry in embryonic retina. Retinoic acid synthesis is reduced in embryonic retina and adult liver. Expression is significantly reduced in the hematopoietic system, but hematopoiesis is not affected. Homozygotes are resistant to diet-induced obesity and insulin resistance and show increased energy dissipation. Approximately 63% of animals are reported to develop mild anterior subcapsular cataracts at 6-9 months of age. This strain may be useful in further characterizing the various functions of the targeted gene. | ||
| 010727 | B6.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. This strain may be useful as a model for Bardet-Biedl syndrome. | ||
| 010728 | B6.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. This strain may be useful as a model for some features of Bardet-Biedl syndrome. | ||
| 009644 | B6.129-Cby1tm1Ktkm/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mice are runted and demonstrate a failure to thrive. Most die before or around weaning age. Mice surviving after postnatal day 25 (P25) usually recover and apparently have normal life spans. All of the mice develop rhinitis and sinusitis and are unable to clear Pseudomonas aeruginosa bacteria from the nasal cavity. There is a complete absence of mucociliary transport caused by a marked lack of motile cilia in the nasal epithelium. Anemia and ductal dilation in the pancreas and kidneys is also observed. Homozygous males have compromised fertility. This strain may be useful as a model of primary ciliary dyskinesia. | ||
| 007064 | B6.129-Crxtm1Clc/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable and fertile and do not display any gross physical abnormalities. These mice do not elaborate photoreceptor outer segments and synaptic termini, and they lack cone and rod activities as assayed by electroretinograms. Circadian entrainment activity is attenuated. Protein is not produced as determined by RT-PCR of retinal RNA extracts. This strain may be useful as a model of retinophathy (e.g., Leber's congenital amaurosis (LCA), cone-rod dystrophy-2 (adCRD2), retinitis pigmentosa (RP)), or circadian rhythm modification. | ||
| 004276 | B6.129-Figntm1Frk/Frk | Cryopreserved - Ready for recovery |
| 012942 | B6.129-Gabra2tm1.1Geh/J | Cryopreserved - Ready for recovery |
| These mutant mice carry substitutions of serine to histidine at amino acid position 270 and leucine to alanine at amino acid position 277 of exon 9. The point mutations confer alcohol and anesthesia insensitivity, while retaining near-normal GABA sensitivity. Approximately half of the homozygous mutant mice (from heterozygous crosses) die between birth and weaning. Homozygotes that survive to adulthood are fertile, normal in size and do not display any gross physical abnormalities. Mutant gene product (mRNA) is detected by RT-PCR analysis of whole brain total RNA. The alpha2 subunit protein levels did not differ between mice homozygous for the mutation and wildtype mice in the cortex and hippocampus. Homozygotes exhibit enhanced fear conditioning, reduced sensitivity to anesthesia (isoflurane), increased alcohol consumption without typical conditioned taste aversion, reduced ethanol induced stimulation of motor activity, and recover more slowly from ethanol?induced hypnosis. Den ..... For more information please see the full phenotype on the strain data sheet | ||
| 004158 | B6.129-Maftm1Gsb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele appear weak, fail to feed and die within a few hours of birth from unspecified causes. Embryos exhibit a slightly foreshortened head and abnormal lens development. No Maf gene transcript is detected. Posterior lens cells from homozygotes fail to elongate. These cells display inappropriately high levels of DNA synthesis and express alpha A crystallin and all of the beta crystallin genes at dramatically reduced levels. Heterozygotes are phenotypically normal. The presence of lacZ in the targeted allele makes it possible to observe Maf expression characteristics. | ||
| 008619 | B6.129-Opn1mwtm1(OPN1LW)Nat/J | Cryopreserved - Ready for recovery |
| A portion of the X-linked mouse opsin 1 (medium-wave-sensitive) "green pigment" gene was replaced by a human opsin 1 (long-wave-sensitive) "red pigment" cDNA in these targeted mutant mice. Heterozyguous female mice are endowed with a unique ability to make chromatic discriminations at long wavelengths. Hemizygous males and homozygous females have greater sensitivity to long wavelength light than normal mice. Heterozygotes, hemizygotes, and homozygotes are normal in size, viability, and fertility. Expression is observed in retinal cone photoreceptors as determined by immunostaining. The knocked-in coding sequences are expressed normally. | ||
| 009042 | B6.129-Pou6f2tm1Nat/J | Cryopreserved - Ready for recovery |
| Heterozygotes and homozygotes are normal in size, viability, and fertility. This transcription factor is normally expressed in retinal neurons, but no obvious phenotype was detected thus far in these targeted ("knockout") mice. | ||
| 004833 | B6.129-Ptprqtm2Bow/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunofluorescence labeling analysis of the inner ear. Homozygotes do not respond to the 20kHz toneburst of a hearing test at 3 months of age. Although embryonic development of the inner ear is normal, newborns exhibit disorganized and defective hair cell bundles. Histological analysis reveals an absence of hair cells in the organ of Corti and some animals are missing the organ of Corti completely. Inner hair cells have missing or defective stereocilia. This mutant mouse strain may be useful in studies related to deafness. | ||
| 005709 | B6.129-Skitm1Cco/J | Cryopreserved - Ready for recovery |
| This mutant was created on a mixed (129 x C57BL/6J) background. Greater than 80% of mice on this mixed background had severe neural tube closure defects (such as exencephaly) while less than 16% exhibited facial clefting. The penetrance of these phenotypes has segregated with further backcross to C57BL/6J. The congenic mutant described here was backcrossed 12-14 times to wildtype C57BL/6J. Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Null mice are distinguishable from wildtype and heterozygous littermates at embryonic day 8.5 (E8.5) with delayed, but complete, cranial neural tube closure (incomplete at the normal E9.5). Ninety percent of null mice alive at E18.5 exhibit facial clefting. Other highly penetrant phenotypes include flattened snout, depressed nasal bridge, excessive orbital separation, elongated subventricular zones, vestigial polydactyly, and malformations of the olfactory bulb, iris, and ventral septum. Heterozy ..... For more information please see the full phenotype on the strain data sheet | ||
| 006853 | B6.129-Ush1ctm1Xzl/Kjn | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ush1ctm1Xzl mutation have circling, head-tossing, and hyperactive behaviors typical of vestibular mutants. Auditory-evoked brainstem assessment shows that homozygotes are completely deaf and scanning electron microscopy shows that the hair cell stereocilia become progressively disorganized with age, with the outer hair cells more affected than the inner hair cells. Although histology at 12 months of age does not reveal any abnormalities, there is a decline in electrotreinogram readings for both rods and cones by 11 months of age. Because the first four exons were replaced by the beta galactosidase reporter cassette, endogenous expression of this gene in phenotypically normal mice can be traced by assessing lacZ expression in heterozygotes. | ||
| 007766 | B6.129P2(Cg)-Olfr160tm6Mom/MomJ | Cryopreserved - Ready for recovery |
| These mice express enhanced green fluorescent protein (EGFP) under the control of the olfactory receptor 160 (M72) promoter. Glomeruli associated with this marker are located primarily on the dorsal surface of the olfactory bulb. Sporadic fluorescence is observed throughout this zone. This strain may be useful in studies of neuronal connectivity and axonal development. | ||
| 008647 | B6.129P2(Cg)-Trpa1tm1Kykw Tyrc-2J/J | Cryopreserved - Ready for recovery |
| Exons encoding the pore domain of the transient receptor potential cation channel, subfamily A, member 1 gene were deleted in this targeted mutation strain. Animals show reduced sensitivity to pain. RT-PCR of dorsal root ganglia confirmed the absence of mRNA in homozygous mutant mice. Homozygotes are viable and fertile. | ||
| 005773 | B6.129P2-Adcy3tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005823 | B6.129P2-Lrp5tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 007767 | B6.129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 005711 | B6.129P2-Prkcqtm1Litt/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted allele are viable, fertile, normal in size, and do not display any behavioral abnormalities. No endogenous or truncated protein product was detected in thymocytes or T cells. Mature T lymphocytes from null mice have blunted proliferative responses with decreased levels of both IL-2 and IL-2 receptor, and defective T cell receptor-initiated IkappaB-degradation/NF-kappaB activation. Homozygous mice exhibit severely impaired Th2, but normal Th1, immune responses as well as abnormal insulin signaling and glucose transport. Mutant mice also have defective regulatory T cell development (very low CD25 expression). This mutant may be suitable for use in studies related to T cell proliferation/signal transduction/immunodeficiency, Th2-mediated disease, asthma, and diabetes.
These mice have been found to also carry the Crb1rd8 allele. | ||
| 005844 | B6.129P2-Sstr1tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005848 | B6.129P2-Trpm5tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 008218 | B6.129S1-Car14tm1Sly/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of brain, heart, kidney, liver, and muscle tissue. Homozygotes exhibit reduced flash electroretinograms (rod/cone a-wave, b-wave, and cone b-wave) when compared to wildtype controls. The abnormal retinal light response of homozygotes is stable over time. This mutant mouse strain may be useful in studies of extracellular retinal pH and carbon dioxide regulation, photoreceptor response and retinal function. | ||
| 002905 | B6.129S1-Cnga2tm1Ngai/J | Cryopreserved - Ready for recovery |
| Heterozygous females are normal. Hemizygous males usually die within 1-2 days of birth from an apparent failure to suckle. A few (~1%) survive to adulthood. They will mate and are fertile. They are completely anosmic. This is an X-linked gene. | ||
| 009379 | B6.129S1-Gpr98tm1Pwh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. A mutant gene product (protein) is detected by Western blot analysis of embryos. High-intensity sound induces audiogenic seizures that often results in death. Cochlear hair cell stereociliary bundles are do not mature properly, lack ankle links and are disorganized. Hair cells and pillar cells in the basal half of the cochlea degenerate and are lost by 2 months of age. Homozygotes become profoundly deaf by 3 weeks of age. Electroretinographic analysis reveals abnormal light-adapted cone-only responses. Mutant mice exhibit abnormal retinal photoreceptor cells ultrastructure and age-related vision loss. This mutant mouse strain may be useful in studies of Usher syndrome type IIC, cochlear development, deafness and blindness. | ||
| 003462 | B6.129S1-Thrbtm1Df/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 002777 | B6.129S2-Adra2atm1Lel/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutation are viable and fertile. They exhibit loss of physiological functions evoked by alpha2-adrenergic receptor agonists and display increased susceptibility to kindling-induced seizures. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 003098 | B6.129S2-Ntrk2tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk2tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus. | ||
| 007768 | B6.129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 007557 | B6.129S2-Oprd1tm1Kff/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first ch ..... | ||
| 002442 | B6.129S4-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 004272 | B6.129S4-Pdyntm1Ute/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted gene product (mRNA or protein) was detected by immunoassay or RT/PCR. Pain withdrawal threshold response of mutant mice is similar to that of wildtype mice. Mutant mice exhibit mild hyperalgesia. This mutant mouse strain represents a model that may be useful in studies of the role of dynorphin in pain, substance abuse and epilepsy. | ||
| 004189 | B6.129S4-Prkcetm1Msg/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the Prkcetm1Msg targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous females produce small litters (0-2 pups). Protein kinase C, epsilon protein was not immunodetectable in dorsal root ganglia or in the central nervous system of mutant mice. Homozygous mutant mice exhibit reduced anxiety, reduced alcohol consumption and reduced responses to nociceptive stimuli. The mice are also supersensitive to acute behavioral effects of allosteric Gamma aminobutyrate (GABA) type A receptor activating drugs. This strain represents a model that may be useful in studies of pharmacological agents for the treatment of alcoholism, anxiety and pain. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 006236 | B6.129S6-Casp6tm1Flv/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile with no gross morphological or behavioral abnormalities. These mutant mice may be useful in studies of mitochondrial events of apoptosis (especially when paired with other executioner caspase mutant models) and lens development. | ||
| 007969 | B6.129S6-Dvl1tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele wa ..... | ||
| 008682 | B6.129S7-Atxn7tm1Hzo/J | Cryopreserved - Ready for recovery |
| Heterozygous mice carrying a 266 CAG repeat knock-in from the human ataxin 7 gene exhibit hypoactivity, progressive weight loss, retarded growth after 5 weeks of age, droopy eyelids (ptosis) and receded eyes, visual impairment, ataxia, muscle wasting, curvature of the spine (kyphosis), and tremors which are triggered whenever they initiate movement. At the terminal stage of the disease, animals became extremely hypokinetic and did not drink nor eat, even when their chow was wetted and placed at the bottom of the cage. Some mice developed myoclonic seizures around 12 weeks of age and many of the heterozygotes die around this age. Homozygous mice show a gene dosage effect, with their phenotype being more severe and disease progression more rapid, resulting in death around 7-8 weeks of age. The heterozygous mice develop retinal degeneration and post-tetanic potentiation (PTP) impairment. The knock-in expression pattern matches that of wildtype mice in the cerebellum, retina, hippocampus a ..... For more information please see the full phenotype on the strain data sheet | ||
| 003336 | B6.129S7-Cdkn1ctm1Sje/J | Cryopreserved - Ready for recovery |
| Mice lacking the Cdkn1c gene have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochrondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; lens cell hyperproliferation and apoptosis. The targeted gene is imprinted. The phenotype differs depending on whether the targeted allele is transmitted from the dam or the sire; maternal inheritance of the null allele is lethal. This is a model for the human Beckwith-Wiedemann syndrome. | ||
| 008116 | B6.129X1(Cg)-Pvrl1tm1Ytk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain extracts from homozygotes. The Donating Investigator reports that homozygous mice are smaller than wild-type littermates until they are six months of age. 30% of homozygotes are born with one or both eyes open. Homozygotes exhibit microthalmia, absent vitreous body, abnormal undulating retinal layers, deformed lenses with adhered ciliary epithelia and lack ciliary processes. At E16.5, the eyelids of homozygotes are not fused and the apex-apex junction of the pigmented and non-pigmented cell layers of the ciliary epithelia are separated. The number of puncta adherentia junctions at the synapses between mossy fibers and CA3 pyramidal cell dendrites is decreased. Mossy fiber projection through the hippocampus is abnormal. Homozygotes have abnormally long hippocampal infrapyramidal ..... For more information please see the full phenotype on the strain data sheet | ||
| 005251 | B6.129X1-Htr3atm1Jul/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of the dorsal root ganglia. Quantitative autoradiography ligand binding assays of solitary tract nucleus, area postrema and trigenimal nucleus caudalis and electrophysiological tests of isolated nociceptor neurons do not detect functional receptor activity. Mutant mice have an impaired response to persistent pain caused by inflammatory tissue injury. This mutant mouse strain may be useful in studies of nociceptive processing, pain response behavior, and peripheral neurogenic inflammation. | ||
| 005289 | B6.129X1-Tulp1tm1Pjn/Pjn | Cryopreserved - Ready for recovery |
| 000783 | B6.A-Ush1gjs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ush1gjs allele are deaf, circle, and toss their heads from side to side. They are viable and fertile but due to their circling gait females may trample their pups and thus should not be used for breeding. No auditory brain response was detected from homozygotes at 14, 21, and 30 days of age. At 10-14 days of age the stereocilia of the outer and macular hair cells are disarrayed or missing although no abnormal phenotype is evident in inner hair cells, or in the gross anatomy of the cochlea or vestibule. The steriocilia degeneration in outer hair cells continues but the inner hair cells remain normal at 30-47 days of age. (Dickie and Deol, 1967; Kitamura et al., 1992.) | ||
| 000517 | B6.BKS-Pcdh15av-J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (Pcdh15av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames waltzer 2J homozygous mutant mice (Pcdh15av-2J/Pcdh15av-2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. Pcdh15av-2J/Pcdh15av-2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (Pcdh15av-3J/Pcdh15av-3J), like Ames waltzer-J (Pcdh15av/Pcdh15av), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 006559 | B6.C-H2-Kbm1/ByBir-Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000256 | B6.C-H2-Kbm1/ByBir-Gusbmps/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Cryopreserved - Ready for recovery |
| 000560 | B6.C-H7b/By KitW-50J/J | Cryopreserved - Ready for recovery |
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Cryopreserved - Ready for recovery |
| 000026 | B6.C3-Gli3Xt-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. | ||
| 000532 | B6.C3-Grxcr1pi/J | Cryopreserved - Ready for recovery |
| Beginning at approximately 10 days of age, pi/pi mice first display backing or crab-like movements and by approximately 14 days of age pirouetting is observed. This pirouetting is a spinning movement that involves swinging the head sharply to one side, either left or right, placing the inner rear foot (with the toes facing outward) close to the outer rear foot which then is used to push the mouse in a tight circling motion. This spinning persists for relatively long periods and cyclostat assessment suggests that these mutants do not develop rotational dizziness. Adult pi/pi mice can not swim on the surface of water or in a coordinated manner and are deaf at 21 to 30 days of age as determined by auditory brainstem response and a failure to respond to a variety of sounds. Although the organ of Corti develops normally, degeneration is found by the second week of life. The tectorial membrane is thickened at 12 days of age and subsequently the hair cells degenera ..... For more information please see the full phenotype on the strain data sheet | ||
| 000122 | B6.C3-KitW-44J/J | Cryopreserved - Ready for recovery |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full phenotype on the strain data sheet | ||
| 002624 | B6.C3-Lmx1adr-6J/J | Cryopreserved - Ready for recovery |
| 000991 | B6.C58-KitW-57J/J | Cryopreserved - Ready for recovery |
| 006562 | B6.CBy(Cg)-Gusbmps Gpi1a-m1J/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 008000 | B6.CBy-Dscamdel17/RwbJ | Cryopreserved - Ready for recovery |
| Mice homozygous for this spontaneous mutation become severely uncoordinated by postnatal day 3, developing spontaneous seizures and kyphosis. On a mixed BALB/cBy and C57BL/6 background some homozygotes survive, are fertile and have a normal lifespan. On the C57BL/6 background, homozygotes exhibit a more severe phenotype and die shortly after birth. With the exception of the caudal folium of the cerebellum, the central nervous system appears normal on a gross level, however, the retinal ganglion cell layer and inner plexiform layer exhibit disorganization by postnatal day 4. Retinal amacrine cells display defects in the arborization of processes and spacing of cell bodies. This mutant mouse strain may useful in studies of the retina and the mechanism of neuronal self-avoidance. | ||
| 000552 | B6.Cg-Aw-J EdaTa-6J Sxr | Cryopreserved - Ready for recovery |
| 001730 | B6.Cg-Aw-J EdaTa-6J Sxrb Hya-/J | Cryopreserved - Ready for recovery |
| 003605 | B6.Cg-Cln6nclf/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the neuronal ceroid lipofuscinosis mutation (nclf) have a phenotype that is very similar to mice homozygous for the motor neuron degeneration mutation (mnd). Homozygous mutant mice display abnormal proteolipid storage by lysosomes termed neuronal ceroid lipofuscinosis. Mice also develop progressive retinal degeneration at an early age. Affected neuronal lysosomes show abnormal morphology. Severe cerebral gliosis and Wallerian degeneration of long neuronal tracts occur late in the disease and account for the motor neuron abnormalities and eventual paralysis. Homozygotes live to approximately 9 months of age. | ||
| 004275 | B6.Cg-Fignfi/Frk | Cryopreserved - Ready for recovery |
| 007787 | B6.Cg-Grxcr1pi-4J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 4 Jackson mutation display bi-directional circling and are completely deaf as early as 5 weeks of age. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 006407 | B6.Cg-Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. These mice have the H2b haplotype typical of inbred C57BL/6 mice. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 002086 | B6.Cg-Gusbmps Tg(Gussx)1Wat/J | Cryopreserved - Ready for recovery |
| Androgen induction of Gus is faster but lower in M. saxicola than in Mus musculus. However, growth hormone induces Gus upregulation in Mus musculus but has no affect on Gus induction in Mus saxicola. When transferred to a Mus musculus background in the absence of endogenous Gus the Mus saxicola derived Gus (Gussx) also showed no growth hormone enhancement of induction supporting the idea that an evolutionary change in regulatory sequence underlies this variation in response. These mice do not exhibit the phenotypic characteristics of Gusmps homozygotes indicating rescue by Gussx. (Niermann and Watson, 1999; Paigen 1989.) | ||
| 000133 | B6.Cg-KitW-24J/J | Cryopreserved - Ready for recovery |
| 000139 | B6.Cg-KitW-25J/J | Cryopreserved - Ready for recovery |
| 000164 | B6.Cg-KitW/J | Cryopreserved - Ready for recovery |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 006337 | B6.Cg-Lgals1tm1Rob/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of dorsal root ganglia and facial motorneuron nucleus and Western blot analysis of adult muscle tissue. Neonate mice homozygous for the mutation have abnormal axon targeting to the caudal region of the olfactory bulb. Mutant mice have fewer neural progenitor cells in the subventricular zone of the forebrain, although the number of apoptotic cells are not affected. Homozygotes exhibit hypoalgesia with a diminished nocifensive withdraw response to thermal testing. Immunohistological analysis of dorsal root ganglia from homozygotes reveals abnormal proportions of axon subpopulations and a larger number of myelinated axons. Mutant mice have a longer recovery of motorneuron function after experimental nerve injury. This mutant mouse strain represents a model that may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/ | ||
| 000071 | B6.Cg-Mcoln3Va/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000158 | B6.Cg-MitfMi-wh/MitfMi/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (MitfMi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac ..... For more information please see the full phenotype on the strain data sheet | ||
| 000184 | B6.Cg-MitfMi-wh/Mitfmi-rw/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (MitfMi-wh/Mitfmi-rw) are mostly white with tan spots and red eyes. | ||
| 000157 | B6.Cg-MitfMi-wh/Mitfmi-sp/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmic but normal skeleton. Both homozygous and heterozygous mice for the microphthalmia-spotted spontaneous mutation (Mitfmi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (MitfMi-wh/Mitfmi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes. | ||
| 000057 | B6.Cg-MitfMi-wh/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. | ||
| 006124 | B6.Cg-Myo6sv-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Snell?s waltzer 2 Jackson mutation display circling and head tossing behavior and are deaf. They are unable to orient in water to swim. | ||
| 003184 | B6.Cg-Myo7ash1-8J/J | Cryopreserved - Ready for recovery |
| Myo7ash1-8J homozygous mice circle and bob their heads; heterozygotes are behaviorally normal. Homozygotes of both sexes are viable and fertile (Samples 2000). The hearing of Myo7ash1-8J mutants has not been examined. However, other Myo7a mutations, whose behavioral phenotypes are virtually identical to that of Myo7ash1-J, are associated with deafness. Mutations in the human ortholog of Myo7a, MYO7A, have been characterized in pedigrees of patients having Usher syndrome type 1 (USH1), an autosomal recessive disorder characterized by profound deafness, vestibular dysfunction and progressive retinitis pigmentosa (Weil et al., 1995; Weston et al., 1996; Adato et al., 1997; Levy et al., 1997; Liu et al., 1998; Espinos et al., 1998; Cuevas et al., 1998, 1999; Janecke et al., 1999). MYO7A mutations have also been identified in patients with autosomal dominant non-sy ..... | ||
| 001104 | B6.Cg-Otop1tlt/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Otop1tlt mutation are viable and fertile. They can be identified outwardly by a tilt in the head posture, which is reported to be detectable in 50-75% of homozygotes. Auditory brainstem responses at four months of age are normal. Although these mice are not deaf and do not show degeneration of the cochlea or vestibular organs, most completely lack otoconia in both the utricle and saccule and thus have problems with spatial orientation. A few giant otoconia have been observed infrequently in a small minority of these mutants, but generally there is agenesis of otoconia. The macular epithelium and otolithic membrane are intact despite the lack of otoconia. Homozygotes are unable to orient themselves in water to find the surface and thus are categorized as non-swimming since they would drown without rescue. Approximately 2% of these homozygotes are able to find the water surface despite somersaults, backflips, or other abnormal motions indic ..... For more information please see the full phenotype on the strain data sheet | ||
| 000024 | B6.Cg-Pldnpa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pallid spontaneous mutation pa and nonagouti (a) are pink-eyed and have a light, yellow-brown coat. The coat is a little lighter than that of pink-eyed dilution homozygotes (p/p). Viability of homozygote mutant mice is slightly reduced. Some homoygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosidase, and a-mannosidase, accompanied by lowered enzyme excretion in the urine. Pallid mice have a deficiency in serum a1-antitrypsi ..... For more information please see the full phenotype on the strain data sheet | ||
| 000567 | B6.Cg-T2J +/+ Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation. | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Cryopreserved - Ready for recovery |
| On an albino background the X-linked transgene Tg(Tyr)3412ARpw permits visual identification of XX versus XY as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother.
This strain also carries Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not female br ..... | ||
| 000571 | B6.Cg-Whrnwi Tyrp1b/+ +/J | Cryopreserved - Ready for recovery |
| At 9 to 10 days of age Whrnwi homozygotes display increased activity, decreased ability to right their selves, and are generally smaller than unaffected siblings. By 14 to 16 days of age homozygotes display head bobbing, circling, and an unsteady gate. Adults display head tossing and circling behavior and deafness is indicated by 20 days of age. Sackler and Weltman reported the average number of circles by a prodded 12-week old female homozygote to be 407 in 10 minutes. They found female homozygotes to have an increased metabolic rate and adrenocorticosteroid activity and decreased body weights. Homozygous males were reported to have decreased blood glucose and liver glycogen levels, decreased white blood cell and eosinophil counts, increased plasma albumin levels, and decreased globulin levels, in addition to decreased weight and increased food intake. (Lane 1963; Sackler and Weltman 1967, 1970, 1971.)
While the organ of Corti in whirler homozygotes shows normal ..... | ||
| 007757 | B6.Cg-hml/J | Cryopreserved - Ready for recovery |
| Homozygotes have a faith-to-thrive phenotype such that they have a smaller body size and unbalanced gait detectable at 10 days of age. Those that survive to 2 months of age can generally live up to 18 months. The inner ear has extensive hypoplasia of the membranous labyrinth, a rudimentary tectorial membrane, and enlarged scala vestibuli and severe hearing loss or complete deafness are found at 19 days of age both by failed response to sounds and auditory brainstem response analysis. Homozygotes also fail to orient in water. | ||
| 010835 | B6.Cg-Tg(Gfap-EGFP)3739Sart/J | Cryopreserved - Ready for recovery |
| Mice harboring the Gfap-EGFP transgene are viable and fertile. The mouse glial fibrillary acidic protein (Gfap) promoter region directs expression of enhanced green fluorescent protein (EGFP) primarily to adult mouse retinal Muller cells. Developmental expression of EGFP mostly parallels GFAP in retinal astrocytes. Expression of EGFP first appears in Muller cells around two weeks of age. However, not all Muller cells express EGFP.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 012588 | B6.Cg-Tg(TH-ALPP)1Erav/J | Cryopreserved - Ready for recovery |
| THpPLAP transgenic mice have the rat tyrosine hydroxylase (TH) promoter directing expression of the human Placental Alkaline Phosphatase (ALPP or hPLAP) gene. Homozygous THpPLAP mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PLAP intensely labels the outer surface of the cell membrane of TH-expressing dopamine (DA) releasing, catecholaminergic amacrines of the retina and the dopaminergic neurons of the brain, including those of the substantia nigra , VTA and olfactory bulb. Furthermore they label, less intensely , the neurons of the locus coeruleus (norepinephrine) and, weakly, the type 2 catecholaminergic amacrines of the retina (transmitter unknown). These mice may be useful for visualizing DA cells, and correlating their physiological properties with their synaptic connections by use of microscopy, electrophysiology, and molecular biology, and for studying the pathophysiology of Parkinson's d ..... For more information please see the full phenotype on the strain data sheet | ||
| 014131 | B6.Cg-Tg(Thy1-CFP)IJrs/GfngJ | Cryopreserved - Ready for recovery |
| These founder line I transgenic mice express Cyan Fluorescent Protein gene under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter. Fluorescence is detected in all motor axons, all retinal ganglion cells, dorsal root ganglion, neurons in cortical layers 2 through 6, and all of the cerebellar mossy fibers. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 000171 | B6.D2-KitW-45J/J | Cryopreserved - Ready for recovery |
| 001563 | B6.D2-KitW-73J/J | Cryopreserved - Ready for recovery |
| 006576 | B6.FVB-Tg(GNAT2-Dta)98Wwk/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "Trc-Tox176" transgene (also called "h-GNAT2pro-DTA") are viable and fertile. Expression of diphtheria toxin (DTA) from the transgene is similar to that of endogenous GNAT2, leading to ablation of both rod and cone photoreceptor development in the ventral retina (the abnormality is a result of abnormal cellular development rather than a consequence of retinal degeneration). The dorsal retina has nearly normal development of rods, but the development of cones is limited to about 10%. These transgenic mice exhibit an absence of cone photoreceptors in the retina, as well as the concomitant absence of rod photoreceptors in the ventral retina. The mice may be useful in studies of photoreceptor development, photoreceptor-related retinal diseases, and to profile photoreceptor genes in adult and in developmental stages. | ||
| 001612 | B6.KB2-Cln8mnd/MsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the motor neuron degeneration (mnd) spontaneous mutation show onset of disease between 5 and 11 months. Disease characterics include hindlimb weakness and ataxia which progresses to severe spastic paralysis of all limbs, with death usually by 9 to 14 months. Histological examination of the nervous system of affected animals shows sudanophyllic, autofluorescent intraneuronal inclusions characteristic of human neuronal ceroid lipofuscinosis suggesting that mnd mice are models for such human disease as Batten's disease. Performance at 14-16 weeks of age in an associative learning task is significantly decreased relative to controls, thus providing an early disease phenotype for this neuronal ceroid lipofuscinosis model. (Wendt KD, et al., 2005) Males and females are equally affected and both are fertile, although breeding efficiency is reduced. Homozygous mnd mice exhibit a retinopathy characterized by an early and progressive degeneration which ..... | ||
| 004620 | B6.L-Whll/J | Cryopreserved - Ready for recovery |
| Whll/+ mice have a moderate circling phenotype accompanied by a mild hearing impairment. | ||
| 001177 | B6.LP-KitW-49J/J | Cryopreserved - Ready for recovery |
| 002492 | B6.MDB-Mbpshi-mld/J | Cryopreserved - Ready for recovery |
| 003951 | B6.P2-P2rx3tm1Ckn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the P2rx3 gene are viable, fertile, normal in size and do not display any gross physical abnormalities. A significantly decreased nociceptive response (hindpaw lifting, licking, biting) is observed in response to injection of ATP, and to a lesser extent formalin. Responses to noxious thermal and mechanical stimuli are similar to that seen in wild-type mice. Aged mice may develop cutaneous hypersensitivity. Mice also exhibit urinary bladder hyporeflexia, characterized by decreased micturition (urination) frequencies and increased bladder capacities. Whole-cell patch-clamp analysis indicates that homozygote null mice lose the rapidly desensitizing ATP-induced currents in dorsal root ganglion. This strain is suitable for use in studies examining afferent sensory pathways. | ||
| 001271 | B6.RBF(C3Fe)-Nek1kat/J | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 007066 | B6.SJL-Tg(Crx-GFP,-ALPP)1Clc/J | Cryopreserved - Ready for recovery |
| Heterozygotes are viable and fertile. Expression of human placental alkaline phosphatase (PLAP) and GFP recapitulates that of the endogenous Crx promoter in the retina at embryonic time points as early as embryonic day 12.5 (E12.5) and in the retina of the adult mouse. This line also shows a more sensitive detection of Crx expression in the optic nerve of the developing retina. PLAP (but not GFP) expression is also found in fresh frozen pineal gland samples collected from adult mice. | ||
| 008616 | B6;129-Cdhr1tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous protocadherin 21 targeted mutation mice are viable and fertile and are normal in size and viability. They exhibit a slow retinal degeneration in which the outer segments of both rods and cones are disorganized and fragmented. Light responses of both rods and cones is only modestly compromised and phototransduction proteins appear to be correctly localized. This strain may be useful in studies of sensory neurons/photoreceptors, and retinal degeneration. | ||
| 011064 | B6;129-Cnga4tm1Reed/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by in situ hybridization analysis of olfactory receptor neurons from homozygotes. Beta-galactosidase expression is faintly detected in an incomplete mimic of the endogenous gene expression pattern, by histochemical analysis of olfactory epithelium and olfactory bulb. Olfactory receptor neuron channels from homozygotes have reduced desensitization rate and decreased affinity for cAMP. Homozygotes exhibit defective odor detection ability and reduced rate of odor adaptation due to impaired Ca2+-calmodulin mediated channel desensitization. | ||
| 004852 | B6;129-Crb1rd8/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 8 weeks of age revealed retinal spots predominantly in the inferior medial quadrant of the fundus, similar to those observed in Crb1rd8 mutants. The results of subsequent complementation tests and sequence analyses showed that these mutants represent the same mutation as rd8, an allele of Crb1, although the phenotypic expression observed in NMF144 is milder than that observed in Crb1rd8 mutants. Male or female mutants have been produced; the mice are fertile, and a colony can be maintained through regular breeding.
Standard pathology work-up on two mutants (69 or 109 days of age) showed bilateral retinal dysplasia in the older mutant and unilateral retinal dysplasia in the younger mutant. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Crb1rd8 (Cr ..... | ||
| 012823 | B6;129-Fzd4tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous Fzd4 (frizzled homolog 4 (Drosophila)) mice have a congenital retinal hypovascularization, a progressive inner ear vascular atrophy, a defect in the blood brain barrier in the cerebellum, and a progressive cerebellar degeneration associated with severe ataxia. Mice also show an absence of a skeletal muscle sheath around the lower esophagus associated with progressive esophageal distension. | ||
| 011078 | B6;129-Fzd4tm2.1Nat/J | Cryopreserved - Ready for recovery |
| This strain combines a conditional knockout and an alkaline phosphatase (AP) reporter of the frizzled 4 (Fzd4; Fz4) gene. LoxP sites flank the 5' and 3' UTR's. Without recombination, homozygotes of this allele are indistinguishable from wild type mice and the AP reporter is not expressed. Following cre-mediated recombination, the coding region is excised, and the downstream AP reporter is expressed under the control of the Fzd4 promoter in a cell/tissue-specific manner. Loss of Fzd4 signaling causes defective vascular growth which leads to chronic but reversible silencing of retinal neurons. Loss of expression in all endothelial cells disrupts the blood brain barrier in the cerebellum. This strain may be useful in studies of vascular growth, remodeling, maintenance and disease. | ||
| 008621 | B6;129-Fzd5tm1Nat/J | Cryopreserved - Ready for recovery |
| These frizzled 5 targeted mutant mice carry a beta galactosidase reporter. Heterozygous embryos show lacZ expression in the neural ridge at the anterior of the neural plate at E8.5, in the telencephalon, optic vesicle, hindgut and midgut at E10.5, and in the retinas at E16.5. Six-week-old animals express lacZ in the parafascicular nucleus and hypothalamus. Homozygous mice have placenta and yolk sac defects, thus die midway through gestation. In situ hybridization has confirmed that transcripts from the targeted gene are absent. | ||
| 008620 | B6;129-Fzd5tm2Nat/J | Cryopreserved - Ready for recovery |
| This is a conditional allele of the frizzled 5 gene in which the coding region was flanked by loxP sites and an alkaline phosphatase (AP) reporter was placed downstream. Cre-mediated recombination eliminates the coding region in a tissue-specific manner, ablates expression of the gene, and causes alkaline phosphatase (AP) to be expressed under the control of the frizzled 5 promoter. If both floxed alleles are excised, mutants are embryonic lethal at day 10 due to a placental defect. If recombination is mediated by an embryonic tissue-specific Cre, such as Sox2-Cre (e.g. Stock No's. 004783, 008454), mice show a loss of cells in the parafasicular nucleus (PFN) of the thalamus and defects in eye development.
When bred to a strain expressing a tamoxifen inducible Cre recombinase (see Stock No. 004847 ..... | ||
| 002201 | B6;129-Gja1tm1Kdr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gja1tm1Kdr targeted mutation die at birth. The cause of death is a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. The cardiac abnormality involves a delay in the normal looping of the ascending limb of the heart tube, which includes the right ventricle and the outflow tract. This predisposes homozygous mutant mice to malformations of the subpulmonary outflow tract and tricuspid valve. The mutation also predisposes mice to lens cataracts and causes a severe reduction of germ cell numbers in homozygous mutant mice of both sexes. Both neonatal and adult mice heterozygous for the Gja1tm1Kdr targeted mutation have slower ventricular epicardial conduction of paced beats in the heart. | ||
| 012287 | B6;129-Ndptm2Nat/J | Cryopreserved - Ready for recovery |
| This targeted mutation allele expresses a non-functional truncated protein from the Ndp (Norrie disease (pseudoglioma)(human)) gene. The C terminus lacks 11 amino acids. Mice display retinal hypovascularization. Vascular mural cells of the retina are thinner and at lower density in mutants as compared to wildtype, resulting in incomplete coverage of veins and capillaries. This strain may be useful in studies of a variety of angiogenic ocular diseases, including diabetic retinopathy and retinopathy of prematurity. | ||
| 005043 | B6;129-nmf166/J | Cryopreserved - Ready for recovery |
| Routine eye examination at 12 weeks of age revealed deep anterior chambers, lens extrusion cataracts, and angle dysgenesis in NMF166 mutants (n=29 eyes examined). Standard pathology work-up on two mutants (84 or 90 days of age) revealed bilateral cataracts and retinal rosettes. Atrophic testes and a lack of sperm (sperm apoptosis in the epididymis) were also noted. Male or female mutants have been produced, although so far males have not mated successfully.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf166 entry. | ||
| 006703 | B6;129P2-Gucy2dtm1Mom/MomJ | Cryopreserved - Ready for recovery |
| A subset of necklace glomeruli demarcating main and accessory portions of the olfactory bulb are labeled by lacZ driven by an axonally-expressed guanylate cyclase 2d (GC-D) promoter. | ||
| 006720 | B6;129P2-Olfr124tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons with the Olfr124 locus actively transcribed can be identified as expressing red fluorescent protein, even though no OLFR124 protein is expressed. The density of these cells in the septal organ is 14 times lower than OLFR124 expressing cells in mice with an intact Olfr124 locus tagged with an IRES-tauGFP. Of the OLFR124 deficient neurons, only 18% in the septal organ and only 14% in the main olfactory epithelium responded to all 5 odorants that stimulate 100% of OLFR124 expressing olfactory sensory neurons. This indicates that OLFR124 is responsible for the unusually broad response profile of the olfactory sensory neurons that express it. | ||
| 006689 | B6;129P2-Olfr151tm19Mom/MomJ | Cryopreserved - Ready for recovery |
| 006675 | B6;129P2-Olfr151tm25Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006676 | B6;129P2-Olfr151tm26Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006596 | B6;129P2-Olfr160tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006595 | B6;129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006712 | B6;129P2-Olfr545tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The Olfr545tm1Mom allele has a fully intact coding sequence with a tauGFP tag permitting bicistronic expression of the endogenous gene and the green fluorescent protein tag. The olfactory sensory neurons that express this tagged allele typically project to a single dorsal-medial and a single anterior-lateral glomerulus per olfactory bulb, and, when co-expressed with Tg(P-taulacZ)8Mom expression is found not to overlap. | ||
| 006713 | B6;129P2-Olfr545tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that select to express Olfr545 are labeled with tauRFP | ||
| 006716 | B6;129P2-Olfr545tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| With the coding sequence of class I olfactory receptor Olfr545 excised and replaced with venusYFP, this strain allows assessment of the role of a specific olfactory receptor in olfactory sensory neuron development. Mice carrying this allele display a normal pattern of labeled axons projecting diffusely to a large subset of glomeruli in the dorsal-medial and anterior-medial olfactory bulb, but also an abnormal finding of labeled axons innervating glomeruli at the caudal margins of the olfactory bulb. Co-staining for five dorsal class I olfactory receptors shows 3.8% co-expressing class I olfactory receptor genes and the disrupted Olfr545tm4Mom allele, while co-staining for five dorsal class II olfactory receptors shows no co-expression with the disrupted Olfr545tm4Mom allele. | ||
| 006667 | B6;129P2-Omptm3Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by GFP. The targeted mutation results in a knockout. Mature olfactory sensory neurons express GFP at high levels. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. Homozygous mice are subfertile. | ||
| 006668 | B6;129P2-Omptm4(cre)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by Cre. The targeted mutation results in a knockout. Mature olfactory sensory neurons express the Cre recombinase at high levels. Homozygous mice are subfertile. As an example, when crossed to a strain with widespread expression of GFP and a loxP-flanked Bgeo reporter (see Stock No. 004178), this mutant mouse strain may be useful in lineage tracing. View cre expression characterization. | ||
| 002466 | B6;129P2-Prkcctm1Stl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Prkcctm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits. | ||
| 006705 | B6;129P2-Sema3btm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Expression of the semaphorin 3B gene is blocked by the removal of the entire open reading frame. Homozygotes are viable, appear normal and are born at Mendelian frequencies. This strain may be useful in studies of axonal patterning in the olfactory nervous system. | ||
| 006710 | B6;129P2-Sema3ftm1Mom/MomJ | Cryopreserved - Ready for recovery |
| These mice carry a targeted mutation of the semaphorin 3F gene. Axonal wiring or some vomeronasal sensory neurons is perturbed by the deficiency. Homozygotes are smaller than wildtype mice during the first few weeks after birth. Fewer homozygotes than predicted by Mendelian ratios are produced from heterozygous crosses. This strain may be useful in studies of olfactory neurobiology. | ||
| 006728 | B6;129P2-Vmn2r26tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| Although the Vmn2r26tm2Mom allele does not express VMN2R26 protein, the vomeronasal sensory neurons actively transcribing this locus express green fluorescent protein. These neurons fail to respond, even at high concentrations, to MHC peptides or urine that stimulate VMN2R26-expressing vomeronasal sensory neurons. However, these non-responsive neurons will flux calcium normally in response to high potassium or a diacylglycerol analog, indicating normal signaling capacity. | ||
| 008686 | B6;129P2-Vmn2r81tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutant is valuable in characterizing the development of vomeronasal sensory neurons and the vomeronasal organ. While the axons of vomeronasal sensory neurons bearing the wild-type Vmn2r81 coalesce into glomeruli at several sites in the posterior accessory olfactory bulb, those of Vmn2r81tm4Mom homozygotes instead spread out diffusely over the posterior accessory olfactory bulb and a few extend into the anterior olfactory bulb. Distinct from normal vomeronasal sensory neurons at 3 weeks of age, 25% of those expressing lacZ, indicative of active transcription at the Vmn2r81 locus, also co-express transcript for another family ABD V2R gene. 68% of wild-type Vmn2r81-expressing neurons co-express Vmn2r2 but rarely co-express Vmn2r1. However, 9.5% of lacZ-bearing neurons also co-express Vmn2r1 and only 8.1% co-express Vmn2r2. 93% of wild-type Vmn2r81-expressing neurons co-express Omp, a marker of matu ..... For more information please see the full phenotype on the strain data sheet | ||
| 003728 | B6;129S-Sparctm1Hwe/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. The development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia. | ||
| 002537 | B6;129S2-Ccnd1tm1Wbg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002544 | B6;129S2-Ntrk2tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk2tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus. | ||
| 002481 | B6;129S2-Ntrk3tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk3tm1 targeted mutation (commonly referred to as trkC) die by 2-3 weeks of age. Homozygous mutant mice lack proprioceptive and cochlear neurons and have a reduction in vestibular neurons. | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by taulacZ, a fusion protein of the microtubule-binding protein tau (from bovine origin) and beta-galactosidase. The targeted mutation results in a knockout. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile. | ||
| 010535 | B6;129S4-Gabrr1tm1Llu/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes exhibit an increased sensitivity to mechanical pain and a decreased inhibition of stimulation-evoked spinal cord response following GABA application. This mutant mouse strain may be useful in studies of GABA-mediated pain sensory pathways. | ||
| 008419 | B6;129S4-Pkd1l3tm1Sul/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No expression was detected when the mice were examined by in situ hybridization of the taste buds. No phenotype has been observed in taste behavioral tests. | ||
| 011031 | B6;129S4-Shhtm1.1Rseg/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not exhibit patterning defects found in Shh null mutants. The R34A and K38A mutations are targeted to the conserved Cardin Weintraub motif and reduce SHH high-affinity proteoglycan binding. Homozygous mice exhibit reduced body weight, small eyes, hypoplasia of the cerebellum and olfactory bulb, reduced precursor cell proliferation in the cerebellar granule cell layer, the spinal cord, the subventricular zone and the hippocampal subgranular layer. This mutant mouse strain may be useful in studies of cell proliferation and SHH-signaling. | ||
| 004768 | B6;129S4-Ush1cdfcr-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for either Ush1cdfcr or Ush1cdfcr-2J display head tossing and hyperactive circling. They are unable to orient themselves in water to swim at the surface. Despite these behavioral traits, these mice are able to breed and have normal life spans. Adult homozygotes have no auditory-evoked brainstem response. This complete deafness was found in an Ush1cdfcr homozygote as early as 21 days of age. Scanning electron micrographs of the organ of Corti at 3 weeks of age reveal disorganized and splayed stereocilia of outer hair cells and, less severely, of inner hair cells along with degeneration of hair cells that yields a disorganized hair cell pattern. While progressive loss of hair cells and a secondary loss of spiral ganglion cells are found and are severe by 8 months of age, no gross morphological abnormalities were discerned in whole mounts of inner ears. At 9 months of age a slight peripheral retinal degeneration i ..... For more information please see the full phenotype on the strain data sheet | ||
| 004953 | B6;129S6-Gucy2etm1Gar/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of eye tissue. Progressive loss of electroretinograms (ERGs) of cone cells from homozygotes begins at age 3 to 5 weeks. ERGs are completely lost in mice older than 8 weeks of age. Histological analysis of mutants between 4 and 5 weeks of age reveals retinal cone cell atrophy and a reduction in the number of cone cells. Isolated retinal rod cells exhibit reduced a-wave and b-wave ERGs, and impaired photoresponse. This mutant mouse strain may be useful in studies of incomplete achromatopsia, progressive cone-rod dystrophy, retinitis pigmentosa and Leber congenital amaurosis. | ||
| 013041 | B6;129S6-Ppp1r14ctm1Uhl/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that the expected number of homozygotes are produced in heterozygous crosses. No gene product (mRNA) is detected by RT-PCR analysis of brain tissue from homozygotes. SNP analysis revealed that the Oprm1 allele variant, which is located close to the targeted gene, is from C57BL/6. Homozygotes exhibit increased phosphatase 1 activity in the thalamus. Homozygotes develop faster morphine tolerance in a hot plate assay ("supraspinal" nociceptive response assessment) and a rightward shift in dose response curve for morphine reward in conditioned place preference when compared to wildtype controls. | ||
| 008645 | B6;129S7-Pou4f3tm1Xia/J | Cryopreserved - Ready for recovery |
| These mice carry a targeted mutation of the POU domain, class 4, transcription factor 3 gene. Homozygotes are deaf, have impaired balance, and display a robust circling behavior due to defects of the inner ear. Auditory and vestibular hair cells are lost during late embryonic and early postnatal periods. A secondary loss of spiral and vestibular ganglion neurons is also seen. This strain may be useful in studies of auditory and vestibular system development. | ||
| 012238 | B6;129X1-Nrtntm1Jmi/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Homozygotes exhibit a decrease in small fiber density in the small intestine, colon and duodenum, reduced myenteric ganglion cell size, and reduced gut motility. By two months of age, mice can be identified by eyelid droopiness, crusting around the eye, eyelid thickening and reduced tear production most likely the result of reduced parasympathetic innervation of the lacrimal gland. Parasympathetic neurons in the submandibular salivary gland and the ciliary ganglion are reduced in number, despite apparently normal function. Otic ganglion cells are reduced in size, but not in number. This mutant mouse strain may be useful in studies of the enteric, parasympathetic and sensory nervous systems. | ||
| 008618 | B6;A-Tg(OPN1LW-lacZ)1Nat/J | Cryopreserved - Ready for recovery |
| Cone photoreceptors in these mice express lacZ driven by the human red cone specific opsin promoter. LacZ is expressed in both the medium and short wavelength cones of the retina. Hemizygotes and homozygotes are normal in size, viability, and fertility. | ||
| 004502 | B6;AKR-Lxl2/GrsrJ | Cryopreserved - Ready for recovery |
| This dominant mutation causes the animal to present with all four limbs at odd angles to the body. There are extra toes on all four limbs and the rear legs are oriented backward. Severe arthritis of the knee was observed in one female, but no other histological lesions were seen. | ||
| 003892 | B6;BKS-Atp2b2dfw-3J/J | Cryopreserved - Ready for recovery |
| 007986 | B6;CBA-Tg(H*/Olfr16-GFP)11Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene provides a control for that used in stocks #007980 and #007981 for investigating the promoter elements important in olfactory receptor expression. It encodes the same full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control of the 405 base pairs of regulatory sequence just upstream of the Olfr16 transcription start site and 9 equally spaced repeats of a mutated homeodomain binding sequence, upstream of this promoter. Each of the homeodomain sequences has two A to G mutations disrupting the binding site. These mutations in the homeobox domains reverse the massive increase in the number of cells expressing this olfactory receptor found in the transgenics with intact homeobox domains. The expression pattern for this transgenic instead resembles that of wild-type endogenous OLFR16 expression. | ||
| 007987 | B6;CBA-Tg(H*/Olfr16-GFP)25Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene provides a control for that used in stocks #007980 and #007981 for investigating the promoter elements important in olfactory receptor expression. It encodes the same full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control of the 405 base pairs of regulatory sequence just upstream of the Olfr16 transcription start site and 9 equally spaced repeats of a mutated homeodomain binding sequence, upstream of this promoter. Each of the homeodomain sequences has two A to G mutations disrupting the binding site. These mutations in the homeobox domains reverse the massive increase in the number of cells expressing this olfactory receptor found in the transgenics with intact homeobox domains. The expression pattern for this transgenic instead resembles that of wild-type endogenous OLFR16 expression. | ||
| 007979 | B6;CBA-Tg(H/Olfr16-GFP)3Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes the full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control of 9 equally spaced repeats of the HD binding sequence and the 405 base pairs of regulatory sequence just upstream of the Olfr16 transcription start site. A massive increase is found in the number of cells that express this olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium, with some transgenic lines having additional narrow ventral domain expression. | ||
| 007980 | B6;CBA-Tg(H/Olfr16-GFP)4Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes the full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control of 9 equally spaced repeats of the HD binding sequence and the 405 base pairs of regulatory sequence just upstream of the Olfr16 transcription start site. A massive increase is found in the number of cells that express this olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium, with some transgenic lines having additional narrow ventral domain expression. | ||
| 007981 | B6;CBA-Tg(H/Olfr16-GFP)6Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes the full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control of 9 equally spaced repeats of the HD binding sequence and the 405 base pairs of regulatory sequence just upstream of the Olfr16 transcription start site. A massive increase is found in the number of cells that express this olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium, with some transgenic lines having additional narrow ventral domain expression. | ||
| 007984 | B6;CBA-Tg(H/Olfr16-taumCherry,-tauGFP)11Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgenic strain encodes two co-injected transgenes that both have 9 equally spaced repeats of the homeodomain binding sequence linked to the 405 base pairs of regulatory sequence just upstream of the transcription start site for Olfr16 driving expression of the full coding sequence of Olfr16 and either an IRES-tauGFP or an IRES-taumCherry just after the stop codon resulting in bicistronic expression of a fluorescent marker with the transgenically expressed olfactory receptor. Similar to the findings in strains bearing just one construct (see stocks #007979, #007980 and #007981) a massive increase is found in the number of cells that express the transgenic olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium. Expression of the co-injected transgenes is mutually exclusive with red and green fluorescence not found to overlap, proving that, despite an increase in ..... For more information please see the full phenotype on the strain data sheet | ||
| 007985 | B6;CBA-Tg(H/Olfr16-taumCherry,-tauGFP)13Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgenic strain encodes two co-injected transgenes that both have 9 equally spaced repeats of the homeodomain binding sequence linked to the 405 base pairs of regulatory sequence just upstream of the transcription start site for Olfr16 driving expression of the full coding sequence of Olfr16 and either an IRES-tauGFP or an IRES-taumCherry just after the stop codon resulting in bicistronic expression of a fluorescent marker with the transgenically expressed olfactory receptor. Similar to the findings in strains bearing just one construct (see stocks #007979, #007980 and #007981) a massive increase is found in the number of cells that express the transgenic olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium. Expression of the co-injected transgenes is mutually exclusive with red and green fluorescence not found to overlap, proving that, despite an increase in ..... For more information please see the full phenotype on the strain data sheet | ||
| 007982 | B6;CBA-Tg(H/Olfr16-taumRFP,-tauGFP)8Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgenic strain encodes two co-injected transgenes that both have 9 equally spaced repeats of the homeodomain binding sequence linked to the 405 base pairs of regulatory sequence just upstream of the transcription start site for Olfr16 driving expression of the full coding sequence of Olfr16 and either an IRES-tauGFP or an IRES-tauRFP just after the stop codon resulting in bicistronic expression of a fluorescent marker with the transgenically expressed olfactory receptor. Similar to the findings in strains bearing just one construct (see stocks #007979, #007980 and #007981) a massive increase is found in the number of cells that express the transgenic olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium. Expression of the co-injected transgenes is mutually exclusive with red and green fluorescence not found to overlap, proving that, despite an increase in the ..... For more information please see the full phenotype on the strain data sheet | ||
| 007983 | B6;CBA-Tg(H/Olfr16-taumRFP,-tauGFP)9Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgenic strain encodes two co-injected transgenes that both have 9 equally spaced repeats of the homeodomain binding sequence linked to the 405 base pairs of regulatory sequence just upstream of the transcription start site for Olfr16 driving expression of the full coding sequence of Olfr16 and either an IRES-tauGFP or an IRES-tauRFP just after the stop codon resulting in bicistronic expression of a fluorescent marker with the transgenically expressed olfactory receptor. Similar to the findings in strains bearing just one construct (see stocks #007979, #007980 and #007981) a massive increase is found in the number of cells that express the transgenic olfactory receptor, relative to the endogenous expression pattern, but the pattern of expression remains predominantly in the dorsal main olfactory epithelium. Expression of the co-injected transgenes is mutually exclusive with red and green fluorescence not found to overlap, proving that, despite an increase in the ..... For more information please see the full phenotype on the strain data sheet | ||
| 007978 | B6;CBA-Tg(Hf/Olfr16-GFP)47Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes the full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control 405 base pairs of regulatory sequence just upstream of the transcription start site with an additional 2.1 kb H element in the forward orientation upstream of this promoter to assess the ability of this element to enhance expression. This line for this transgenic construct expresses a mildly enhanced but normal pattern of expression for this olfactory receptor. | ||
| 007974 | B6;CBA-Tg(Olfr160-taulacZ)V4-7Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 135 base pairs upstream of the Olfr160 transcription start site and 163 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows mosaic expression of LacZ in the main olfactory epithelium with the expression ventralized compared to the normal pattern of Olfr160 expression. | ||
| 006743 | B6;CBA-Tg(P-taulacZ)11Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)11Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006793 | B6;CBA-Tg(P-taulacZ)13Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)13Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006742 | B6;CBA-Tg(P-taulacZ)8Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)8Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. When mice co-express both this transgene and a YFP labelled null allele of Olfr545, a class I olfactory receptor, they label distinct regions; when mice co-express both this transgene and a GFP labelled null allele of Olfr160, a class II olfactory receptor, they label the same reg ..... For more information please see the full phenotype on the strain data sheet | ||
| 006033 | B6;CByJ-nmf445/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf445 entry. | ||
| 012341 | B6;SJL-Tg(Thy1-COP3/EYFP)1Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012344 | B6;SJL-Tg(Thy1-COP3/EYFP)4Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut ..... For more information please see the full phenotype on the strain data sheet | ||
| 000126 | B6By.Cg-Sd Mcoln3Va-J Krt25Re/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-J) are more pigmented than the original varitint waddler mice (Mcoln3 Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying two other mutations, rex (Krt25Re) and Danforth's short tail (Sd). | ||
| 000836 | B6By.Cg-Sig/J | Cryopreserved - Ready for recovery |
| 000505 | B6C3 Aw-J/A-Mutedmu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the muted spontaneous mutation (Mutedmu) have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths from the sacculus and utriculus of one or both ears. The bony labyrinth is normal; the mice are not deaf and do not circle. Mutant mice have prolonged bleeding times and a platelet storage pool deficiency (SPD) associated with abnormalities of the dense granules of the blood platelets. The combination of pigment, otolith, and SPD abnormalities also occurs in two other mouse mutants, pallid and mocha (Ap3d1mh), and is also seen in human Hermansky-Pudlak syndrome. | ||
| 000506 | B6C3Fe a/a-Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 001037 | B6C3Fe a/a-Agtpbp1pcd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Purkinje cell degeneration spontaneous mutation (pcd) show a moderate ataxia beginning at 3 to 4 weeks. Homozygous mutant mice are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic nuclei begin to appear in the photoreceptor cells between 18 and 25 days, and the outer rod segments become disorganized. Degeneration of the photoreceptor cells proc ..... For more information please see the full phenotype on the strain data sheet | ||
| 000636 | B6C3Fe a/a-Lmx1adr-J/J | Cryopreserved - Ready for recovery |
| Lmx1a encodes a LIM homeodomain (LIM-hd) protein that is expressed in the roof plate along the neuraxis during CNS development. The Lmx1adr-J mutation replaces a conserved cysteine in the LIM1 domain of the protein with a tyrosine (Millonig et al. 2000). Mice homozygous for Lmx1adr-Jare identifiable at birth by a thin filament extending from the end of the tail, which drops off within a few days, and a short or blunt tail. They may also have a head bleb. When fur develops, there may be a white belly spot. Lmx1adr-J/Lmx1adr-J mice are ataxic and hyperactive and have difficulty righting themselves, and they do not reproduce (Sweet and Wahlsten 1983). They also exhibit circling behavior, are deaf, and have inner ear and vertebral malformations (Manzanares et al. 2000).
Lmx1adr-J homozygotes exhibit defects of three classes of anatomic structures: the hindbrain roof plate, neural crest derived ..... | ||
| 001280 | B6C3Fe a/a-Lse/J | Cryopreserved - Ready for recovery |
| Lse/+ pups can be identified at birth by the presence of an open auditory meatus, which in normal mice remains closed until approximately day 13, when the eyes also open. Fewer than the expected 50% affected pups are born, and about 50% of pups identified as Lse/+ fail to survive until weaning. Homozygotes either die prenatally or are indistinguishable from heterozygotes. The ears of Lse/+ mice are positioned lower and further forward than those of normal mice and are abnormally formed. These mice are not deaf. In addition to the ear abnormalities, Lse/+ mice are smaller than their normal littermates and have opaque corneas (Theiler and Sweet 1986). | ||
| 001573 | B6C3Fe a/a-MitfMi/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the MitfMi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 000181 | B6C3Fe a/a-Otogtwt/J | Cryopreserved - Ready for recovery |
| When mice homozygous for the twister spontaneous mutation (twt) are picked up by the tail, all affected mice tuck their heads. Homozygous mutant mice may show circling behavior or tilted heads and none can swim. These mice are deaf. | ||
| 002078 | B6C3Fe a/a-Pcdh15av-2J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (av) that have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames waltzer 2 Jackson homozygous mutant mice (av2J/av2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av2J/av2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3 Jackson homozygotes (av3J/av3J), like Ames waltzer Jackson homozygotes (avJ/avJ), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 000230 | B6C3Fe a/a-Tcirg1oc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the osteosclerotic spontaneous mutation (oc) can be recognized at about 10 days by failure of eruption of the incisors, clubbed feet, and circling behavior. Homozygous mutant mice may also have a kinked tail. They grow normally for about the first 10 days of life, then lose weight or at least fail to gain. | ||
| 000063 | B6C3Fe a/a-sy/J | Cryopreserved - Ready for recovery |
| Most mice homozygous for the shaker-with-syndactylism mutation (sy) die within the first month, and none have lived to breed. Homozygous mutant mice may be syndactylous on all four feet; the forefeet may often be normal and possibly one or both hindfeet very occasionally so. The remainder of the skeleton shows many slight anomalies in addition to small size. The shafts of the long bones are considerably thinner than normal, and there are differences in shape of the sacral vertebrae and the scapula. Abnormal behavior appears during the first week. It consists of head-tossing and some circling, and the affected mice are always deaf. Abnormalities of the labyrinth can be seen at E13. | ||
| 000296 | B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-J) are more pigmented than the original varitint waddler mice (Mcoln3Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes of the two alleles (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying the semidominant hypodactyly spontaneous mutation (Hoxa13Hd). Heterozygous hyp ..... For more information please see the full phenotype on the strain data sheet | ||
| 003301 | B6C3FeF1 a/A-Eya1bor/J | Cryopreserved - Ready for recovery |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. The Eya1bor/Eya1bor mice are deaf and their behavior is marked by circling and head-bobbing. They lack all but the most basal one-quarter of the cochlea, and the organ of Corti is completely absent. They have foreshortened, narrower semicircular canals and in some the common crus is incomplete. Their kidneys are absent or dysmorphic with greater severity generally on the left side. Fewe ..... For more information please see the full phenotype on the strain data sheet | ||
| 000956 | B6CB-Mitfmi-rw/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. | ||
| 000287 | B6CBACa Aw-J/A-Plp1jp EdaTa/J | Cryopreserved - Ready for recovery |
| Hemizygous males carrying the X-linked jimpy spontaneous mutation (Plp1jp) appear normal when sitting quietly, but beginning at about 3 weeks of age they show a marked tremor of the hindquarters when attempting movement. After 3 weeks of age convulsions may occur. These males die between 20 and 40 days of age. In males, the CNS is very deficient in myelin, but the PNS is normally myelinated. Heterozygous jimpy females have normal lifespans with no overt phenotype. However, jimpy heterozygous females are reported to have reduced numbers of oligodendrocytes compared to wildtype females. While the mutation is recessive, only partial phenotypic rescue was attained by the transgenic expression of the two major isoforms, PLP and DM20, suggesting a dominant negative action from this allele (Nandon et al., 1994). This stock is also carrying the X-linked tabby mutation (EdaTa). | ||
| 000288 | B6CBACa Aw-J/A-we a Mafbkr/J | Cryopreserved - Ready for recovery |
| 002557 | B6Ei.GL-Nox3het/J | Cryopreserved - Ready for recovery |
| Head tilt (het) is an autosomal recessive mutation that can cause abnormal circling behavior and hyperactivity in affected mice. Homozygotes also exhibit a subtle head tilt. Together, the abnormal behavioral phenotype is consistent with that of a vestibular disorder. Evoked auditory brainstem response profiles are normal indicating that the mutants are not deaf. het/het mutants are unable to sense orientation under water and therefore, cannot swim properly. If held by the tail, het/het mice retract, rather than extend, their limbs; they also flex ventrally, instead of dorsally as wild type mice do. When lowered quickly by the tail, het/het mice fail to extend their forelimbs in a normal manner and have difficulty righting themselves if dropped vertically from a short distance. Morphological assessment of the inner ear of homozygotes reveals an abnormal appearance of the saccule and utricle owing to a complete absence of otoliths. Otoliths are tiny cal ..... For more information please see the full phenotype on the strain data sheet | ||
| 000551 | B6EiC3 a/A-Tbx15de-H/J | Cryopreserved - Ready for recovery |
| 000503 | B6EiC3Sn a/A-Gy/J | Cryopreserved - Ready for recovery |
| Gyro (Gy) is an X-linked dominant mutation that causes circling behavior and defects in phospate metabolism. It is allelic with the hypophosphatemia mutation (PhexHyp). Hemizygous males and heterozygous females are characterized by hypophosphatemia, rickets, circling behavior, and inner ear abnormalities. Affected males are also sterile. | ||
| 002432 | B6J x B6.C-H2-Kbm1/ByJ-Cdh23v-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the waltzer Jackson spontaneous mutation (Cdh23v-J) exhibit the circling, head-tossing, deafness, and hyperactivity typical of circling mutants. Homozygous mutant mice are very similar to other waltzer mutants (Cdh23v and Cdh23v-2J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (Cdh23v/+ Myo7ash1/+) become deaf by 3 to 6 months of age. Double heterozygotes show degeneration in the organ of Corti, stria vascularis, and spiral ganglion similar to that of Cdh23v-J homozygotes, but less severe and with much later onset. Viability and breeding ability are somewhat reduced. | ||
| 004771 | BALB/cBy-Ush1cdfcr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for either Ush1cdfcr or Ush1cdfcr-2J display head tossing and hyperactive circling. They are unable to orient themselves in water to swim at the surface. Despite these behavioral traits, these mice are able to breed and have normal life spans. Adult homozygotes have no auditory-evoked brainstem response. This complete deafness was found in an Ush1cdfcr homozygote as early as 21 days of age. Scanning electron micrographs of the organ of Corti at 3 weeks of age reveal disorganized and splayed stereocilia of outer hair cells and, less severely, of inner hair cells along with degeneration of hair cells that yields a disorganized hair cell pattern. While progressive loss of hair cells and a secondary loss of spiral ganglion cells are found and are severe by 8 months of age, no gross morphological abnormalities were discerned in whole mounts of inner ears. At 9 months of age a slight peripheral retinal degeneration is fou ..... For more information please see the full phenotype on the strain data sheet | ||
| 005348 | BALB/cByJ Agtpbp1pcd-3J-Bmp5cfe-se6J/GrsrJ | Cryopreserved - Ready for recovery |
| The ear pinnae of homozygotes are ragged around the edges, yet uniform, and smaller than normal. | ||
| 006274 | BALB/cByJ-Dfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the deaf ballerina mutation display circling and head tossing behavior, are deaf, and lack the corpus callosum. Heterozygous females do not breed. | ||
| 003756 | BALB/cByJ-nr/J | Cryopreserved - Ready for recovery |
| On the BALB/cByJ background nervous homozygotes have a delayed expression of the mutant phenotype relative to that on the C3HeB/FeJ background (see Stock No. 000229). At 8 to 9 weeks of age homozygotes have a ruffled and disheveled appearance and are slightly smaller than their affected littermates. They are ataxic, having an unsteady gait particularly in the hindquarters, but do not display tremors. They are more active than their littermates. Males and females are affected equally and have a normal lifespan. These mice are good breeders with few non-productive matings. A cross between C3Fe.CGr(Cg)-nr/J homozygotes and BALB/cByJ-nr/J homozygotes produced compound heterozygotes most of which presented with the nervous phenotype by 4 weeks of age, although some had onset delayed as much as to 7 weeks of age (Giggey and Thompson, 2005). There is a 90% loss of Purkinje cells between 23 and 50 days in homozygous mu ..... | ||
| 002026 | BALB/cHeA-Foxe3dyl/J | Cryopreserved - Ready for recovery |
Dysgenetic lens (Foxe3dyl) was originally characterized as an autosomal recessive mouse mutant but Foxe3 haploinsufficiency can also yield a similar phenotype characterized by defective lens development and cataracts. Homozygotes are viable and fertile. The most prominent abnormality is the irregular shape and reduced size of the lens. The pupil is also smaller and exhibits abnormal reactivity. The major morphological hallmark of homozygous Foxe3dyl mice is the persistent attachment of the lens to the corneal epithelium. The iris can also be fused with the lens but the retina remains unaffected. The lens contains fewer secondary fibers but when present, these fibers are very disorganized and the tissue contains large vacuoles. The developing lens initially forms properly as the lens placode is induced within the anterior neural ectoderm but around embryonic day 10 the mutant lens vesicle does not completely close and detach from the ..... | ||
| 005226 | BALB/cJ-Mbpshi-J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the shiverer Jackson mutation can be identified at 12 days of age by a generalized tremor during locomotion and the severity of the phenotype progresses with age and includes a loss of coordination of the hindlimbs. Deficiency of myelin from the central nervous system has been found at 7 weeks of age, the earliest time-point assessed. | ||
| 000652 | BDP/J | Cryopreserved - Ready for recovery |
| 004949 | BKS(Cg)-Grxcr1pi-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 3 Jackson mutation display bi-directional circling and head bobbing and are completely deaf by ABR assessment. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 004176 | BKS.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 003929 | BXA4/Pgn-Tmiesr-J/J | Cryopreserved - Ready for recovery |
| 006816 | BXA7/Pgn-Slc26a4pdsm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pdsm mutation display head bobbing, circling, and occasional head tilt, evident by 3 weeks of age. The inner ear defects include diminished or absent otoconia, hair cells and spiral ganglion cells, malformed tectorial membrane, a reduction in the number of cochlear turns, degeneration of the organ of Corti, and displacement of Reissner's membrane resulting in enlarged scala media. Serum chemistry and histology failed to detect any signs of hypothyroidism. | ||
| 002368 | C.129S4(B6)-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 002439 | C3.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet | ||
| 005494 | C3.129S1(B6)-Grm1rcw/J | Cryopreserved - Ready for recovery |
| Visibly, Grm1rcw/Grm1rcw mice are identifiable by 2.5 - 3 weeks of age. Their constant wobbly gait frequently throws them off balance, but only briefly, as they show immediate and normal righting response. When walking, they often brace for balance with their fore- and hindfeet extended forward or sideways. Their heads lurch mildly and the mutants often sit on their haunches when motion falters. Their forefeet show normal grip strength when the mutant mice are pulled gently backwards over a cage cover. When picked up by the tail, they may clasp their hindfeet. However, they show sufficient hindlimb strength to prevent their falling when placed on an edge. Mutants live through adulthood, and mice of both sexes breed. Grm1rcw has been mapped between the flanking markers D10Mit49, at map position 6.3 Mb and D10Mit80, at map position 11.4 Mb. | ||
| 002000 | C3.Cg-CrygeElo/J | Cryopreserved - Ready for recovery |
| Heterozygotes and homozygotes have microphthalmia with normal ocular structures except for the lens. Homozygotes are viable and fertile. At embryonic day 12 there is poor elongation of the basal cytoplasm of the central lens fibers and the lens cavity remains open. At embryonic day 13 the elongation of the lens fiber and the convex nuclear arrangement shows poor progression, the central lens fibers are deranged, and the lens fibers are detached from the capsule at the basal surface. At birth the lens is approximately half the normal size and is deformed, with the lens cavity remaining open. In heterozygotes and homozygotes the lens degenerates by 30 days of age. | ||
| 001768 | C3.Cg-Irs1Sml H2b/GrsrJ | Cryopreserved - Ready for recovery |
| The small mutation causes hyperinsulinemia with only mild insulin resistance, a paucity of body fat, deficiencies in bone development and homeostasis, and hearing loss. Homozygotes can be distinguished by 2 weeks of age by their smaller body size and thin short tails, and adult homozygotes are visibly smaller with a tail that is 20% shorter than in wild-type controls. Hearing loss was shown through increased ABR threshold values when assessed between 8 and 12 weeks of age. The skeletal defects include shortened femurs with smaller growth plates, decreased cortical and trabecular thickness and abnormal trabecular number, with an increase in the number of osteoclasts and osteoblasts per bone perimeter but impaired osteoblast proliferation and differentiation in culture. This spontaneous point mutation is semidominant in some aspects of phenotype, unlike targeted mutations of this gene. Heterozygotes are statistically smaller than wild-type controls, but the severity of dwarfing is not ..... For more information please see the full phenotype on the strain data sheet | ||
| 000509 | C3.Cg-Lystbg-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the beige 2J spontaneous mutation (Lystbg-2J) display characteristics very similar to the original beige mutation (Lystbg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet | ||
| 001957 | C3A Pde6brd1.O20/A-Prph2Rd2/J | Cryopreserved - Ready for recovery |
| 005973 | C3Bir.129P2(B6)-Il10C3Bir/LtJ | Cryopreserved - Ready for recovery |
| This is a control strain for C3Bir.129P2(B6)-Il10tm1Cgn/Lt (Stock No. 004326), developed in parallel with the latter until backcrossing was complete. As such, it does not exhibit the Il10-deficient phenotype. | ||
| 003968 | C3Bir.129P2(B6)-Il10tm1Cgn/LtJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000229 | C3Fe.CGr(Cg)-nr/J | Cryopreserved - Ready for recovery |
| Nervous homozygotes on this C3HeB/FeJ congenic background display a mutant phenotype by 3 to 4 weeks of age, much earlier than on the BALB/cByJ background (see Stock No. 003756). Because this earlier onset occurs at wean age, the affected pups may have to stay with the mother an extra week or two. Homozygotes are somewhat smaller than their littermates and are ataxic with a slight head bobbing motion but do not display tremors. They often fall over on their side and have a sort of backwards lurching movement. They have a tendency to look up and are hyperactive compared to their littermates. Males and females are equally affected and have a normal lifespan. They are poor breeders with a higher than normal incidence of non-productive matings. A cross between C3Fe.CGr(Cg)-nr/J homozygotes and BALB/cByJ-nr/J homozygotes produced compound heterozygotes most of which presented with the nervous phenotype by 4 weeks of age, ..... For more information please see the full phenotype on the strain data sheet | ||
| 000638 | C3FeB6 A/Aw-J-Spnb4qv-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering-Jackson spontaneous mutation (Spnb4qv-J) are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their young. | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 001904 | C3H-Atcayji-hes/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hesitant spontaneous mutation (Atcayji-hes) can be recognized at 14 days of age by their slightly smaller size and hesitant walking motion. From 3 weeks of age on, the hindlimbs of homozygous mutant mice hesitate after lifting and then are placed flat on the surface and stiffly extended causing the posterior to rise. No body tremors, spasticity, or muscle degeneration is observed. Homozygotes of both sexes are fertile, although fertility in males may be reduced. | ||
| 000511 | C3H/HeJ-Ap3d1mh-2J/J | Cryopreserved - Ready for recovery |
| The mh-2J allele of Ap3d causes a similar yet less severe pigment dilution than that caused by the mh allele, but each causes a different neurological phenotype. These homozygotes are recognizable by a lighter coat color and decreased pigmentation in the eyes. For the Ap3dmh allele, this coat color dilution has been shown to result from smaller and fewer melanin granules in the hairs. While both alleles cause similar degrees of hyperactivity, the cochlear degeneration and accompanying head tilt is observed less frequently in the Ap3dmh-2J homozygotes and the auditory evoked brain responses in these mice are similar to wildtype. At three months of age, mice homozygous for the Ap3dmh allele have significantly increased auditory evoked potentials after the first of two paired tones. Ap3dmh-2J homozygotes also show an increased response to the first tone, but this has not been proven with stat ..... For more information please see the full phenotype on the strain data sheet | ||
| 001276 | C3H/HeJ-Atp2b2dfw/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the deaf waddler spontaneous mutation (Atp2b2dfw) are deaf, walk with a hesitant, wobbly gait, and bob their heads. Both sexes are fertile. | ||
| 000784 | C3H/HeJ-Faslgld/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. | ||
| 000627 | C3H/HeJ-KitW-x/J | Cryopreserved - Ready for recovery |
| 002433 | C3H/HeJ-Spnb4qv-lnd2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive Spnb4qv-lnd2J mutation are identifiable by two weeks of age by their small size relative to their littermates. Their bodies quiver, and their movements are less coordinated than those of littermates. Mutants become progressively wasted and die by four weeks of age. (Cook 1995; Samples 2003) Their phenotype is more severe than that of mice homozygous for the original Spnb4qv-lnd allele, which survive at least 10 months. Spnb4qv-lnd/Spnb4qv-lnd mice were found to have dystrophic axons in the lower lumbar and sacral spinal cord. The dystrophic axons were observed in both white and gray matter, but particularly in dorsolateral white matter (Bronson et al. 1992). The acoustic brainstem response ABR) pattern of Spnb4qv-lnd2J homozygous mice exposed to click stimuli of 80, 70, 60 and 50 decibels exhibited only the first expected peak, indicating the mice have norm ..... For more information please see the full phenotype on the strain data sheet | ||
| 005972 | C3H/HeJBirLtJ | Cryopreserved - Ready for recovery |
| Under conventional housing conditions, C3H/HeJBirLtJ mice develop spontaneous colitis. It should be noted that the phenotype of cecocolitis in this strain requires an interaction with an as yet undefined component of the enteric flora. Inflammation is present mainly in the cecum and right colon. Colitis develops early in life and resolves by three months of age. The colitis is characterized by acute and chronic inflammation, ulcerations, crypt abscesses, regenerative hyperplasia and submucosal scarring. A mild recurrence of the disease can occur after one year. Small lesions at the anorectal junction are common throughout life. | ||
| 001824 | C3H/HeJSxJ | Cryopreserved - Ready for recovery |
| 000474 | C3H/HeSn | Cryopreserved - Ready for recovery |
| 000316 | C3H/HeSn-Gpr161vl/J | Cryopreserved - Ready for recovery |
| 001431 | C3H/HeSn-ocd/J | Cryopreserved - Ready for recovery |
| 002235 | C3H/HeSnJ-Ctnna2cdf/J | Cryopreserved - Ready for recovery |
| Cerebellar deficient folia (cdf) is a recessive mutation which maps to chromosome 6. Homozygotes display a constant side-to-side wobble in their gait that is apparent as early as 2 weeks of age. Additionally, they often hold their tails off the surface or arch them over their heads while moving. Smaller size is detectable in homozygotes by two weeks of age, at weaning they weigh approximately 25% less than littermate controls, and as adults they weigh, on average, 50% less. These mutants live a normal life span (one-and-a-half to two years on the C3H/HeJ background), but homozygous males rarely breed and homozygous females are poor mothers requiring transfer of litters to foster mothers. The cdf mutation causes a hypoplastic and dysmorphic cerebellum. On the C3H/HeJ background, homozygotes have only 7 cerebellar folia rather than the 10 present in wildtype, and the folia pattern is abnormal. Their vermis is one-third smaller than wildtype in rostro-caudal length ..... | ||
| 002333 | C3H/HeSnJ-gri/J | Cryopreserved - Ready for recovery |
| On an agouti background gri homozygotes resemble Tyrc-ch homozygotes. There is a graying of the coat due to a lighter than normal phaeomelanin band. There is no change in eye color. gri homozygotes are slightly smaller than their unaffected littermates. Homozygous females breed well, but homozygous males often do not breed. Testis biopsies failed to identify any sperm abnormalities. The gri mutation does not cause a clotting disorder. (Davisson et al., 2000.) | ||
| 003532 | C3HeB.129S7-Kcna1tm1Tem/J | Cryopreserved - Ready for recovery |
| Homozygous null mice display an epileptic phenotype (episodic eye blinking, twitching of vibrissae, forelimb paddling, arrested motion, hyperstartle response) beginning during the third postnatal week. Quantitative RNase protection analysis on brain tissue indicates that in heterozygous mice the Kcna1 transcript is reduced to approximately half that observed in wild-type littermates. No transcripts were detected in homozygous mice. Approximately 50% of the homozygous mice die between the third and fifth weeks of life. Mice surviving this period survive for varying periods, depending on genetic background; congenic C3HeB/FeJ mice usually die at 6-8 weeks; hybrid N:NIHS-BC mice have been maintained for over 12 months during which they continue to display spontaneous seizures. A similar phenotype with spontaneous seizures has been observed in mice having 129/Sv, C3HeB/FeJ, C57BL/6 X 129/Sv, and 129/Sv X N:NIHS-BC backgrounds. | ||
| 006435 | C3HeB.SW-Soaa/MonJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the dominant a allele exhibit an taster (avoidance as low as <.001mM concentration) phenotype to the bitter compound sucrose octaacetate. This strain may be useful in studies related to the mechanisms of taste. | ||
| 001434 | C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Zeb1Tw/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the twirler mutation (Zeb1Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1rE-so) and extra toes-Jackson (Gli3St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube a ..... For more information please see the full phenotype on the strain data sheet | ||
| 001576 | C3HeB/FeJ-Atp7btx-J/J | Cryopreserved - Ready for recovery |
| 002588 | C3HeB/FeJ-Eya1bor/J | Cryopreserved - Ready for recovery |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. During mapping crosses using CAST/Ei and C3H/HeJ, it was found that genetic background impacts both the kidney and inner ear phenotypes, and modifier genes in humans also may impact the severity of Branchio-Oto-Renal-Syndrome. | ||
| 001533 | C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. This strain is homozygous for the sombre mutation (Mc1rE-so). | ||
| 004406 | C3HeB/FeJ-Pou3f4del-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pou3f4del-J display head shaking and circling behavior by three weeks of age. Homozygous females and males hemizygous for this X-linked mutation have profound deafness, although heterozygous females do not. They have cochlear hypoplasia, a reduced number of cochlear turns, failure to fully form the bony structure of the modiolus, and detachment of the stria vascularis. | ||
| 001886 | C3HeB/FeJLe a/a-gnd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the generalized neuroaxonal dystrophy spontanteous mutation (gnd) have large numbers of dystrophic axons in all white matter funiculi and in central grey matter at all levels of the spinal cord. Dystrophic axons also common throughout the brain stem. In the forebrain, some can be seen in the optic nerves and tracts, corpus callosum, rostral commissure, and fornix. Mutant mice are identifiable between 2 and 3 weeks of age by their small size, dull fur, and nervous behavior. Adults are smaller than littermates and have a humped back and slender torso. They walk with a shaky gait and restricted hip movement. Hindlimbs paralyzed by 8 months of age. They rarely breed. | ||
| 001908 | C3HfB/BiJ | Cryopreserved - Ready for recovery |
| 001502 | C3Sn.B6-Epha4rb/EiGrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the rb allele of Epha4 can be visibly identified by 2.5 - 3 weeks of age by a constant hopping gait of the hind limbs; the forelimbs may show a hopping gait or move normally. When picked up by the tail homozygotes clasp their hindlimbs and show reduced ability to hold on to an edge; forelimbs show normal strength. | ||
| 000847 | C3Sn.B6-KitW-39J/J | Cryopreserved - Ready for recovery |
| 001547 | C3Sn.Cg-Cm/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the coloboma spontaneous mutation (Cm) show abnormal posture, head shaking or bobbing, and circling. Heterozygous mutant mice are extremely hyperactive, locomotor activity being three times that of normal mice. | ||
| 001380 | C3Sn.Cg-KitlSl-con/J | Cryopreserved - Ready for recovery |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 001906 | C3fBAnl.Cg-Catb/AnlJ | Cryopreserved - Ready for recovery |
| 007662 | C57BL/6-Arctm1Stl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. A destabilized form of GFP (d2EGFP) is expressed under the control of the endogenous Arc promoter which is activated by neuronal stimulation in forebrain regions. The half-life of EGFP expression is shortened to approximately two hours which is comparable to the decay time of ARC protein. Homozygous mice have a reduced orientation specificity in the visual cortex. The loss of Arc mRNA expression in homozygous mice was verified by RT-PCR analysis of brain total RNA preparations. This strain may be useful in studies of cortical functions. | ||
| 016609 | C57BL/6-Rr13tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| Each olfactory sensory neuron selects for expression of one of approximately 1,200 olfactory receptor genes. This targeted deletion of regulatory region 13, also known as the P element, has been shown to alter the selection for expression of specific olfactory receptor genes with diminished selection for expression of nine olfactory receptor genes and increased selection of olfactory receptor 715. All ten of these genes are located in the telomeric segment of a cluster of 24 olfactory genes that are centromeric of the P element on Chromosome 7. Heterozygotes have an intermediary level of expression between that of homozygotes and C57BL/6J controls consistent with cis regulatory control. | ||
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile, although the donating investigator reports that hemizygous mice have breeding problems likely resulting from a social anxiety-related phenotype. These "BDNF (line A9)" mice express the rat brain-derived neurotrophic factor (BDNF) primarily in forebrain regions, including the neocortex and hippocampus. Weak transgenic BDNF expression is detected also in cerebellum. Within the primary visual cortex, transgene expression is highest in the superficial layers. Hemizygous mice exhibit accelerated maturation of GABAergic innervation and inhibition, earlier termination of the critical period for ocular dominance plasticity, and accelerated development of visual acuity. These transgenic mice may be useful for studies involving BDNF overexpression and synaptic maturation and plasticity in the visual cortex. | ||
| 000338 | C57BL/6J Aw-J-EdaTa-6J/J | Cryopreserved - Ready for recovery |
| 000569 | C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J | Cryopreserved - Ready for recovery |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby mutation (EdaTa) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 005598 | C57BL/6J-Arsbm1J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Arsbm1J mutation have a combination of delayed muscle and nerve degeneration along with a skeletal phenotype consisting of a shortened snout, wide-set eyes and shortened limbs that becomes more noticeable with age. Mutants can be poor breeders yielding small litters. Of 10 litters the average number of pups was 3.9. | ||
| 004764 | C57BL/6J-Cdh23v-8J/J | Cryopreserved - Ready for recovery |
| The mutants were initially detected based on abnormal pre-pulse-inhibition test results. They were subsequently observed to exhibit a slight head tilt and circling behavior (onset at approximately 4 weeks of age), and the mutant line was established based on the overt phenotype. Testing of auditory brainstem responses revealed the mutants (n=4) to be deaf. The vestibular abnormality of nmf112 was mapped as a recessive phenotype in 19 affected and 20 unaffected (C57BL/6J-nmf112 x BALB/cByJ) F2 intercross mice, and the best linkage was to D10Mit138 (LOD = 7.0) and D10Mit15 (LOD = 6.1). Because of the map position of this mutation and its phenotypic similarity to the waltzer mutations, a series of complementation tests was performed to determine if allelic relationships exist between NMF112, NMF181, NMF252 and Cdh23. The results showed NMF112 to be an allele of NMF181 (one mating produced 2 mutants in a total of 7 progeny), of NMF252 (one mating produced 2 mutants in a total of 5 p ..... For more information please see the full phenotype on the strain data sheet | ||
| 004819 | C57BL/6J-Cdh23v-9J/J | Cryopreserved - Ready for recovery |
| The mutants exhibit circling and head tossing behavior by weaning age (at 3-4 weeks), and three animals tested at four weeks of age for Auditory brain stem response were deaf. Mutants of either gender have been produced and the colony is maintained through regular breeding. Serial sections of the ears of two mutants (24 and 29 days of age) and additional whole ear histology on one mutant (33 days of age) revealed no abnormalities. Standard pathology work-up on all three animals showed no other abnormalities. Because of the map position of this mutation, and its phenotypic similarity to the waltzer mutations, a series of complementation tests has been performed to determine if allelic relationships exist between NMF181, NMF112, NMF252 and Cdh23. The results showed NMF181 to be an allele of NMF112(one mating produced 2 mutants in a total of 7 progeny), of NMF252(one mating produced 2 mutants in a total of 8 progeny) and therefore of Cdh23, since NMF252 has been identified a ..... For more information please see the full phenotype on the strain data sheet | ||
| 005095 | C57BL/6J-Clcn2nmf240/J | Cryopreserved - Ready for recovery |
| Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum ..... For more information please see the full phenotype on the strain data sheet | ||
| 003129 | C57BL/6J-Epha4rb-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Epha4rb-2J allele can be visibly identified by 2.5 - 3 weeks of age by a constant hopping gait of the hind limbs; the forelimbs may show a hopping gait or move normally. When picked up by the tail mutants clasp their hindlimbs and show reduced ability to hold on to an edge; forelimbs show normal strength. More severely affected homozygous mutant mice also lean frequently to either side, a phenotype not reported in mice homozygous for the rb allele of Epha4. Homozygous females may deliver 2-3 pups per litter but often exhibit poor nurturing. | ||
| 004820 | C57BL/6J-Kcne12J/J | Cryopreserved - Ready for recovery |
| The mutants show circling and head tossing behavior, and a slight head tilt, observable at 4 weeks of age (+/-1 week; n=18). Two mutants tested for Auditory brainstem responses were found to be deaf. Serial sections of the ears of one mutant (32 days of age) showed a thickened tectorial membrane with mineralization and adhesion to Reissner's membrane; whole ear exam of one other mutant (30 days of age) showed abnormally shaped maculae. Standard pathology work-up showed no other abnormalities.
Because of the map position of this mutation, and its phenotypic similarity to Kcne1 mutations (potassium voltage-gated channel, Isk-related subfamily, member 1, see also Vetter et al., 1996), complementation tests with Kcne1pkr (Kcne1 punk rocker Letts et al., 2000) have been performed to determine if NMF190 represents an allele of Kcne1. Two litters of heterozygote matings between NMF190 and Kcne1pkr yielded 2 mutants in a total of 12 pro ..... | ||
| 004703 | C57BL/6J-Kcnq2Nmf134/J | Cryopreserved - Ready for recovery |
| The mutants exhibit a low threshold to electroconvulsive clonic seizures, i.e. when stimulated transcorneally with the CC3 for minimal seizures in C57BL/6J mice (6.5 mA females, or 8.0 mA males), the majority responds not with minimal, but with intense, seizures. Therefore, NMF134 mutants might be useful for studying neurobiological mechanisms related to epilepsy.
This seizure phenotype was mapped as a binary dominant trait in 17 affected and 24 unaffected (C57BL/6J-Nmf134 x BALB/cByJ)F1 X BALB/cByJ N2 backcross mice. The apparent molecular interval was D2Mit148 - 2.5 cM - (Nmf134, D2Frk1=Kcnq2), with a peak LOD score of 4.2 at D2Frk1. Nmf134 is presently examined for mutations in Kcnq2. Standard pathology work-up on two mutants that died during ECT testing (42 days of age) revealed no abnormalities; standard pathology performed on two additional mutants (68 days of age) that survived ECT testing also showed no abnormalities. View strain phenotype and add ..... | ||
| 000166 | C57BL/6J-KitW-17J/J | Cryopreserved - Ready for recovery |
| 000167 | C57BL/6J-KitW-18J/J | Cryopreserved - Ready for recovery |
| 000169 | C57BL/6J-KitW-20J/J | Cryopreserved - Ready for recovery |
| 000117 | C57BL/6J-KitW-34J/J | Cryopreserved - Ready for recovery |
| 000128 | C57BL/6J-KitW-35J/J | Cryopreserved - Ready for recovery |
| 000134 | C57BL/6J-KitW-37J/J | Cryopreserved - Ready for recovery |
| 000062 | C57BL/6J-KitW-39J/J | Cryopreserved - Ready for recovery |
| 000121 | C57BL/6J-KitW-40J/J | Cryopreserved - Ready for recovery |
| 000119 | C57BL/6J-KitW-41J/J | Cryopreserved - Ready for recovery |
| 000127 | C57BL/6J-KitW-42J/J | Cryopreserved - Ready for recovery |
| 000129 | C57BL/6J-KitW-43J/J | Cryopreserved - Ready for recovery |
| 000990 | C57BL/6J-KitW-55J/J | Cryopreserved - Ready for recovery |
| 001179 | C57BL/6J-KitW-62J/J | Cryopreserved - Ready for recovery |
| 003252 | C57BL/6J-KitlSl-20J/J | Cryopreserved - Ready for recovery |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. | ||
| 005094 | C57BL/6J-Lama1nmf223/J | Cryopreserved - Ready for recovery |
| Homozygotes have retinal vasculopathy, characterized by vitreal fibroplasias and vessel tortuosity. There is thinning of the peripheral inner nuclear layer and variable cell loss in the retinal ganglion cell layer, along with reduced dark and light adapted electroretinogram amplitudes. There is abnormal migration of retinal astrocytes into the vitreous and the persistence of hyaloid vaculature. While targeted disruption of the alpha 1 laminin gene causes a more severe phenotype, including the absence of the inner limiting membrane, this hypomorph nevertheless displays ectopic cells and blood vessels within the vitreous indicative of reduced integrity of the inner limiting membrane. | ||
| 002611 | C57BL/6J-Mitfmi-bws/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. | ||
| 005749 | C57BL/6J-Myo6sv-3J/J | Cryopreserved - Ready for recovery |
| 005468 | C57BL/6J-Myo7ash1-11J/J | Cryopreserved - Ready for recovery |
| The mutants were identified through head tilt, body leaning and bi-directional circling behavior at wean (average onset at 3.5 +/- 0.6 weeks of age; n=31); they also show head tossing behavior. ABR testing showed the mutants to be deaf at all frequencies (8, 16, 32KHz) tested. Because of phenotypic and genotypic similarities to mutants of Myo7a, complementation tests were performed with B6.Cg-Myo7ash1-8J/J (JR#3184); the results of two heterozygous by homozygous matings (5 affected in a total of 24 progeny) suggest that nmf371 represents an allele of Myo7a. Serial sections of the ears of two mutants (160 days of age) revealed a virtual absence of organ of corti,spiral ganglion cells, hair cells or normal otoconia; whole ear exam also showed defective otoconia. Standard pathology work-up revealed no further abnormalities.
View strain phenotype and additional information on the Neuroscience Muta ..... | ||
| 002854 | C57BL/6J-Nek1kat-2J/J | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 004851 | C57BL/6J-Nmf128/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 8 weeks of age revealed unusual spots on the retina and in the vitreous body, in addition to scarring and scleralization of the cornea. The colony is maintained through normal breeding. Standard pathology work-up on one mutant (122 days of age) showed a cataract and dysplastic retina with folds in one eye; the other eye appeared normal. There was also a mineral deposit in the wall of the middle ear.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf128 entry. | ||
| 005007 | C57BL/6J-Nmf191/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 12 weeks of age identified a grainy appearance of the retina in NMF191 mutants; electroretinographic recordings were normal (n=7). Standard pathology work-up on two mutants (92 days of age) revealed no gross morphological abnormalities.
The mutants breed well, and the colony is maintained through regular breeding.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf191 entry. | ||
| 005014 | C57BL/6J-Nox3het-4J/J | Cryopreserved - Ready for recovery |
| These mutants were detected through routine inspections for overt abnormal behavior and the onset of head- and body tilt has been determined to be at 4 weeks of age (+/- 0.3 weeks); occasional circling behavior has also been observed. Results of Auditory brainstem recordings (n=2) were normal. Complementation analysis, i.e. matings between heterozygous nmf250 (female) and homozygous Nox3 mice (male, JR#002557, B6Ei.GL-Nox3het/J) resulted in 5 mutants in a total of 7 progeny, demonstrating that nmf250 represents an allele of Nox3. Standard pathology work-up on two mutants (43 or 112 days of age) revealed no abnormalities. Serial sections of the ears of the older mouse showed a lack of otoconia in the ear, which was confirmed by examination of ear whole mounts of two other mutants. No other abnormalities were observed. Male or female mutants have been produced and the colony can usually be maintained through homozygous matings.
View strain phenotype and ad ..... | ||
| 005008 | C57BL/6J-Nphp4nmf192/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination revealed mutants with retinal spots or mottled retina. Histology performed on a single eye surgically removed from a mutant at 186 days of age, revealed severe photoreceptor degeneration. Male mutants do not breed well, and the colony is maintained through heterozygote matings.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf192 entry. | ||
| 000531 | C57BL/6J-Otx1jv/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Jackson waltzer mutation run in circles and shake their heads. The lateral semicircular canal and its cristae are absent, and the sacculus and utriculus may be morphologically abnormal. However, hearing is unaffected. This pheontype is similar to that reported for the Otx1tm1Asim targeted mutation and complementation testing with this targeted mutation showed jv to be an allele of Otx1. (Note that C57BL/6J is homozygous for ahl, the age related hearing loss 1 mutation, which on this strain background causes progressive hearing loss with onset after 10 months of age.) Homozygotes can swim. | ||
| 002072 | C57BL/6J-Pcdh15av-3J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames wa ltzer 2J homozygous mutant mice (av2J/av2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av2J/av2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (av3J/av3J), like Ames waltzer-J (avJ/avJ), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 003484 | C57BL/6J-Pou4f3ddl/J | Cryopreserved - Ready for recovery |
| 004821 | C57BL/6J-Prph2Nmf193/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 8 weeks of age revealed a mottled retina, indicating potential retinal degeneration in NMF193 mutants.
Male or female mutants have been produced and the colony is maintained through regular breeding. Standard pathology work-up on two mutants (74 days of age) revealed slight, bilateral, pan retinal photoreceptor degeneration of the outer nuclear layer, which consisted of 8 instead of 11 cell layers.
Eye histology on two additional mutants (224 and 432 days of age) showed thinning of the peripheral retina, which was more severe in the older mutant. No other abnormalities were noted.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf193 entry. | ||
| 005096 | C57BL/6J-Rpgrip1nmf247/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 12 weeks of age showed retinal spots and vitreal fibroplasia in NMF247 mutants. Standard pathology work-up on two mutants (84 or 91 days of age) revealed severe photoreceptor degeneration. Mutants breed well, and a colony can be maintained through homozygous matings.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Rpgrip1nmf247 entry. | ||
| 004105 | C57BL/6J-Scn8a5J/J | Cryopreserved - Ready for recovery |
| Mice develop bilateral hind limb paralysis between 14-22 days (average onset 16.9 +/- 2.1 days) followed by death between 3-4 weeks of age. Mutants of either gender have been produced.
A complementation test between NMF5 and C3HeB/FeJ-Scn8med-J (JR#3798) revealed that the motor phenotype of NMF5 represents a new allele of Scn8a, which encodes a type VIII voltage-gated sodium channel alpha polypeptide. Affected mice were found in each of 3 litters from heterozygote matings (NMF5 x Scn8med-J). Of the 25 mice born, 28% were affected (4/8, 1/9, 2/8, litters 1-3, respectively). Additional complementation tests showed NMF5 to be an allele of NMF58, and recent sequencing data confirmed the allelic relationship of NMF58 and Scn8a, and therefore of NMF5 and Scn8a (Mammalian Genome, 15,4, 2004).
However, we note that the retinal phenotype detected in NMF5 has not been reported for any Scn8a allele. To determine whe ..... | ||
| 000219 | C57BL/6J-Slc30a4lm/J | Cryopreserved - Ready for recovery |
| Female mice homozygous for the lethal milk mutation (Slc30a4lm, formerly Znt4lm) produce milk that is lethal to mice nursed during the first week of life and detrimental to mice nursed thereafter. The lethal and detrimental effects are due to a deficiency of zinc in the milk. If foster nursed on normal dams, lethal milk homozygotes survive and become reproductively mature. Zinc supplementation of the drinking water of dams enables them to nurse their young successfully. All homozygous mutant mice lack utricular otoliths and this defect is not prevented by zinc supplementation. They have varying loss of saccular otoliths and show mild behavioral abnormalities related to the otolith defect. Homozygotes over eight months of age show progressive hair loss, dermatitis, and skin lesions, symptoms of zinc deficiency. | ||
| 000563 | C57BL/6J-Sobpjc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Jackson circler spontaneous mutation (Sobpjc) show erratic circling behavior which becomes more pronounced with age. Homozygous mutant mice are very active, bobbing up and down and flexing head and trunk ventrally towards the tail and mice can swim. Mice can be identified at weaning by a characteristic flexing behavior when suspended by tail. | ||
| 001028 | C57BL/6J-Spnb4qv-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering 3 Jackson spontaneous mutation (Spnb4qv-3J) are very similar to mice homozygous for the quivering-Jackson mutation (Spnb4qv-J). Homozygous quivering mutant mice are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are st ..... For more information please see the full phenotype on the strain data sheet | ||
| 000543 | C57BL/6J-Tmiesr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spinner spontaneous (Tmiesr) show the typical head tossing, circling, deafness, and hyperactivity of the shaker and waltzer mutants. Abnormal behavior in homozygous mutant mice can be recognized as early as 7 days. Inner ear abnormalities consist of degeneration of the organ of Corti and spiral ganglion, reduction in size of the stria vascularis of the cochlea, and degeneration of the saccular macula. Both sexes are fertile, but females are not good mothers. | ||
| 006948 | C57BL/6J-hstp/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the high stepper mutation display an abnormal gait in which they pull their rear legs up to the body as they walk. They also draw the rear legs to the belly when picked up by the tail. Electroretinogram recordings are abnormal for all homozygotes on a pure C57BL/6J background or on a (C57BL/6J x CAST/EiJ)F2 background. Histology of the eye shows rosettes and misplaced ganglion cells by approximately 2 weeks of age. | ||
| 004811 | C57BL/6J-nmf110/J | Cryopreserved - Ready for recovery |
| The mutants are small and exhibit an unsteady gait, which can be detected at 4 weeks of age (+/- 0.48; n=21). A colony can be maintained through heterozygote matings. Two female mutants tested showed weights slightly (approximately 10%) below normal. Two mutants were tested for Fear-potentiated-startle and Acoustic startle response, and for each screen one mutant showed abnormal, one normal results. Unaffected littermates showed normal results (n=5). Similarly, auditory brainstem responses (at 6 weeks of age) showed one mutant to be deaf and one to be severely hearing impaired (only a late response to a 8kHz stimulus at 90db was observed), while two unaffected littermates tested normal.
Standard pathology work-up on 3 mutants (113 - 161 days of age) showed dystrophic axons and a few abnormal muscle fibers. Large lobules of lymphocytes in the lung and mild hydrocephaly were also present in one mutant. Retinal degeneration, and a loss of hair cells, supporting cells and ganglionic c ..... | ||
| 004812 | C57BL/6J-nmf111/J | Cryopreserved - Ready for recovery |
| The mutants can easily be identified at wean by their small size and all develop a subtle body tremor that is apparent by 8 weeks of age, but may appear as early as 3-4 weeks (average time of onset 47.2+/-18.2 days); they walk low on their hind limbs, which also intermittently show a prolonged extension, making their movement appear to be 'hesitant'. A colony can be maintained through normal breeding. Standard pathology work-up on two mutants (183 days of age) showed thinning along the periphery of the retina.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf111 entry. | ||
| 004747 | C57BL/6J-nmf118/J | Cryopreserved - Ready for recovery |
| The mutants are small, show body tremor, and slightly abnormal movement of hind limbs; toes are frequently curled and the foot pads do not make proper contact with the ground. In addition, abnormal results in two phenotypic screens were observed: grip strength and auditory brainstem response (ABR). Of two mutants tested for grip strength, one showed reduced values, and of four mutants tested for ABR, two were deaf, one showed reduced hearing ability at 16 and 32 Hz, and one tested normal. These results, combined with the pathology findings, suggest that these are mutants with hearing abnormalities.
Standard pathology work-up on two mutants (110 or 150 days of age) showed degenerating muscle fibers mixed with giant fibers in the spinal muscle. A deficiency of neurons in the spiral ganglia and an absence of hair cells were noted in the ear. Standard pathology performed on a much younger mutant (36 days of age) revealed no abnormalities. View strain phenotype and additional i ..... | ||
| 005006 | C57BL/6J-nmf131/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination showed hyaloid remnants and vitreal fibroplasia with white retinal spots in the majority of mutants, and cataracts, corneal scarring, microphthalmia, and/or cataracts in some mutants. The colony can be maintained through regular breeding; however, because of the low penetrance of the phenotype, which requires a large number of animals to be tested, and our limited testing capacity, we chose to cryopreserve the line. NMF131 is not available live; if you are interested in these mutants please inquire about details of availability.
Standard pathology work-up on 3 mutants (100, 116 or 173 days of age) showed variable retinal and vitreal abnormalities which include retinal dysplasia, topical degeneration and vitreal fibroplasia. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf131 entry. | ||
| 004818 | C57BL/6J-nmf172/J | Cryopreserved - Ready for recovery |
| The mutants exhibit (bi-directional) circling and head tossing behavior by 4 weeks of age, and of 3 mutants tested for auditory brainstem responses (at 6 weeks of age) 2 were found to be deaf and 1 hearing impaired. Standard pathology work-up on two mutants (95 or 173 days of age), including serial sections of the ears of one animal (95 days of age) showed no abnormalities. Whole ear exam performed on a third mutant (47 days of age) also showed no abnormalities.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf172 entry. | ||
| 005009 | C57BL/6J-nmf195/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 12 weeks of age revealed a grainy appearance of the retina, suggesting a pigmentation defect. Standard pathology work-up on two mutants (93 or 347 days of age) revealed no gross abnormalities. Additional pathology is in progress.
The colony is maintained through normal breeding.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf195 entry. | ||
| 004831 | C57BL/6J-nmf219/J | Cryopreserved - Ready for recovery |
| The mutants exhibit circling and head tossing behavior by weaning age (average date of onset 3.7 weeks of age +/- 0.66; n=20), and two animals tested for Auditory brainstem response at 6 weeks of age were found to be deaf. Standard pathology work-up on four mutants (29, 36 or 111 days of age) revealed abnormal development of the ears of three mutants. Serial sections of the ears of a 29 and a 111 day old mutant showed a lack of organization, no properly formed hair cells were observed in the older mouse; the semicircular canals also appeared very small. However, whole ear histology performed on an additional mutant (29 days of age) revealed no abnormalities. In the 36 day old mutant, macrophages were present in spinal and trigeminal nerve roots, as well as in the white matter of the CNS. No other abnormalities were observed. Male or female mutants have been produced and a colony can be maintained through heterozygote or mutant breeding (though heterozygotes breed better than mutants).
..... For more information please see the full phenotype on the strain data sheet | ||
| 005101 | C57BL/6J-nmf268/J | Cryopreserved - Ready for recovery |
| Routine ophthalmoscopic examination at 11 weeks of age showed white spots on mutant retina. Standard pathology work-up on one mutant (211 days of age) revealed no abnormalities. NMF268 mutants breed well and a colony can be maintained through heterozygote or homozygote matings.
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf268 entry. | ||
| 004656 | C57BL/6J-nmf88/J | Cryopreserved - Ready for recovery |
| nmf88 mutants have an increased propensity for seizure triggered by PTZ or transcorneal stimulation. For further details see the Neuroscience Mutagenesis Facility web page for the nmf88 entry. | ||
| 005408 | C;129P2-Npy1rtm1Pern/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross behavioral abnormalities. At age 3 to 5 months female mutant mice exhibit increased body weight. Northern blot analysis detects mRNA encoding beta-galactosidase and not the endogenous mRNA. Beta galactosidase activity pattern mimic the endogenous gene expression pattern, with expression observed in the forebrain (dorsal horn). Mice homozygous for the mutation exhibit hyperalgesia, hypersensitive cutaneous and visceral nociception, loss of sensitivity to the analgesic effects of neuropeptide Y and resistance to barbiturates. Unlike wildtype mice, homozygotes fail to display capsaicin-induced neurogenic inflammatory responses. This mutant mouse strain may be useful in studies of the role of the neuropeptide Y receptor and the physiological effects of its ligand. | ||
| 002124 | C;129S-Ngfrtm1Jae/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death. | ||
| 001490 | C;AK-Gja8Lop10/J | Cryopreserved - Ready for recovery |
| The lens opacity 10 mutation in Gja8 is semidominant. Homozygotes are microphthalmic with foamy cataract of the entire lens apparent when the eyes open at 12 days of age and increasing in opaqueness with age. Bladder cells are found adjacent to the anterior and posterior subcapsular regions of the lens before birth, the lens nucleus begins to liquefy by 4 days of age and ruptures posteriorly, then the lens capsule thickens. Gja8Lop10 Heterozygotes are not microphthalmic and the phenotype associated with the mutation varies according to the genetic background. A nuclear haze or snowflake nuclear opacity is found in F1 heterozygotes of some backgrounds while a more severe dense nuclear opacity is evident by 4 weeks of age in F1 heterozygotes of other backgrounds including AKR/J and BALB/cJ. Mice homozygous for the Gja8tm1Paul targeted mutation, a recessive mutation in which the entire coding region is removed, do not display posterior lens r ..... For more information please see the full phenotype on the strain data sheet | ||
| 003711 | CAST.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 010826 | CB.129S-Tectatm1.1Ogha/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygous mice have a thickened and shortened tectorial membrane, which covers only the first of the three rows of the cochlear outer hair cells. In homozygotes the membrane is thicker, appears to be detached from the sensory epithelium, loosely connected to the spiral limbus and elevated from the organ of Corti. Heterozygous and homozygous mice exhibit, respectively, reduced and absent forward transduction, partial and severe hearing loss, partial and severe disruption of the fibrils surrounding the edges of the tectorial membrane. Both genotypes exhibit enhanced reverse transduction. | ||
| 006169 | CBA.Cg-Tmc1dn/AjgJ | Cryopreserved - Ready for recovery |
| Homozygotes for this spontaneous mutation exhibit degeneration in the spiral ganglion neurons as well as the organ of Corti and the saccular macula. Mice are deaf throughout life. This strain may be used to research inherited deafness. | ||
| 002489 | CBA/CaGnLe-Cryaalop18/J | Cryopreserved - Ready for recovery |
| Mice homozygous for Cryaalop18 develop large, dense nuclear cataracts. At embryonic day (E) 10 the lens vesicle in these homozygotes buds out from the surface ectoderm. At E14 tiny vacuoles develop in the lens, these are larger at E16, and by four months of age there is advanced degeneration of the cortex with posterior migration of the lens epithelial nuclei and the posterior pole of the lens shows abnormal lens fibers. However, the cataracts were not found to progress further after this age. (Chang et al., 1996.) | ||
| 000813 | CBA/J-Atp7aMo-pew/J | Cryopreserved - Ready for recovery |
| The Atp7 genes encode Cu2+ ATPases. Atp7a is the mouse ortholog of the human ATP7A gene, which is mutated in children with Menke's syndrome. The range of defects in both Menke's syndrome and in mice having mutations of Atp7a--the mottled series of mutants--are due to deficiencies in a number of copper-requiring enzymes, in turn attributed to an intracellular copper transport defect. Thus, it is likely that the Atp7a gene product functions as a copper transport protein. (For brief review and references, see Levinson et al., 1994.) Atp7aMo-pew, the mottled-pewter mutation, has the mildest effect of the known mutations at this locus. The sole phenotype noted in hemizygous males and homozygous females is their pale, silvery gray coat color. The coats of affected mice of both sexes are initially agouti; males become pewter by about 4 weeks and females at 5-6 weeks of age. Heterozygous females have normal, agouti coats throug ..... | ||
| 002457 | CBA/J-wl3J/J | Cryopreserved - Ready for recovery |
| 012426 | CBACa.129S6(Cg)-Ush1ctm1Bkts/J | Cryopreserved - Ready for recovery |
| These mice contain a mutation designed to replace gene function of the endogenous mouse Ush1c gene with the human USH1C function. They also contain a mutation (216G->A) designed to retain the endogenous mouse Ush1c sequence. Mice with this mutation carry the same truncated USH1C mRNA transcript and splicing defect as found in the cochleae and retinas of Usher 1C patients. Mice homozygous for Ush1c216A are viable, fertile, and exhibit behavioral characteristics of deaf mice; they are hyperactive, display circling and head tossing behavior, and do not have a Preyer reflex. They also develop retinal degeneration, as evident by absent auditory-evoked brainstem responses and progressive loss of rod photoreceptors, providing a novel resource to study the disease mechanism and the development of therapies. | ||
| 000965 | CBACa.C3-KitW-x/J | Cryopreserved - Ready for recovery |
| 005696 | CBACaJ;129S-Chrna9tm1Bedv/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable and fertile and have normal balance, movement, cochlear duct morphology, and gross development and position of the olivo-cochlear (OC) bundle. However, most outer hair cells are innervated by one large OC efferent fiber terminal instead of multiple smaller terminals as in wildtype. OC terminal plexus in close apposition to the inner hair somata are absent in homozygotes. Null mice fail to show electrophysiological cochlear responses during efferent fiber activation. This mutant may be suitable for use in studies related to auditory-related studies of the inner ear, including the cochlea, organ of Corti, and hair cells as well as acetylcholine receptor/neurotransmitter or olfactory research. | ||
| 000805 | CBy.RF-Tshrhyt/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hypothyroid spontaneous mutation (Tshrhyt) are characterized by growth retardation, low thyroid hormone levels, elevated thyroid stimulating hormone (TSH) and hypoplastic thyroid glands. Homozygous mice of both sexes are infertile but fertility as well as growth can be restored by treatment with thyroid hormone. The mice do not respond to exogenous TSH. Homozygous mutant mice also display audiotory defects characterized by morphologic abnormalities of the stereocilia on both inner and outer hair cell systems | ||
| 002894 | CByJ.A-Atp2b2dfw-2J/J | Cryopreserved - Ready for recovery |
| The deaf waddler 2J allele (Atp2b2dfw-2J) arose spontaneously in a congenic substrain of BALB/cByJ mice, CByJ.A-fsn/J. Homozygous mutant mice are viable, but neither sex will breed. They are recognizable by 12-14 days of age by their hesitant, wobbly gait and head bobbing behavior. Homozygotes also develop a slight body tremor and become increasingly lethargic. Homozygous mutant mice are profoundly deaf, exhibiting no discernible auditory brainstem responses (ABR) to stimuli up to 100 dB. Heterozygous Atp2b2dfw-2J mutant mice also show age-dependent changes in ABR and progressive hearing loss as a result of a modifier allele (ahl) present in BALB/cByJ mice. | ||
| 005016 | CByJ;B6-Cdh23v-10J/J | Cryopreserved - Ready for recovery |
| The mutants exhibit circling behavior and a slight head tilt and tossing behavior by weaning age; two mice tested for Auditory brain stem response (at 6 weeks of age) were found to be deaf. Because of the map position of this mutation, and its phenotypic similarity to the waltzer mutations, a complementation test has been performed to determine if NMF252 represents an allele of Cdh23. One mating between NMF252 and Cdh23v-2J mice produced 2 mutants in a total of 6 progeny, suggesting that NMF252 represents a new allele of Cdh23. Therefore, NMF252 mutants might be useful for studying neurobiological mechanisms related to Usher syndrome and human deafness. Standard pathology on two mutants (49 days of age) revealed no abnormalities; whole ear exam and serial sections of the ears also showed no abnormalities. Male or female mutants have been produced, and a colony can be maintained through homozygous matings.
View strain phenotype and additional information ..... | ||
| 000293 | CHMU/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the congenital hydrocephalus (Foxc1ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Mutedmu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths ..... For more information please see the full phenotype on the strain data sheet | ||
| 004223 | CHa.SWV(C3Fe)-Mbpshi/J | Cryopreserved - Ready for recovery |
| 002927 | CNCr.129P2-Cd40tm1Kik/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation. | ||
| 000660 | DA/HuSnJ | Cryopreserved - Ready for recovery |
| 004641 | DBA/2J-Grxcr1pi-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 2 Jackson mutation display bi-directional circling and head bobbing and are completely deaf by ABR assessment. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 000252 | DC/LeJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004). | ||
| 000092 | FL/1Re-KitW/J | Cryopreserved - Ready for recovery |
| Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 000023 | FL/1ReJ | Cryopreserved - Ready for recovery |
| Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 000025 | FL/4ReJ | Cryopreserved - Ready for recovery |
| 000619 | FS/EiJ | Cryopreserved - Ready for recovery |
| The FS/Ei strain was originally used as a linkage testing stock for gene mapping. It is homozygous for several visible recessive mutations including brown (Tyrp1b), pink-eyed dilution (Oca2p), chinchilla (Tyrc-ch), frizzy (fr), and the neurological mutation shaker 1 (Myo7ash1). It is also homozygous for a couple allelic variants that can be easily typed (Mod2b and Hbbd). Mice homozygous for the shaker 1 show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist ..... For more information please see the full phenotype on the strain data sheet | ||
| 003024 | FVB.129P2(B6)-Fmr1tm1Cgr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fmr1tm1Cg targeted mutation show macroorchidism (enlarged testes), learning deficits, and hyperactivity. Macroorchidism in caused by an increased rate of Sertoli cell proliferation during embryogenesis which may be independent of FSH signalling. Comparison of homozygotes to wildtype littermates in hidden- and visible-platform water maze learning showed deficits in spatial learning and motor performance. | ||
| 002539 | FVB.129P2-Abcb4tm1Bor/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Abcb4tm1Bor mutation lack the ability to secrete phospholipid into the bile from the liver. They develop a degenerative liver disease. Portal inflammation ensues at an early age followed by hepatocellular carcinoma development after the age of 1 year. Bile from heterozygous mice has half the level of phospholipid when compared to bile from homozygotes. No liver pathology has been shown in heterozygotes. | ||
| 002935 | FVB.129S2(B6)-Ccnd1tm1Wbg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002953 | FVB.Cg-Tg(MMTVTGFA)254Rjc/J | Cryopreserved - Ready for recovery |
| Mice carrying the (MMTVTGFA)254Rjc transgene are viable and fertile, but lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgenic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females transgene expression was localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also revealed some stromal staining in the hyperplastic areas. Egfr mRNA expression was also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic mice and TGFB1 transgenic mice demonstrate that these growth factors oppose each oth ..... For more information please see the full phenotype on the strain data sheet | ||
| 003170 | FVB.Cg-Tg(Myh6-tTA)6Smbf/J | Cryopreserved - Ready for recovery |
| This strain expresses the tetracycline-controlled transactivator protein (tTA) under the regulatory control of the rat alpha myosin heavy chain promoter, which directs expression of tTA, specifically, in cardiac myocytes. When these Myh6-tTA (also called 2.9alphatTA or MHCAtTA) transgenic mice are mated to a second transgenic strain carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE), conditional expression of the target gene in cardiac myocytes may be controlled by the administration of tetracycline or doxycycline. | ||
| 003078 | FVB.Cg-Tg(WapIgf1)39Dlr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the WapIgf1 transgene are viable and fertile. The transgene is expressed at high levels during lactation and post-lactation. There were no obvious changes in mammary gland histomorphology during lactation, but at 5 to 10 days post-laction, there was a delay in involution and decreased apoptosis. | ||
| 002456 | FVB/N-Tg(CryHIVPR)72Gjj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the expression of HIV-1 protease (HIVPr) linked to the lens alphaA-crystallin promoter are viable and fertile. Homozygotes develop bilateral cataracts at 23 - 24 days of age, beginning in the perinuclear region of the lens. Proteolysis begins with the loss of betaB1-, betaB3- and betaA3-crystallins and the appearance of crystallin fragments, accompanied by protein leakage and breakdown of cytoskeletal elements. It appears that the HIV-1 protease works in concert with other endogenous proteases to induce the changes that eventually result in opacification of the lens. | ||
| 002384 | FVB/N-Tg(UcpDta)1Kz/J | Cryopreserved - Ready for recovery |
| Transgenic mice fed a "Western diet" developed marked obesity, insulin resistance, hyperglycemia, and hyperlipidemia. Mice hemizygous for the TgN(UcpDta)1Kz transgene develop early obesity in the absence of hyperphagia indicating an increased metabolic efficiency. Hyperphagia does follow and is present in mice over 7 weeks of age. | ||
| 003487 | FVB/NJ-Tg(XGFAP-lacZ)3Mes/J | Cryopreserved - Ready for recovery |
| Mice carrying this transgene express beta galactosidase in the nuclei of astrocytes. The donating investigator reports that more recent studies on this particular line indicate low level expression of the lacZ reporter gene in many neuronal populations as well. The transgene integrated on the X chromosome and therefore undergoes X-inactivation. This strain may be useful for cell culture and transplantation studies. | ||
| 001491 | FVB/NMob | Cryopreserved - Ready for recovery |
| 000259 | JE/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the jerker spontaneous mutation (Espnje) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes ar ..... For more information please see the full phenotype on the strain data sheet | ||
| 000262 | LS/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the lethal spotting mutation (Edn3ls) resemble piebald mice (Ednrbs/Ednrbs) mice. Homozygous mutant mice exhibit considerable white spotting and like homozygotes for the piebald-lethal allele (Ednrbs-l) usually develop megacolon. Lethal spotting mutant mice usually die in the third week of life from the megacolon abnormality, which is associated with deficiency of intrinsic ganglion cells in the lower colon. A few homozygotes may survive and breed. This strain is also homozygous for the black and tan coat color mutation (at). | ||
| 002757 | MK;B6-Slc12a2sy-ns/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker with no syndactylism spontaneous mutation (Slc12a2sy-ns) is allelic with the original radiaton-induced shaker-with-syndactylism mutation (sy). Homozygous mutant mice exhibit deafness and balance defects but have a normal foot morphology. Two other spontaneous alleles of sy, fused phalanges and fused phalanges 2 Jackson, do not affect hearing or behavior. Tests for allelism among mice with four different mutant alleles at the shaker-with-syndactylism locus (sy, syfp, syfp-2J, and Slc12a2sy-ns) indicate that sy is a deletion including at least two genes associated with distinct phenotypes. Mice homozygous for sy have syndactylous feet and other skeletal malformations, are deaf, and exhibit abnormal behavior characteristic of vestibular dysfunction. Complementation test results indicate that sy, syfp and syfp-2J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000734 | MOLD/RkJ | Cryopreserved - Ready for recovery |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of Stock No. 000550, MOLF/EiJ (Wade et al. 1993, Capparelli et al, 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect expression. | ||
| 000265 | MY/HuLeJ | Cryopreserved - Ready for recovery |
| 005053 | NOD.Cg-Prkdcscid Gusbmps/SndsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 000993 | NZB/BlNJ-KitW-59J/J | Cryopreserved - Ready for recovery |
| 001981 | O20/A-Prph2Rd2/J | Cryopreserved - Ready for recovery |
| 005052 | PN/nBSwUmabJ | Cryopreserved - Ready for recovery |
| PN/nBSwUmabJ mice develop a predominantly female lupus-like syndrome with age (Walker et al., 1978). Characteristics of the systemic lupus erythemoatosus syndrome include: abnormalities in B and T cell function, hypergammaglobulinemia, antibody production against multiple autoantigens, severe systemic perivasculitis and vasculitis, and immune complex-mediated glomerulonephritis (Walker et al.,1978, Luzina et al., 1999, Davidson et al., 1982, Handwerger et al.,1999). Perivascular and vascular infiltrates are composed of unusual phenotypic markers characteristic of both T and B cells (Luzina et al, 1999). By three months of age 88-100% of mice have IgG autoantibodies (Handwerger et al., 1999). Death usually occurs earlier in females as a result of glomerulonephritis and arteritis. The disease progression is accelerated in the female offspring of NZB and PN F1 crosses (Walker et al., 1986). PN/nBSwUmabJ mice develop hearing loss and otic capsule sclerosis demonstrating some paralle ..... For more information please see the full phenotype on the strain data sheet | ||
| 000807 | RBJ/DnJ | Cryopreserved - Ready for recovery |
| 000682 | RF/J | Cryopreserved - Ready for recovery |
| Derived from an unknown stock at the Rockefeller Institute, RF/J are commonly used in research in genetics, immunology, oncology and virology. This strain displays a high cancer incidence including leukemia (reportedly between 40 and 66%) and reticulum cell sarcomas (approximately 50%). Mice also have a high incidence of spontaneous glomerular hyalinisation and glomerulosclerosis developing between eight and twenty months. | ||
| 000268 | RSV/LeJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000269 | SB/LeJ | Cryopreserved - Ready for recovery |
| The SB/Le inbred strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full phenotype on the strain data sheet | ||
| 010968 | SB;C3Sn-Lrp4mdig-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Lrp4mdig-2J mutation have toes missing from each foot, have a coarse tail, and some, but not all, have one or two extra upper incisors. | ||
| 002747 | SENCARB/PtJ | Cryopreserved - Ready for recovery |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 000271 | SH1/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 1 spontaneous mutation (Myo7ash1) show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist of degeneration of the organ of Corti, the spiral ganglion, and the stria vascularis in the cochlea, and of the saccular macula and the vestibular ganglion in the vestibular labyrinth. | ||
| 005651 | SJL.AK-Thy1a/TseJ | Cryopreserved - Ready for recovery |
| This SJL/J congenic strain carries the T lymphocyte specific Thy1a (Thy1.1) allele. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis. SJL/J mice are a model of experimental autoimmune encephalomyelitis (EAE). This congenic is useful for EAE research requiring an adoptive transfer system. | ||
| 003961 | SJL.Cg Thy1a-Noxo1hslt/J | Cryopreserved - Ready for recovery |
| 002335 | SKH2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa ..... For more information please see the full phenotype on the strain data sheet | ||
| 000308 | SSL/LeJ | Cryopreserved - Ready for recovery |
| This inbred strain carries both the piebald (Ednrbs) and piebald lethal (Ednrbs-l) alleles. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. Homozygous piebald lethal mice are almost completely white with dark eyes and only an occasional small pigmented spot on the head or rump. Piebald-piebald lethal heterozygotes (Ednrbs/Ednrbs-l) mice resemble piebald mice in the degree of spotting. The piebald mutations disrupt the development of melanocytes derived from the neural crest. All piebald lethal homozygotes develop megacolon with a lack of enteric ganglion cells in the posterior end of the colon. On the SSL/Le background, although many Ednrbs-l homozygotes die between 2 and 4 weeks of age, significant numbers survive and may breed. The incidence of megacolon is reduced in piebald and piebald-piebald lethal ..... For more information please see the full phenotype on the strain data sheet | ||
| 000688 | ST/bJ | Cryopreserved - Ready for recovery |
| 002130 | STOCK Agpsbs2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the blind-sterile 2 mutation display nuclear cataracts, microphthalmia, smaller than normal lens with improper differentiation of lens epithelial cells to fiber cells with vacuolation, morganian globules, bladder cells and detachment of the apical-apical junctions of epithelial and fiber cells, although the lens epithelial cells appear normal at the anterior of the lens. Males have abnormally small testes with disrupted seminiferous tubules lacking mature spermatozoa or elongating spermatids. Although male homozygotes are sterile, female homozygotes are not. | ||
| 002267 | STOCK Bdnftm1Jae/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Bdnftm1Jae mutation show about 1/2 normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 001646 | STOCK CrygdLop12/J | Cryopreserved - Ready for recovery |
| 007674 | STOCK Esrrbtm1.1Nat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nr3b2CKO allele possess loxP sites flanking exon 2 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exon containing the initiator methionine codon and encoding the N-terminal 132 amino acids (including part of the DNA-binding domain) deleted in the cre-expressing tissue(s). Of note, if the conditional Nr3b2CKO is deleted by Cre recombinase in the placenta and embryo, embryonic lethality will result (placental defect). If the conditional Nr3b2CKO is deleted by Cre recombinase only in the embryo, the resulting mice exhibit an inner ear defect (decreased endolymph production) resulting in deafness and defective balance. These Nr3b2CKO mutant mice may be useful in generating conditional mutations to study disorders of hearing and balance, inner ear development (such as endolymph-producing epithelia withi ..... For more information please see the full phenotype on the strain data sheet | ||
| 001743 | STOCK Gtg1dwg/J | Cryopreserved - Ready for recovery |
| Mice homozgyous for the dwarf grey spontaneous mutation (Gtg1dwg) are viable but do not breed. Homozygous mutant mice have grey coats, are smaller than littermates, and develop cataracts by 3-4 weeks of age. Additional characteristics include increased numbers of osteoclasts, reduced bone mass, reduced red pulp area of the spleen, and slightly reduced thyroxin levels. | ||
| 001880 | STOCK Gusbmps Tg(GUSB)4Sly/BirJ | Cryopreserved - Ready for recovery |
| 000979 | STOCK KitlSl-16J/J | Cryopreserved - Ready for recovery |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. | ||
| 008581 | STOCK Largemyd-3J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the myodystrophy 3 Jackson mutation generally begin to display evidence of muscle degeneration at two to three months of age, although some exhibit symptoms as early as wean age. Inability to splay the hind legs outward when held up by the tail is an initial phenotype and this progresses with age to include swaying gait then dragging of the hind legs. Homozyogtes also display retinoschisis and males are sterile. | ||
| 004808 | STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis. | ||
| 002352 | STOCK MipCat-Fr/J | Cryopreserved - Ready for recovery |
| 001253 | STOCK MitfMi-wh +/+ Wnt7apx/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7apx) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet | ||
| 000109 | STOCK Myo15sh2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 spontaneous mutation (Myo15sh2) are viable and fertile, showing only a slight reduction in both compared to wildtype mice. Homozygous mutant mice display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. Homozygotes appear to be deaf from the beginning, and the saccular macula is abnormal at birth. The stria vascularis appears normal by light microscopy at 2 weeks, but begins to show degenerative changes shortly thereafter. Many of the cells contain electron-dense inclusions filled with a fine granular material. At 2.5 months, the type I hair cells of the cristae ampullares and maculae utriculi contain rod-shaped inclusion bodies composed of actin filaments. The visible phenotype of the shaker-2 Jackson (Myo15sh2-J, Stock No. 002048<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002919 | STOCK Myo7ash1-7J/J | Cryopreserved - Ready for recovery |
| Myo7ash1-7J homozygotes exhibit circling behavior, a slight head tilt and side-to-side head bob. They develop progressive hearing loss, becoming totally deaf by 60 days of age. Heterozygotes are normal. (Samples et al., 2000). Mutations of the human ortholog of Myo7a, MYO7A, have been characterized in pedigrees of patients having Usher syndrome type 1 (USH1), an autosomal recessive disorder characterized by profound deafness, vestibular dysfunction and progressive retinitis pigmentosa (Weil et al., 1995; Weston et al., 1996; Adato et al., 1997; Levy et al., 1997; Liu et al., 1998; Espinos et al., 1998; Cuevas et al., 1998, 1999; Janecke et al., 1999). MYO7A mutations have also been identified in patients with autosomal dominant non-syndromic deafness (Liu et al., 1997) and autosomal recessive isolated deafness (Liu et al., 1997; Weil et al., 1997). | ||
| 002139 | STOCK Nr2e3rd7/J | Cryopreserved - Ready for recovery |
| Nr2e3 is a retinal transcription factor important in the developmental pathways of photoreceptor cells. In mice homozygous for Nr2e3rd7, evenly distributed white spots cover the retina and have been detected by Fundus examination as early as 16.5 days of age. Whorls and rosettes in the outer nuclear layer can first be detected at 12.5 days of age, before the eyes open. These whorls likely underlie the appearance of the white spots on the retina and the white spots and whorls are both present at one month of age then are reduced in number by 5 months, and disappear by 16 months. Electroretinographs give normal signals until 5 months of age when both rod and cone signals begin to show a progressive reduction. Attenuated retinal vessels and mottled pigment are found by 16 months of age, and the outer nuclear layer is only half normal thickness subsequent to progressive loss of cones and rods. Immunohistochemical assessment revealed that the whorls are filled ..... For more information please see the full phenotype on the strain data sheet | ||
| 006702 | STOCK Ntstm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Through bicistronic expression of enhanced green fluorescing protein and neurotensin, this strain permits the visualization of the mitral and tufted cells of the main olfactory bulb thereby permitting developmental analysis in the lateral olfactory tract. | ||
| 006645 | STOCK Olfr151tm12(Olfr16)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region of the olfactory receptor Olf151 was replaced by that of the mouse olfactory receptor Olfr16. Olfactory sensory neurons that express the mutated locus co-express taulacZ by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006691 | STOCK Olfr151tm14(Adrb2)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006635 | STOCK Olfr151tm15(V1rb2)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region of the olfactory receptor Olfr151 (formerly M71) was replaced by that of the V1rb2 vomeronasal receptor (termed VRi2 in Rodriguez et al.,1999, Cell 97, 199-208). Olfactory sensory neurons that express the mutated locus co-express taulacZ by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of b-galactosidase enzymatic activity, or by immunofluorescence with anti-b-galactosidase antibodies. | ||
| 006692 | STOCK Olfr151tm16(Olfr160/Olfr161)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006693 | STOCK Olfr151tm17Mom/MomJ | Cryopreserved - Ready for recovery |
| 006688 | STOCK Olfr151tm18(GFP)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006694 | STOCK Olfr151tm20Mom/MomJ | Cryopreserved - Ready for recovery |
| 006695 | STOCK Olfr151tm21Mom/MomJ | Cryopreserved - Ready for recovery |
| 006690 | STOCK Olfr151tm23Mom/MomJ | Cryopreserved - Ready for recovery |
| 006677 | STOCK Olfr151tm28(cre)Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the Cre recombinase by virtue of IRES-mediated co-translation. | ||
| 006652 | STOCK Olfr160tm2(GFP)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006696 | STOCK Olfr160tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| 006678 | STOCK Olfr160tm6Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006669 | STOCK Olfr17tm7Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 000942 | STOCK Pitx3ak/2J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pitx3ak mutation exhibit microphthalmia (small eyes) and aphakia (no lens) related to arrested lens development. The mesencephalic dopamine system is malformed and as a result homozygotes fail to develop dopaminergic neurons of the substantia nigra (Smidt et al., 2004). Homozygotes display sensorimotor deficits specific to the nigrostriatal pathway such as the challenge beam and pole test and the test for spontaneous exploratory activitiy in a cylinder. These deficits can be reversed by L-DOPA administration (Hwang et al., 2005). This mutant mouse strain may be useful in studies of Parkinson's disease. | ||
| 004510 | STOCK Rom1tm1Mci/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and normal in size. When heterozygous mice are bred together, homozygous animals occur at a greatly reduced frequency (~6%). No gene product (protein) is detected in retinal tissue from homozygotes by Western blot analysis. Onset of progressive retinal degeneration occurs at 2 months of age beginning with a thinning of the outer nuclear layer of retinal cells. Rod outer segments in 2 month old mice display disorganized arrangement, irregular gaps and amorphous aggregates. At 4 months of age organization of rod outer segments improves. TUNEL assay of mutant retinal tissue show photoreceptor degeneration is due to apoptotic cell death. Ultra structural organization of rod outer segment disks is disorganized, often with patches of enlarged disks. Electroretinogram a-wave analysis of photoreceptor function reveals a diminished maximal photoreceptor response (50% lower than wildtype). This mutant mouse strain may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 013197 | STOCK Sagtm1Jnc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice are photosensitive and if not maintained under low light conditions will develop progressive retinal degeneration. No gene product (protein) is detected by Northern blot analysis of retinas from homozygous mice maintained in cyclic (12 hour light: 12 hour dark) conditions. Photoreceptor loss in homozygotes maintained in cyclic light conditions begins at approximately 100 days of age, progressing to loss of more than half of the photoreceptors by 1 year of age. After 1 week of constant light exposure, homozygotes lose 30% of photoreceptors; after 3 weeks of constant light exposure, more than 60% of photoreceptors are lost. Homozygotes maintained under cyclic light conditions exhibit disorganized and 25% shorter retinal rod outer segment layer, as well as reduced levels of retinal rhodopsin. Recovery phase respon ..... For more information please see the full phenotype on the strain data sheet | ||
| 005128 | STOCK Sema7atm1Alk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis. By age embryonic day 16, homozygotes exhibit abnormal lateral olfactory tract outgrowth. The lateral olfactory tract (LOT) from mutants have a more narrow morphology when compared to wildtype controls. In many mutants, no LOT is detected in the most caudal regions. This mutant mouse strain may be useful in studies of lateral olfactory tract development and axonal growth. | ||
| 003318 | STOCK Shhtm1Amc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Shhtm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.
When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e ..... | ||
| 001385 | STOCK Srebf2lop13/J | Cryopreserved - Ready for recovery |
| Lens opacity 13 is a recessive mutation that causes bilateral cataracts that do not affect the cortex of the lens. This presents at 3 to 4 weeks of age as a white area in the center of the lens. The size of the eyes is normal. (Varnum, 1981.) | ||
| 006104 | STOCK Ush1cdfcr-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the deaf circler 3 Jackson mutation display head bobbing and rapid circling and are deaf. This strain is maintained segregating for coat color alleles resulting in agouti and albino mice. | ||
| 006633 | STOCK Vmn1r49tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutation causes a deletion of the coding region of the vomeronasal receptor V1rb2 and encodes two detectable tags. Vomeronasal sensory neurons that express the mutated locus co-express GFP and the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, by immunofluorescence with anti-GFP antibodies, by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. There is a three fold diminution in neurons expressing this disrupted allele relative to those that express a tagged endogenous sequence, and the pattern of innervation of the accessory olfactory bulb differs, with axons failing to converge onto distinct glomeruli. | ||
| 002648 | STOCK a/a Cln6nclf/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the neuronal ceroid lipofuscinosis mutation (nclf) have a phenotype that is very similar to mice homozygous for the motor neuron degeneration mutation (mnd). Homozygous mutant mice display abnormal proteolipid storage by lysosomes termed neuronal ceroid lipofuscinosis. Mice also develop progressive retinal degeneration at an early age. Affected neuronal lysosomes show abnormal morphology. Severe cerebral gliosis and Wallerian degeneration of long neuronal tracts occur late in the disease and account for the motor neuron abnormalities and eventual paralysis. Homozygotes live to approximately 9 months of age. | ||
| 000302 | STOCK a/a MitfMi-wh +/+ Itpr1opt/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalities of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the opisthotonus spontaneous mutation (Itpr1opt) display a characteristic upward arching of head and tail. Homozygous mutant mice can be recognized at about 10 days of age by their loss of balance when standing or moving. Typical behavior of 15 to 20 day old homozygotes consists of falling over and struggling to get up. Agitation and s ..... For more information please see the full phenotype on the strain data sheet | ||
| 003148 | STOCK chky/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the chick yellow mutation on an albino background have a pale yellow coat color evident by approximately 10 days of age when the first coat of hair comes in. Cataracts, lens extrusion, and retinal degeneration develop. Independent of the chick yellow mutation, mice of this background, which is an inbred of an ICR outbred population, may develop polydipsia with age. | ||
| 001985 | STOCK eyl2/J | Cryopreserved - Ready for recovery |
| 80% of mice homozygous for the eyeless 2 Jackson mutation were reported to have anophthalmia, and those with intact globes have microphthalmia and are often found to have congenital corneal perforations and collapse of the anterior chamber (Chang et al., 2005). | ||
| 000279 | STOCK gr +/+ Ap3d1mh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the mocha spontaneous mutation (Ap3d1mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1mh allele have si ..... For more information please see the full phenotype on the strain data sheet | ||
| 000312 | STOCK stb + a/+ Fignfi a/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fidget spontaneous mutation (Fignfi) toss their heads from side to side and tend to run in circles. Homozygous fidgit mice are hypersensitive to sound in early life, but later lose hearing ability. Corneal lesions are common, and hind foot polydactylism occurs. The bony labyrinth is quite defective. Other abnormalities including small eyes, absence of lachrymal glands, dislocation of the hip, and displaced parafloccular lobes of the cerebellum. Viability of homozygotes is usually less than normal and fertility is poor. The STOCK is also carrying the stubby spontaneous mutation (stb). Homozygous stubby mice are recognizable at 4 or 5 days by a domed head and thick short tail. Adult stubby mice have shorter heads, bodies, and legs compared to wildtype mice. Most females are fertile but males do not breed. Male mice do produce normal numbers of motile sperm. Cartilage histology is within normal limits, but chondrogenesis stops earlier than ..... For more information please see the full phenotype on the strain data sheet | ||
| 001032 | STOCK In(1)38Rk/J | Cryopreserved - Ready for recovery |
| 000852 | STOCK In(5)30Rk/J | Cryopreserved - Ready for recovery |
| 003304 | STOCK Rb(16.17)7Bnr-Myo15sh2-2J/J | Cryopreserved - Ready for recovery |
| 000583 | STOCK T(X;16)16H +/+ EdaTa | Cryopreserved - Ready for recovery |
| 006674 | STOCK Tg(Olfr16,taulacZ)2030Mom/MomJ | Cryopreserved - Ready for recovery |
| Hemizygous mice express a mini-transgene for the olfactory receptor MOR23. Olfactory sensory neurons that express MOR23 co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. These mice may be useful in studies of axon guidance and mechanisms of olfactory receptor specificity in the olfactory bulb. | ||
| 003198 | STOCK Tg(huS100B)5Daoh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this transgene are viable and fertile. They have impaired learning and electrophysiological disturbances in the hippocampus. This strain may serve as a model of the mild learning impairment seen in human beings with Down syndrome (trisomy 21). | ||
| 004770 | SW.B6-Soab/J | Cryopreserved - Ready for recovery |
| 002023 | SWR.M-Emv21 Emv22/J | Cryopreserved - Ready for recovery |
| This strain carries a pair of linked retroviral insertions that occurred simultaneously on Chr 18 in a MEV substrain related to MEV/1Ty. Homozygosity for one of the insertions causes a juvenile lethal wasting condition that results in death at approximately 16 days of age. The proviruses rarely recombine; during development of this incipient congenic strain, a mouse was never found to have Emv21 in the absence of Emv22. There is no evidence that either of these viruses causes germline or somatic infection resulting in integration of new germline copies. (brs per personal communication from B. Taylor) | ||
| 000939 | SWR/J-Clcn1adr-mto/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the myotonia spontaneous mutations exhibit classical myotonia similar to that described in human myotonic diseases. Homozygotes are recognizable at 2 weeks of age or earlier by prolonged, stiff extension postures of the limbs when the cage is shaken or the mouse is dropped from about 10 cm. This behavior persists throughout life. When undisturbed, affected animals walk almost normally, although somewhat stiffly. They grow more slowly and weigh about 40% less than controls in adulthood. Electromyographic studies revealed changes characteristic of myotonia. These discharges do not originate in peripheral nerves, and there is no evidence of muscle fiber necrosis. | ||
| 000275 | V/LeJ | Cryopreserved - Ready for recovery |
| This strain was originally used as a linkage stock for gene mapping. It is homozygous for several visible recessive mutations all located on different chromosomes including nonagouti (a), fuzzy (fz), leaden (Mlphln), and piebald (Ednrbs) and is segregating for the neurological mutation, waltzer (Cdh23v). Homozygous waltzer mice show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. Homozygous piebald mice have dark eyes. The white areas of the coat are completely lacking in melanocytes and there is a reduction in the number of melanocytes in the choroid layer of the eye. | ||
| 000161 | WB.D2-KitlSl-d/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 000147 | WLHR/LeJ | Cryopreserved - Ready for recovery |
| WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v ..... For more information please see the full phenotype on the strain data sheet | ||
| 000933 | YBR/EiJ | Cryopreserved - Ready for recovery |
| 005005 | ZRDCT Rax+/ChUmdJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Rax+ (Stock No. 005005) mutation are normal eyed. This control strain was developed in parallel with ZRDCT Raxey1 (Stock No. 005004). | ||
| 005004 | ZRDCT Raxey1/ChUmdJ | Cryopreserved - Ready for recovery |
| Ninety percent of mice homozygous for Raxey1 are anophthalmic and 10% are microphthalmic. Anophthalmic mice have orbits and eyelids but lack eyes and optic tracts (Chase et al. 1941). Microphthalmic mice have one or two small eyes, and may have an optic nerve (Chase et al. 1941). The phenotype is first distinguished at approximately embryonic day ten. Optic vesicles develop, however, they are reduced in size and contact poorly with surface ectoderm (Chase et al. 1941). A normal eyed control strain, ZRDCT Rax+/ChUmdJ (Stock No. 005005) was developed in parallel with ZRDCT Raxey1. Raxey1 mice exhibit an abnormal hypothalmus (Silver 1977) and altered circadian rhythm (Laemle et al. 1998). This strain serves as a model for human anophthalmia. | ||
| 000395 | 129S1/Sv-Vsx2or-J/J | Research Strain |
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Research Strain |
| Mice homozygous for the recessive Dstncorn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstncorn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstncorn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat ..... | ||
| 005379 | B6(A)-Rpe65rd12/J | Research Strain |
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Research Strain |
| 003684 | B6.C3Ga-Mfrprd6/J | Research Strain |
| Male and female mice homozygous for rd6develop a slowly progressive retinal degeneration affecting both rod and cone cells beginning at 3-4 weeks of age, soon after the retina develops. Ophthalmoscopic examination reveals small, evenly distributed white spots throughout the retina from the time the mice are 8 weeks old. The spots remain clearly visible until about 7 months, when clinical signs of retinal degeneration first become evident, and become less easily distinguishable as degeneration progresses. Retinal blood vessels appear pale and attenuated by 7 months and are undetectable by 15 months, when the fundus appears mottled, lightly pigmented and granular. Aberrations of the photoreceptor layer are histologically evident at 3-4 weeks; by one year, only one to three cell layers (of the normal 10-12) remain. The time and distribution of the ophthalmoscopically detectable retinal spots correlate with histologic observation of putative phagocytic cells in the subretinal space ..... For more information please see the full phenotype on the strain data sheet | ||
| 005350 | B6.CAST(Cg)-Largevls/Pjn | Research Strain |
| Mice homozygous for the veils (Largevls) allele appear runted with muscle wasting. By five months of age, mild to moderate multifocal areas of cardiomyocyte degeneration are observed in the myocardium of homozygotes. Homozygote mice exhibit extensive ocular abnormalities including: retinal dysplasia, a disorganized ganglion cell layer, thinning of the inner nuclear layer, a progressive diminution of photoreceptor cells with aging, as well as, defects in the inner limiting membrane and outer plexiform layer. (Lee Y, et al., 2005) | ||
| 002756 | B6.CAST-Cdh23Ahl+/Kjn | Research Strain |
| C57BL/6 mice develop severe and progressive late-onset hearing loss. Histopathological changes associated with age-related hearing loss includes the disruption of both outer and inner hair cells. C57BL/6 mice are also more susceptible to noise-induced hearing loss. Age related hearing loss 1 (Ahl), a major gene responsible for this hearing loss, was mapped in an intersubspecific backcross by measuring elevated auditory-evoked brainstem response (ABR) thresholds. Ahl is located on Chromosome 10 near marker D10Mit5. B6.CAST- +Ahl is a congenic strain that carries the wildtype allele of Ahl producing C57BL/6 mice that are not susceptible to age related hearing loss. | ||
| 004297 | B6.CXB1-Pde6brd10/J | Research Strain |
| 003678 | B6.CXB1-Pde6ccpfl1/J | Research Strain |
| As early as 3 weeks of age electroretinograms show no cone-mediated responses, although rod-mediated responses are normal. There is normal retina structure but as early as 3 weeks of age vacuolization of a small subset of cells in the photoreceptor layer is found and cone photoreceptor cell degeneration becomes extensive such that very few cone cells can be found at 5 months of age. This mutant is a model for achromatopsia. | ||
| 012283 | B6.Cg-Cep290rd16/Boc | Research Strain |
| Degeneration of outer segments and decreased thickness of the outer nuclear layer of the retina is found in homozygotes as early as 19 days of age, but other cellular layers do not appear to be involved. White retinal vessels appear at one month of age and large pigment patches are found at two months of age. | ||
| 004643 | B6.Cg-Nr2e3rd7/J | Research Strain |
| Nr2e3 is a retinal transcription factor important in the developmental pathways of photoreceptor cells. In mice homozygous for Nr2e3rd7, evenly distributed white spots cover the retina and have been detected by Fundus examination as early as 16.5 days of age. Whorls and rosettes in the outer nuclear layer can first be detected at 12.5 days of age, before the eyes open. These whorls likely underlie the appearance of the white spots on the retina and the white spots and whorls are both present at one month of age then are reduced in number by 5 months, and disappear by 16 months. Electroretinographs give normal signals until 5 months of age when both rod and cone signals begin to show a progressive reduction. Attenuated retinal vessels and mottled pigment are found by 16 months of age, and the outer nuclear layer is only half normal thickness subsequent to progressive loss of cones and rods. Immunohistochemical assessment revealed that the whorls are filled ..... For more information please see the full phenotype on the strain data sheet | ||
| 002529 | B6;129S7-Vldlrtm1Her/J | Research Strain |
| Mice homozygous for the Vldlrtm1Her targeted mutation are viable and fertile. They are smaller and leaner than normal wildtype siblings. The high level of expression in muscle and adipose tissue suggests a role in VLDL triacylglycerol delivery. Plasma levels of cholesterol, triacylglycerol, and lipoproteins were normal when mice were fed normal, high-carbohydrate or high fat diets. However, homozygous mice do show a modest decrease in body weight, body mass index, and adipose tissue mass as determined by the weights of epididymal fat pads. Many homozygous pups in the colony at the Jackson Lab have patchy fur (hair loss) at weaning but look normal at about 6 weeks of age. In a segregation analysis crossing homozygous females with normal "C57BL6/2J" mice, offspring that were homozygous for this Vldlrtm1Her mutation are associated with subretinal neovascularization and were found to have a neovascularization process similar to a type seen in patients wi ..... For more information please see the full phenotype on the strain data sheet | ||
| 001912 | C3A.BLiA-Pde6b+/J | Research Strain |
| 001979 | C3A.Cg-Pde6b+ Prph2Rd2/J | Research Strain |
| 002134 | C57BL/6J-Mitfmi-vit/J | Research Strain |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitfmi-vit are only mildly affected compared to other Mitf alleles. Homozygous mutant mice have a lighter initial coat color than normal with extensive white spotting. After eight weeks of age, the mice producing increasing numbers of white hairs with each hair cycles resembling human vitiligo. Homozygotes exhibit uneven pigmentation of the retina and slow, progressive photoreceptor cell loss, eventually leading to blindness. | ||
| 004766 | C57BL/6J-Pde6brd1-2J/J | Research Strain |
| Ophthalmoscopic examination showed a mottled retina, indicative of retinal degeneration, and white retinal vessels initially observed at 24 days of age (n=3). A complementation test between NMF137 and C3H/HeJ (RD1; JR#000659) revealed that the retinal degeneration phenotype observed in NMF137 represents a new allele of Pde6b that is different from rd1, and might be useful for studying neurobiological mechanisms related to retinitis pigmentosa. All 14 progeny resulting from two homozygote matings of NMF137 x C3He/J were affected. Electroretinogram recordings revealed that homozygotes have no rod or cone responses at eight weeks, while heterozygotes test normally. The mutants showed extensive and progressive degeneration of the outer nuclear layer of the retina, which appears to be less severe than the degeneration observed in rd1 mutants.
View strain phenotype and additional information on the > ..... | ||
| 003391 | C57BL/6J-Rd9/Boc | Research Strain |
| This semidominant X-linked mutation causes a blond appearance to the fundus in homozygous females and hemizygous males, while heterozygous females develop diffuse white spots covering the retina beginning at 6 weeks of age. | ||
| 000516 | C57BLKS-Rpl24Bst/J | Research Strain |
| Belly spot and tail (Rpl24Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1 ..... For more information please see the full phenotype on the strain data sheet | ||
| 001489 | CALB/RkJ | Research Strain |
| 010614 | CBACa.B6-Cdh23ahl/Kjn | Research Strain |
| 012438 | D2.B6-Fscn2+/Kjn | Research Strain |
| This congenic expresses the C57BL/6J derived sequence of Fscn2, rather than the Fscn2ahl8 sequence, and has a resulting amelioration of the early onset hearing loss characteristic in DBA/2J mice. Distinct from the DBA/2J host background these congenic mice have click, 8 kHz, and 16 kHz ABR thresholds at 2 months of age that are equivalent to those of C57BL/6J, although the 32 kHz thresholds are elevated similar to those of DBA/2J. This congenic rescue is similar to that found in the transgenic rescue in DBA/2J-Tg(RP24-180N9)2Kjn/Kjn (stock #012440). | ||
| 012440 | DBA/2J-Tg(RP24-180N9)2Kjn/Kjn | Research Strain |
| The Tg(RP24-180N9)2Kjn transgene gives expression of Fscn2 and rescues the Fscn2ahl8 related early onset hearing loss on the DBA/2J background. At one month of age the 16 kHz ABR threshold of the hemizygote is close to that of DBA/2NCrl controls, a subline that does not have Fscn2ahl8. This transgenic rescue is similar to that found in the congenic rescue in D2.B6-Fscn2+/Kjn (stock #012438). | ||
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