Search Criteria: Research Area is "Sensorineural Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001026 | BALB/cByJ | Level 1 |
| 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. | ||
| 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. 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. 000664; C57L/J, Stock No. 00066
..... 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 | ||
| 000656 | CBA/J | Level 1 |
| 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). | ||
| 000671 | DBA/2J | Level 1 |
| 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 3-4 weeks of age) and becoming severe by 2-3 months of age. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral hearing loss. Young
..... 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 <
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..... 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, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glome
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| 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 inbred strain is used 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, Sto
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| 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). | ||
| 000635 | C3H/HeOuJ | Level 2 |
| 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 2 |
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 2 |
| 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 | ||
| 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). | ||
| 001140 | DBA/1LacJ | Level 2 |
| 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 | ||
| 000486 | MRL/MpJ | Level 2 |
| 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<
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..... 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 | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| 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. | ||
| 004326 | C3Bir.129P2(B6)-Il10tm1Cgn/Lt | Level 3 |
| 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 | ||
| 000662 | C57BLKS/J | Level 3 |
| 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 8 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. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 000676 | LP/J | Level 3 |
| 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. | ||
| 000680 | PL/J | Level 3 |
| 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 T, et al, 2004). | ||
| 100299 | PLSJLF1/J | Level 3 |
| 000689 | SWR/J | Level 3 |
| 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 | ||
| 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. | ||
| 002065 | 129T2/SvEmsJ | 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. | ||
| 000661 | C3H/HeSnJ | Level 4 |
| 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. | ||
| 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/LtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/LtJ. | ||
| 000726 | RBF/DnJ | Level 4 |
| 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. | ||
| 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. | ||
| 004337 | 129(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 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. | ||
| 004293 | 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
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| 001137 | 129P1/ReJ | Repository- Live |
| 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 | 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 (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. | ||
| 000395 | 129S1/Sv-Vsx2or-J/J | Repository- Live |
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Repository- Live |
| 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
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| 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/LtJ 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 similarities to the NOD/ShiLtJ mice, ALR/LtJ mice do not develop
..... 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 wk 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, which exhibit impaired glucose tolerance in the presence
..... 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 | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| 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
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| 005543 | B6(129)-Duox2thyd/J | Repository- Live |
| 005379 | B6(A)-Rpe65rd12/J | Repository- Live |
| 003916 | B6(Cg)-Col2a1sedc/J | Repository- Live |
| 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). | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Repository- Live |
| 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)-Tmhshscy/J | Repository- Live |
| Mice homozygous for the Tmhshscy 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). | ||
| 001809 | B6-Aw-J.Cg-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. | ||
| 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 | ||
| 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. | ||
| 007557 | B6.129S2-Oprd1tm1Kff/J | Repository- Live |
| 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
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| 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
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| 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
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| 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. | ||
| 006236 | B6.129S6-Casp6tm1Flv/J | Repository- Live |
| 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 | 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 (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
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| 000783 | B6.A-Ush1gjs/J | Repository- Live |
| 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.) | ||
| 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 | ||
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Repository- Live |
| 003684 | B6.C3Ga-Mfrprd6/J | Repository- Live |
| 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 | ||
| 002756 | B6.CAST-Cdh23Ahl+/Kjn | Repository- Live |
| 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. | ||
| 006562 | B6.CBy(Cg)-Gusbmps Gpi1a-m1J/BrkJ | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 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 | ||
| 005051 | B6.Cg-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 | ||
| 006337 | B6.Cg-Lgals1tm1Rob/J | Repository- Live |
| 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 | ||
| 006124 | B6.Cg-Myo6sv-2J/J | Repository- Live |
| 004643 | B6.Cg-Nr2e3rd7/J | Repository- Live |
| 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 | ||
| 001104 | B6.Cg-Otop1tlt/J | Repository- Live |
| 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 | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Repository- Live |
| On an albino background Tg(Tyr)3412ARpw permits the identification of gender 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 is also homozygous for 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 brain (Dewing et al., 20
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| 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 | ||
| 002504 | B6.D2-Pmp22Tr-J/J | Repository- Live |
| Mice heterozygous for the trembler-Jackson spontaneous mutation (Pmp22Tr-J) are similar to heterozygotes carrying the original trembler mutation (Pmp22Tr). However, the behavior and neuropathology of trembler-Jackson heterozygotes is less severe. The tremor phenotype cannot be reliably recognized before 20 to 25 days. There are no obvious seizures and only a mild gait abnormality. In the PNS, the myelin deficiency is considerably less severe than that of trembler mice. Homozygous trembler-Jackson mice are recognizable by 8 days of age after which they become progressively disabled. Homozygous mutant mice are unable to walk normally and can right themselves only with great difficulty; most are dead by 18 days. It should be noted that although trembler homozygotes are more severely demyelinated than trembler-Jackson homozygotes, the trembler mice live a normal lifespan while trembler-Jackson mice die prior to weaning. Survival of trembler homozygotes
..... For more information please see the full phenotype on the strain data sheet | ||
| 006576 | B6.FVB-Tg(GNAT2-Dta)98Wwk/J | Repository- Live |
| 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. | ||
| 007066 | B6.SJL-Tg(Crx-GFP,-ALPP)1Clc/J | Repository- Live |
| 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. | ||
| 006675 | B6;129P2-Olfr151tm25Mom/MomJ | Repository- Live |
| 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 | Repository- Live |
| 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 | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 006667 | B6;129P2-Omptm3Mom/MomJ | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Repository- Live |
| 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. | ||
| 002529 | B6;129S7-Vldlrtm1Her/J | Repository- Live |
| 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 | ||
| 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 | ||
| 000636 | B6C3Fe a/a-Lmx1adr-J/J | Repository- Live |
| 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
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| 001280 | B6C3Fe a/a-Lse/J | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 001022 | B6C3FeF1/J a/a | Repository- Live |
| 000314 | B6CBACa Aw-J/A-EdaTa/J-XO | Repository- Live |
| 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 | ||
| 002557 | B6Ei.GL-Nox3het/J | Repository- Live |
| 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 | ||
| 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 Tim/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. | ||
| 004771 | BALB/cBy-Ush1cdfcr/J | Repository- Live |
| 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 | ||
| 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 | ||
| 008292 | BALB/cJ-Agtpbp1pcd-8J/J | Repository- Live |
| 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). | ||
| 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
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..... For more information please see the full phenotype on the strain data sheet | ||
| 001979 | C3A.BLiA-Pde6b+.O20-Prph2Rd2/J | Repository- Live |
| 001912 | C3A.BLiA-Pde6b+/J | Repository- Live |
| 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 | ||
| 001276 | C3H/HeJ-Atp2b2dfw/J | Repository- Live |
| 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. | ||
| 006435 | C3HeB.SW-Soaa/MonJ | Repository- Live |
| 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. | ||
| 004406 | C3HeB/FeJ-Pou3f4del-J/J | Repository- Live |
| 003648 | C3Sn.BLiA-Pde6b+/Dn | Repository- Live |
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Repository- Live |
| 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. | ||
| 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 | ||
| 002552 | C57BL/6J-Cdh23v-2J/J | Repository- Live |
| 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. | ||
| 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. | ||
| 002134 | C57BL/6J-Mitfmi-vit/J | Repository- Live |
| 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. | ||
| 000531 | C57BL/6J-Otx1jv/J | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 004766 | C57BL/6J-Pde6brd1-2J/J | Repository- Live |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pde6b2J entry. | ||
| 000563 | C57BL/6J-Sobpjc/J | Repository- Live |
| 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. | ||
| 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.) | ||
| 000516 | C57BLKS-Rpl24Bst/J | Repository- Live |
| 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 | ||
| 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 7 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.N
..... 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). | ||
| 001489 | CALB/RkJ | Repository- Live |
| 006169 | CBA.Cg-Tmc1dn/AjgJ | Repository- Live |
| 000805 | CBy.RF-Tshrhyt/J | Repository- Live |
| 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 | ||
| 000657 | CE/J | Repository- Live |
| CE/J mice are 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 breeding the female can ameliorate this trait.<
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| 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. | ||
| 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. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/ | ||