Search Criteria: Research Area is "Sensorineural Research: Hearing Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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 | ||
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997.
In response to challenge, 129X1/SvJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulo ..... | ||
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A/J inbred strain is widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, ..... | ||
| 001026 | BALB/cByJ | Level 2 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000656 | CBA/J | Level 2 |
| CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965). The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al. 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al. 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter 1977, Leiter et al. 1977). | ||
| 000670 | DBA/1J | Level 2 |
| DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). There is high incidence of calcified lesions of the tongue with age. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975). | ||
| 000671 | DBA/2J | Level 2 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between three to four weeks of age) and becoming severe by two to three months of age. The age related hearing loss 8 mutation arose spontaneously in DBA/2J between 1951 and 1975. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroven ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 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. | ||
| 000662 | C57BLKS/J | Level 4 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after eight weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background ..... For more information please see the full phenotype on the strain data sheet | ||
| 000668 | C57L/J | Level 4 |
| C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE) and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences. | ||
| 001140 | DBA/1LacJ | Level 4 |
| Historical reports indicate DBA/1J and DBA/1LacJ mice immunized with type II collagen develop a severe polyarthritis mediated by an autoimmune response. Recent in-house studies suggest that the response to collagen induction in the DBA/1LacJ strain is not as robust as indicated by earlier studies. Arthritis models such as B10.RIII-H2r H2-T18b/(71NS)SnJ (Stock No. 000457) and BUB/BnJ (Stock No. 000653) can be used as alternatives to DBA/1LacJ. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1 mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000676 | LP/J | Level 4 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 000486 | MRL/MpJ | Level 4 |
| The MRL/MpJ mice are large but docile to the point that males rarely fight. They are the parent and control strain for for MRL/MpJ-Faslpr (Stock Nos. 000485, 006825). Despite carrying the normal Fas gene, MRL/MpJ mice also exhibit autoimmune disorders, but symptoms are manifested much later in life compared to those the MRL/MpJ-Faslpr mice. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-Faslpr mouse but not in the wildtype control, MRL/MpJ. Also beginning at 3 months Faslpr mice exhibit very severe poliferative glomerulonephritis, whereas in the MRL/MpJ controls usually only mild glomerular lesions are detected. MRL/MpJ inbred female typically die at 73 weeks of age and males die at 93 weeks. This compares to a lifespan of 17 weeks in the female and 22 weeks for males in the mouse homozygous for Faslpr. See MRL/MpJ-Faslpr<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/ShiLtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/ShiLtJ. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 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. | ||
| 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. | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the ..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males ..... For more information please see the full phenotype on the strain data sheet | ||
| 013127 | B6.129-Accn3tm1Wsh/J | Repository- Live |
| Homozygous Accn3 (amiloride-sensitive cation channel 3) targeted mutation mice display alterations in normal and pain-associated cutaneous mechanosensitivity and inflammatory pain sensation, visual loss associated with night blindness, and age-induced hearing loss. Mice show increased sensitivity of mechanoreceptors detecting light touch. Sensitivity of mechanoreceptors responding to noxious pinch is decreased as is the response of acid- and noxious heat-sensitive nociceptors. No mRNA is detectable by RT-PCR in the dorsal root ganglion. Protein is not found in trigeminal and dorsal root ganglion. This strain may be useful in further elucidating the role of this gene in mechanosensation. | ||
| 016162 | B6.129-Gfi1tm2Tmo/J | Repository- Live |
| These mutant mice express EGFP (Enhanced Green Fluorescent Protein) from the endogenous Gfi1 locus. No endogenous gene product (protein) is detected in thymocytes from homozygotes, as detected by FACS analysis. Homozygotes exhibit neutropenia, decreased thymocyte number, and defective B cell and T cell differentiation. The Donating Investigator reports that homozygous mice must be maintained under spf conditions and have a lifespan of 1 year. GFP fluorescence expression mimics the expression pattern of the endogenous gene. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Almost all thymocytes from heterozygotes fluoresce. Fluorescence of thymocytes from homozygotes is more intense than fluorescence observed in heterozygotes. At embryonic day 17.5, homozygous embryos exhibit disorganized inner ear sensory epithelia, with abnormal outer hair cells morphology. Neonate ..... For more information please see the full phenotype on the strain data sheet | ||
| 016163 | B6.129-Gfi1tm3(Gfib1)Tmo/J | Repository- Live |
| These mutant mice express mouse Gfi1b (growth factor independent 1B) from the endogenous Gfi1 locus. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Higher expression levels of Gfi1b transcript is detected in inner ears as measured by RT-PCR analysis. The Gfi1b knock-in did not completely rescue the Gfi1 knock out phenotype (see STOCK No. 016161). Homozygotes have slightly fewer granulocytes in bone marrow, a small accumulation in bone marrow of immature myeloid cells and monocytes, and fewer mature circulating granulocytes when compared to wildtype controls. At 3 to 3.5 months in age, homozygotes are deaf, do not display a Preyer reflex, abnormal auditory brainstem response (over 100 dB at 8 kHz and over 90 dB at 16 and 32 kHz), and exhibit head bobbing and abnormal reaching response. In neonatal mutants, the cochlear inner hair cells are morphol ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 010546 | B6.129S1-Jag2tm1Grid/J | Repository- Live |
| Mice that are homozygous for this targeted mutation have a perinatal lethal phenotype, dying shortly after birth due to craniofacial defects (cleft palate, due to fusion of unelevated palatal shelves with the tongue). Embryos homozygous for the mutation and aged embryonic day 10.5-11.5, display a hyperplastic thick apical ectodermal ridge of the limb buds. Homozygous neonates have bilateral cleft of the secondary palate and syndactyly (fused digits) of both forelimbs and hindlimbs, although the hindlimbs are more affected. The number of inner ear hair cells is increased in mutants. Histological analysis reveals an increased number of inner ear hair cells and disorganized stereocilia bundles in mutants. Homozygotes exhibit abnormal thymic morphology and decreased gamma-delta T cell number. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygotes have abnormal inner ear morphology (increased number of hair c ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 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 | ||
| 013193 | B6;129S-Barhl1tm1Xia/J | Repository- Live |
| In this strain, the entire coding region of the endogenous BarH-like 1 (Barhl1) gene is replaced with a lacZ (β-galactosidase) reporter gene and a loxP-flanked neomycin resistance (neo) cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size, with β-gal staining in Barhl1 expressing tissues. LacZ expression in embryos and neonates is evident in all hair cells, but is more abundantly observed in the cochlear outer hair cells. LacZ expression in adults is strong in the outer hair cells, and weak in the inner and vestibular hair cells, with persistent expression in hair cells of the organ of Corti. These mice exhibit age-related progressive degeneration of both cochlear outer and cochlear inner hair cells in the organ of Corti, resulting in hearing loss. The progression is apical-to-basal for outer hair cell and basal-to-apical for inner hair cells. Barhl1-/- mice have elevated audit ..... For more information please see the full phenotype on the strain data sheet | ||
| 001923 | B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J | Repository- Live |
| The Tim mutation (translocation induced circling mutation) was induced by ethylene oxide in a mutagenesis experiment. The mutation was induced simultaneously with a reciprocal translocation between Chrs 4 and 17. Because the mutation has so far been inseparable from the translocation, it may be that one of the translocation breakpoints has disrupted a gene on Chr 4 or 17. Heterozygotes exhibit circling, head tossing, poor limb coordination, and corneal clouding. The affected mice are usually smaller than wildtype littermates. Inner ear studies have not been done. The mutants swim poorly but can orient themselves in the water. One mutated copy of the gene is dominant over two normal alleles because segmentally trisomic mice with two normal Chrs 4 and 17 and the small 417 translocation product have the behavioral abnormalitites. Breeding is generally poor. | ||
| 005412 | BALB/cByJ-Fgfr1Eask/GrsrJ | Repository- Live |
| The ear askew mutation is homozygous embryonic lethal. Heterozygotes have unilateral or bilateral low-set ears and malformed pinna. There is variable expressivity. Heterozygotes are viable and fertile, but auditory brainstem response assessment shows severe hearing loss at 6 months of age. | ||
| 000653 | BUB/BnJ | Repository- Live |
| BUB/BnJ mice carry a specific T cell receptor V beta mutation, making this strain highly susceptible to collagen-induced arthritis. This T cell receptor V beta restriction works in concert with other uncharacterized modifying genes present in BUB/BnJ mice. BUB/BnJ mice carry no detectable endogenous ecotropic MuLV DNA sequences. Mice are also reported to have high serum complement activity. In response to challenge, BUB/BnJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). BUB/BnJ mice are homozygous for the Mass1frings allele (monogenic, audiogenic seizure susceptibility 1) and are susceptible to audiogenic seizures prior to 25 days of age (Skradski, et al 2001). In addition, the Mass1frings allele acounts for early onset hearing impairment by 3-4 weeks of age (Johnson KR, et al 2005). | ||
| 001768 | C3.Cg-Irs1Sml H2b/GrsrJ | Repository- Live |
| The small mutation causes hyperinsulinemia with only mild insulin resistance, a paucity of body fat, deficiencies in bone development and homeostasis, and hearing loss. Homozygotes can be distinguished by 2 weeks of age by their smaller body size and thin short tails, and adult homozygotes are visibly smaller with a tail that is 20% shorter than in wild-type controls. Hearing loss was shown through increased ABR threshold values when assessed between 8 and 12 weeks of age. The skeletal defects include shortened femurs with smaller growth plates, decreased cortical and trabecular thickness and abnormal trabecular number, with an increase in the number of osteoclasts and osteoblasts per bone perimeter but impaired osteoblast proliferation and differentiation in culture. This spontaneous point mutation is semidominant in some aspects of phenotype, unlike targeted mutations of this gene. Heterozygotes are statistically smaller than wild-type controls, but the severity of dwarfing is not ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 000661 | C3H/HeSnJ | Repository- Live |
| 014165 | C57BL/6-Myo3atm1.1Mckg/J | Repository- Live |
| These Myo3aKI/KI mice contain the nonsense mutation TAT>TAG at codon 1041 of the myosin IIIA (Myo3a) gene. This mutation introduces a premature stop codon in exon 28, analogous to a Myo3a mutation found in humans with adult on-set hearing loss (DFNB30). Homozygotes are viable, fertile, and normal in size. DFNB30 is an inherited progressive hearing loss first identified in a Middle Eastern family, Family N. Myo3a is normally expressed in the vestibular hair cells of the inner ear. These mice exhibit significant hearing loss during the third month of life, beginning at high frequencies and eventually progressing to all frequencies. The inner and outer hair cells of these mice exhibit degeneration by 10 and 17 months of age, respectively, showing greater loss towards the base of the cochlea. These mice may be useful for studying adult on-set human hearing loss DFNB30. | ||
| 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. | ||
| 000667 | C57BR/cdJ | Repository- Live |
| C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD ..... For more information please see the full phenotype on the strain data sheet | ||
| 000669 | C58/J | Repository- Live |
| This strain was developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock. A mating of the same male but a different female gave rise to the commonly used C57BL group of strains. C58/J mice exhibit a high incidence of leukemia (>90% by one year of age). C58/J mice also exhibit an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). | ||
| 014182 | CByJ.Cg-Fgfr3m1J/GrsrJ | Repository- Live |
| Mice homozygous for the recessive Fgfr3m1J allele have skeletal deformities that result in kyphosis, scoliosis, and a bent tail, which is often found to exit the pelvis at an abnormal angle. ABR threshold assessment shows hearing loss to the point of deafness at 3 to 4 weeks of age, the earliest age assessed. Male homozygotes display infertility, but females do breed and rear pups. Homozygotes have not been found to have a reduced lifespan, distinct from the reduced lifespan or prenatal lethality found in homozygotes for targeted deletions of this gene. | ||
| 004070 | CByJ.Cg-hml/GrsrJ | Repository- Live |
| Homozygotes have a faith-to-thrive phenotype such that they have a smaller body size and unbalanced gait detectable at 10 days of age. Those that survive to 2 months of age can generally live up to 18 months. The inner ear has extensive hypoplasia of the membranous labyrinth, a rudimentary tectorial membrane, and enlarged scala vestibuli and severe hearing loss or complete deafness are found at 19 days of age both by failed response to sounds and auditory brainstem response analysis. Homozygotes also fail to orient in water. | ||
| 000657 | CE/J | Repository- Live |
| CE/J mice are very responsive to phytohemagglutinin and resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breed ..... | ||
| 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. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002106 | KK/HlJ | Repository- Live |
| KK/HlJ male mice exhibit diabetic symptoms that includes hyperglycemia, hyperinsulinemia, and insulin resistance. This strains serves as a model of noninsulin dependent diabetes mellitus, type 2. | ||
| 000675 | LG/J | Repository- Live |
| LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis (Peng et al., 1996). LG/J was the predominant strain used to develop the MRL/LpJ (Stock No. 000486) inbred strain, a model for autoimmunity. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975). | ||
| 000677 | MA/MyJ | Repository- Live |
| A characteristic of MA/MyJ is the spontaneous mutation hf (hepatic fusion), which results in varying degrees of fusion in the hepatic lobes. | ||
| 000679 | P/J | Repository- Live |
| P/J mice exhibit a high incidence of lymphatic leukaemia. They also show a high susceptibility to audiogenic and electroconvulsive seizures. P/J mice are also homozygous for a number of other mutations including nonagouti (a), brown (Tyrp1b), pink-eyed dilution (Oca2p), short ear (Bmp5se), dilute Myo5ad), and retinal degeneration 1 (Pdeb1rd1). | ||
| 004339 | STOCK Bdnftm3Jae/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this ..... | ||
| 003392 | STOCK Crb1rd8/J | Repository- Live |
| 005051 | STOCK KitW-sh/HNihrJaeBsmJ | Repository- Live |
| Kit mutations affect melanogenesis, hematopoiesis and gametogenesis. The sash mutation affects melanoblast survival. Melanoblast density is severely reduced in homozygotes by E12 (Cable et al., 1995). Homozygote are white with black eyes and some pigment around the ears. Heterozygotes are black with a white sash at the midline. The KitW-sh mutation affects Kit expression in a tissue specific manner. Kit expression is abolished in mast cells and mutant mice have a mast cell deficit (Tono et al., 1992, Berrozpe et al., 1999). However, young animals (<4 weeks) have been reported to have mast cells in skin (Yamakazi et al., 1994). KitW-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the KitW and KitW-v mutations, KitW-sh germ cells and erythrocytes are not affected. Homozygtes have some ..... For more information please see the full phenotype on the strain data sheet | ||
| 006104 | STOCK Ush1cdfcr-3J/J | Repository- Live |
| Mice homozygous for the deaf circler 3 Jackson mutation display head bobbing and rapid circling and are deaf. This strain is maintained segregating for coat color alleles resulting in agouti and albino mice. | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J-KitlSl/KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet | ||
| 002756 | B6.CAST-Cdh23Ahl+/Kjn | Research Strain |
| C57BL/6 mice develop severe and progressive late-onset hearing loss. Histopathological changes associated with age-related hearing loss includes the disruption of both outer and inner hair cells. C57BL/6 mice are also more susceptible to noise-induced hearing loss. Age related hearing loss 1 (Ahl), a major gene responsible for this hearing loss, was mapped in an intersubspecific backcross by measuring elevated auditory-evoked brainstem response (ABR) thresholds. Ahl is located on Chromosome 10 near marker D10Mit5. B6.CAST- +Ahl is a congenic strain that carries the wildtype allele of Ahl producing C57BL/6 mice that are not susceptible to age related hearing loss. | ||
| 002134 | C57BL/6J-Mitfmi-vit/J | Research Strain |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitfmi-vit are only mildly affected compared to other Mitf alleles. Homozygous mutant mice have a lighter initial coat color than normal with extensive white spotting. After eight weeks of age, the mice producing increasing numbers of white hairs with each hair cycles resembling human vitiligo. Homozygotes exhibit uneven pigmentation of the retina and slow, progressive photoreceptor cell loss, eventually leading to blindness. | ||
| 010614 | CBACa.B6-Cdh23ahl/Kjn | Research Strain |
| 012438 | D2.B6-Fscn2+/Kjn | Research Strain |
| This congenic expresses the C57BL/6J derived sequence of Fscn2, rather than the Fscn2ahl8 sequence, and has a resulting amelioration of the early onset hearing loss characteristic in DBA/2J mice. Distinct from the DBA/2J host background these congenic mice have click, 8 kHz, and 16 kHz ABR thresholds at 2 months of age that are equivalent to those of C57BL/6J, although the 32 kHz thresholds are elevated similar to those of DBA/2J. This congenic rescue is similar to that found in the transgenic rescue in DBA/2J-Tg(RP24-180N9)2Kjn/Kjn (stock #012440). | ||
| 012440 | DBA/2J-Tg(RP24-180N9)2Kjn/Kjn | Research Strain |
| The Tg(RP24-180N9)2Kjn transgene gives expression of Fscn2 and rescues the Fscn2ahl8 related early onset hearing loss on the DBA/2J background. At one month of age the 16 kHz ABR threshold of the hemizygote is close to that of DBA/2NCrl controls, a subline that does not have Fscn2ahl8. This transgenic rescue is similar to that found in the congenic rescue in D2.B6-Fscn2+/Kjn (stock #012438). | ||
| 002908 | 129-Col4a3tm1Dec/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Col4a3tm1Dec targeted mutation develop glomerulonephritis and die at about 8.5 weeks of age. Survival time of homozygous mutant mice is extended to about 14 weeks of age in mice maintained on a mixed genetic background. | ||
| 003009 | 129-Kcne1tm1Sfh/J | Cryopreserved - Ready for recovery |
| This strain is characterized by inner ear defects with a phenotype similar to shaker and waltzer. There is loss of hair cells and many supporting cells in the organ of Corti as well as in all vestibular end organs. The time course of hair cell degeneration is different for each portion of the inner ear. Heart abnormalities of homozygous mutant mice included a longer QT interval at slow heart rates, a paradoxical shorter QT interval at fast heart rates, and an overall exacerbated QT-heart rate adaptation compared with wild-type controls. This mutant serves as a model for Jervell and Lange-Nielsen disease in which patients suffer cardian arrhythmias and profound bilateral deafness. | ||
| 002357 | 129P3/JEmsJ | Cryopreserved - Ready for recovery |
| 000212 | 129P4.Cg-Axin1Fu/J | Cryopreserved - Ready for recovery |
| The fused mutation is dominant and generally more severe in homozygotes, but has highly varying penetrance in both the heterozygote and homozygote, to the extent that some homozygotes do not have an abnormal phenotype. Phenotypic traits of mice carrying the Axin1Fu allele include shortened, bifurcated, or absent tails, kinked tails with fused vertebrae, other asymmetrical fusions of vertebrae, axial duplications, and ribs fused at the proximal ends. Imperforate anus, anemia at birth, waltzing movement, deafness, and missing or abnormal kidneys have also been reported. Both heterozygotes and homozygotes are generally fertile although female carriers transmit with a lower penetrance than males do. (Reed, 1936; Dunn and Gluecksohn-Waelsch, 1954; Theiler and Gluecksohn-Waelsch, 1956.) | ||
| 001198 | 129P4/RrRkJ | Cryopreserved - Ready for recovery |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 007965 | 129S-Dvl1tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders. | ||
| 009083 | 129S-Dvl3tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have a perinatal lethal phenotype. Neonates have breathing difficulties and are often cyanotic. Homozygous embryos exhibit cardiac conotruncal abnormalities such as persistent truncus arteriosis (PTA) and double outlet right ventricle (DORV), and cochlear defects (disoriented stereociliary bundles). This mutant mouse strain may be useful in studies of cardiac development, neural tube formation and development of the inner ear. | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full phenotype on the strain data sheet | ||
| 006446 | B10.Cg-H2h4 Sh3pxd2bnee/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the nose eyes ear mutation are runted, with proportionally smaller skeletons, shortened noses, shortened and domed skulls, reduced areal bone mineral density, diminished visceral and subcutaneous white adipose tissue, but not brown adipose tissue, and abnormal eyes and middle ears. The eyes have an enlarged anterior chamber, cloudy cornea, and severe peripheral anterior synechia of the irideocorneal angle. The middle ear shows inflammation as serous fluid with diffuse neutrophils with thickened epithelium. Elevated ABR thresholds are found in all homozygotes and homozygotes are infertile. | ||
| 000593 | B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the MitfMi spontaneous mutation are characterized by decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Cryopreserved - Ready for recovery |
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil ..... | ||
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Cryopreserved - Ready for recovery |
| 005543 | B6(129)-Duox2thyd/J | Cryopreserved - Ready for recovery |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet | ||
| 003916 | B6(Cg)-Col2a1sedc/J | Cryopreserved - Ready for recovery |
| Newborn homozygotes are smaller than normal, have a shortened trunk, and often display head bobbing. Decreased body weight persists into adulthood, and the noses, trunks, tails, skulls, and long bones of adults are shortened relative to those of normal siblings. Abnormal epiphyses, with dysplasia of the vertebrae, femora, and tibias are found. Although light microscopy failed to detect any abnormalities in the inner ear, the head bobbing characteristic accompanying this mutation is usually associated with inner ear defects. Auditory brainstem response threshold analysis of 10-15 week old homozygotes does show hearing impairment. Clefts develop between the inner and outer aspects of the inner nuclear layer of the retina (retinoschisis). | ||
| 008834 | B6(Cg)-Tmiesr-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spinner 2 Jackson mutation display head tilting and circling and are deaf. | ||
| 000562 | B6(Cg)-Tubtub/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p ..... For more information please see the full phenotype on the strain data sheet | ||
| 004640 | B6(MOR)-Lhfpl5hscy/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Lhfpl5hscy mutation circle rapidly, shake their heads from side to side, fail to swim, and are congenitally deaf. Although hair cells appear normal at birth, they degenerate. At 4 months of age, degeneration of the organ of Corti is also found, more pronounced in the basal region of the cochlea than the apex, with loss of inner and outer hair cells and decreased spiral ganglia (Longo-Guess et al., 2005). | ||
| 002552 | B6(V)-Cdh23v-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the waltzer 2J spontaneous mutation (Cdh23v-2J) show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Homozygous mutant mice are very similar to the other waltzer mutants (Cdh23v and Cdh23v-J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (v/+ Myo7ash1/+) are deaf beginning at 3 to 6 months. Double heterozygotes have changes similar to those of the homozygotes in the organ of Corti, stria vascularis, and spiral ganglion, but less severe and with much later onset. Viability and breeding ability are somewhat reduced. | ||
| 009592 | B6.129(Cg)-Kcnn2tm1.1Jpad/J | Cryopreserved - Ready for recovery |
| Homozygous SK2-delta (SK2-null) mice are viable but subfertile (homozygous males exhibit poor reproductive success and homozygous females are nurturing but produce small, infrequent litters). No RNA or protein expression from the targeted allele is observed in brain tissues, and no EGFP expression is reported. Homozygous mice are smaller than wild-type until approximately 5 weeks of age. SK2-deficient mice exhibit whole body tremor beginning around 10 days of age, with ataxia and impaired righting reflex when placed on their back at young ages. Homozygotes also have inner ear abnormalities (impaired exocytotic response of immature inner hair cells and impaired function/long-term survival of olivocochlear fibers and efferent synapses on cochlear outer hair cells). These SK2-delta mice may be useful in studying the role of small-conductance calcium-activated potassium (SK) channels in after-hyperpolarization and action potentials of neuronal, inner ear (cochlea), and urinary bladder tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 004276 | B6.129-Figntm1Frk/Frk | Cryopreserved - Ready for recovery |
| 004833 | B6.129-Ptprqtm2Bow/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunofluorescence labeling analysis of the inner ear. Homozygotes do not respond to the 20kHz toneburst of a hearing test at 3 months of age. Although embryonic development of the inner ear is normal, newborns exhibit disorganized and defective hair cell bundles. Histological analysis reveals an absence of hair cells in the organ of Corti and some animals are missing the organ of Corti completely. Inner hair cells have missing or defective stereocilia. This mutant mouse strain may be useful in studies related to deafness. | ||
| 006853 | B6.129-Ush1ctm1Xzl/Kjn | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ush1ctm1Xzl mutation have circling, head-tossing, and hyperactive behaviors typical of vestibular mutants. Auditory-evoked brainstem assessment shows that homozygotes are completely deaf and scanning electron microscopy shows that the hair cell stereocilia become progressively disorganized with age, with the outer hair cells more affected than the inner hair cells. Although histology at 12 months of age does not reveal any abnormalities, there is a decline in electrotreinogram readings for both rods and cones by 11 months of age. Because the first four exons were replaced by the beta galactosidase reporter cassette, endogenous expression of this gene in phenotypically normal mice can be traced by assessing lacZ expression in heterozygotes. | ||
| 009379 | B6.129S1-Gpr98tm1Pwh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. A mutant gene product (protein) is detected by Western blot analysis of embryos. High-intensity sound induces audiogenic seizures that often results in death. Cochlear hair cell stereociliary bundles are do not mature properly, lack ankle links and are disorganized. Hair cells and pillar cells in the basal half of the cochlea degenerate and are lost by 2 months of age. Homozygotes become profoundly deaf by 3 weeks of age. Electroretinographic analysis reveals abnormal light-adapted cone-only responses. Mutant mice exhibit abnormal retinal photoreceptor cells ultrastructure and age-related vision loss. This mutant mouse strain may be useful in studies of Usher syndrome type IIC, cochlear development, deafness and blindness. | ||
| 003462 | B6.129S1-Thrbtm1Df/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 003098 | B6.129S2-Ntrk2tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk2tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus. | ||
| 000783 | B6.A-Ush1gjs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ush1gjs allele are deaf, circle, and toss their heads from side to side. They are viable and fertile but due to their circling gait females may trample their pups and thus should not be used for breeding. No auditory brain response was detected from homozygotes at 14, 21, and 30 days of age. At 10-14 days of age the stereocilia of the outer and macular hair cells are disarrayed or missing although no abnormal phenotype is evident in inner hair cells, or in the gross anatomy of the cochlea or vestibule. The steriocilia degeneration in outer hair cells continues but the inner hair cells remain normal at 30-47 days of age. (Dickie and Deol, 1967; Kitamura et al., 1992.) | ||
| 000517 | B6.BKS-Pcdh15av-J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (Pcdh15av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames waltzer 2J homozygous mutant mice (Pcdh15av-2J/Pcdh15av-2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. Pcdh15av-2J/Pcdh15av-2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (Pcdh15av-3J/Pcdh15av-3J), like Ames waltzer-J (Pcdh15av/Pcdh15av), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Cryopreserved - Ready for recovery |
| 000560 | B6.C-H7b/By KitW-50J/J | Cryopreserved - Ready for recovery |
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Cryopreserved - Ready for recovery |
| 000532 | B6.C3-Grxcr1pi/J | Cryopreserved - Ready for recovery |
| Beginning at approximately 10 days of age, pi/pi mice first display backing or crab-like movements and by approximately 14 days of age pirouetting is observed. This pirouetting is a spinning movement that involves swinging the head sharply to one side, either left or right, placing the inner rear foot (with the toes facing outward) close to the outer rear foot which then is used to push the mouse in a tight circling motion. This spinning persists for relatively long periods and cyclostat assessment suggests that these mutants do not develop rotational dizziness. Adult pi/pi mice can not swim on the surface of water or in a coordinated manner and are deaf at 21 to 30 days of age as determined by auditory brainstem response and a failure to respond to a variety of sounds. Although the organ of Corti develops normally, degeneration is found by the second week of life. The tectorial membrane is thickened at 12 days of age and subsequently the hair cells degenera ..... For more information please see the full phenotype on the strain data sheet | ||
| 000122 | B6.C3-KitW-44J/J | Cryopreserved - Ready for recovery |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full phenotype on the strain data sheet | ||
| 002624 | B6.C3-Lmx1adr-6J/J | Cryopreserved - Ready for recovery |
| 000991 | B6.C58-KitW-57J/J | Cryopreserved - Ready for recovery |
| 004275 | B6.Cg-Fignfi/Frk | Cryopreserved - Ready for recovery |
| 007787 | B6.Cg-Grxcr1pi-4J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 4 Jackson mutation display bi-directional circling and are completely deaf as early as 5 weeks of age. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 000133 | B6.Cg-KitW-24J/J | Cryopreserved - Ready for recovery |
| 000139 | B6.Cg-KitW-25J/J | Cryopreserved - Ready for recovery |
| 000164 | B6.Cg-KitW/J | Cryopreserved - Ready for recovery |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/ | ||
| 000071 | B6.Cg-Mcoln3Va/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000158 | B6.Cg-MitfMi-wh/MitfMi/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (MitfMi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac ..... For more information please see the full phenotype on the strain data sheet | ||
| 000184 | B6.Cg-MitfMi-wh/Mitfmi-rw/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (MitfMi-wh/Mitfmi-rw) are mostly white with tan spots and red eyes. | ||
| 000157 | B6.Cg-MitfMi-wh/Mitfmi-sp/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmic but normal skeleton. Both homozygous and heterozygous mice for the microphthalmia-spotted spontaneous mutation (Mitfmi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (MitfMi-wh/Mitfmi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes. | ||
| 000057 | B6.Cg-MitfMi-wh/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. | ||
| 006124 | B6.Cg-Myo6sv-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Snell?s waltzer 2 Jackson mutation display circling and head tossing behavior and are deaf. They are unable to orient in water to swim. | ||
| 003184 | B6.Cg-Myo7ash1-8J/J | Cryopreserved - Ready for recovery |
| Myo7ash1-8J homozygous mice circle and bob their heads; heterozygotes are behaviorally normal. Homozygotes of both sexes are viable and fertile (Samples 2000). The hearing of Myo7ash1-8J mutants has not been examined. However, other Myo7a mutations, whose behavioral phenotypes are virtually identical to that of Myo7ash1-J, are associated with deafness. Mutations in the human ortholog of Myo7a, MYO7A, have been characterized in pedigrees of patients having Usher syndrome type 1 (USH1), an autosomal recessive disorder characterized by profound deafness, vestibular dysfunction and progressive retinitis pigmentosa (Weil et al., 1995; Weston et al., 1996; Adato et al., 1997; Levy et al., 1997; Liu et al., 1998; Espinos et al., 1998; Cuevas et al., 1998, 1999; Janecke et al., 1999). MYO7A mutations have also been identified in patients with autosomal dominant non-sy ..... | ||
| 000567 | B6.Cg-T2J +/+ Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation. | ||
| 000571 | B6.Cg-Whrnwi Tyrp1b/+ +/J | Cryopreserved - Ready for recovery |
| At 9 to 10 days of age Whrnwi homozygotes display increased activity, decreased ability to right their selves, and are generally smaller than unaffected siblings. By 14 to 16 days of age homozygotes display head bobbing, circling, and an unsteady gate. Adults display head tossing and circling behavior and deafness is indicated by 20 days of age. Sackler and Weltman reported the average number of circles by a prodded 12-week old female homozygote to be 407 in 10 minutes. They found female homozygotes to have an increased metabolic rate and adrenocorticosteroid activity and decreased body weights. Homozygous males were reported to have decreased blood glucose and liver glycogen levels, decreased white blood cell and eosinophil counts, increased plasma albumin levels, and decreased globulin levels, in addition to decreased weight and increased food intake. (Lane 1963; Sackler and Weltman 1967, 1970, 1971.)
While the organ of Corti in whirler homozygotes shows normal ..... | ||
| 007757 | B6.Cg-hml/J | Cryopreserved - Ready for recovery |
| Homozygotes have a faith-to-thrive phenotype such that they have a smaller body size and unbalanced gait detectable at 10 days of age. Those that survive to 2 months of age can generally live up to 18 months. The inner ear has extensive hypoplasia of the membranous labyrinth, a rudimentary tectorial membrane, and enlarged scala vestibuli and severe hearing loss or complete deafness are found at 19 days of age both by failed response to sounds and auditory brainstem response analysis. Homozygotes also fail to orient in water. | ||
| 000171 | B6.D2-KitW-45J/J | Cryopreserved - Ready for recovery |
| 001563 | B6.D2-KitW-73J/J | Cryopreserved - Ready for recovery |
| 004620 | B6.L-Whll/J | Cryopreserved - Ready for recovery |
| Whll/+ mice have a moderate circling phenotype accompanied by a mild hearing impairment. | ||
| 001177 | B6.LP-KitW-49J/J | Cryopreserved - Ready for recovery |
| 002492 | B6.MDB-Mbpshi-mld/J | Cryopreserved - Ready for recovery |
| 012823 | B6;129-Fzd4tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous Fzd4 (frizzled homolog 4 (Drosophila)) mice have a congenital retinal hypovascularization, a progressive inner ear vascular atrophy, a defect in the blood brain barrier in the cerebellum, and a progressive cerebellar degeneration associated with severe ataxia. Mice also show an absence of a skeletal muscle sheath around the lower esophagus associated with progressive esophageal distension. | ||
| 002544 | B6;129S2-Ntrk2tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk2tm targeted mutation (commonly referred to as trkB) die by 2-3 weeks of age. Homozygous mutant mice show a complete lack of nodose, vestibular, and cochlear neurons. In addition, mice display CNS deficits including cell death in dentate gyrus, cortical layers II-III and V-VI, striatum and thalamus. | ||
| 002481 | B6;129S2-Ntrk3tm1Bbd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Ntrk3tm1 targeted mutation (commonly referred to as trkC) die by 2-3 weeks of age. Homozygous mutant mice lack proprioceptive and cochlear neurons and have a reduction in vestibular neurons. | ||
| 004768 | B6;129S4-Ush1cdfcr-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for either Ush1cdfcr or Ush1cdfcr-2J display head tossing and hyperactive circling. They are unable to orient themselves in water to swim at the surface. Despite these behavioral traits, these mice are able to breed and have normal life spans. Adult homozygotes have no auditory-evoked brainstem response. This complete deafness was found in an Ush1cdfcr homozygote as early as 21 days of age. Scanning electron micrographs of the organ of Corti at 3 weeks of age reveal disorganized and splayed stereocilia of outer hair cells and, less severely, of inner hair cells along with degeneration of hair cells that yields a disorganized hair cell pattern. While progressive loss of hair cells and a secondary loss of spiral ganglion cells are found and are severe by 8 months of age, no gross morphological abnormalities were discerned in whole mounts of inner ears. At 9 months of age a slight peripheral retinal degeneration i ..... For more information please see the full phenotype on the strain data sheet | ||
| 008645 | B6;129S7-Pou4f3tm1Xia/J | Cryopreserved - Ready for recovery |
| These mice carry a targeted mutation of the POU domain, class 4, transcription factor 3 gene. Homozygotes are deaf, have impaired balance, and display a robust circling behavior due to defects of the inner ear. Auditory and vestibular hair cells are lost during late embryonic and early postnatal periods. A secondary loss of spiral and vestibular ganglion neurons is also seen. This strain may be useful in studies of auditory and vestibular system development. | ||
| 004502 | B6;AKR-Lxl2/GrsrJ | Cryopreserved - Ready for recovery |
| This dominant mutation causes the animal to present with all four limbs at odd angles to the body. There are extra toes on all four limbs and the rear legs are oriented backward. Severe arthritis of the knee was observed in one female, but no other histological lesions were seen. | ||
| 003892 | B6;BKS-Atp2b2dfw-3J/J | Cryopreserved - Ready for recovery |
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut ..... For more information please see the full phenotype on the strain data sheet | ||
| 000126 | B6By.Cg-Sd Mcoln3Va-J Krt25Re/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-J) are more pigmented than the original varitint waddler mice (Mcoln3 Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying two other mutations, rex (Krt25Re) and Danforth's short tail (Sd). | ||
| 000505 | B6C3 Aw-J/A-Mutedmu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the muted spontaneous mutation (Mutedmu) have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths from the sacculus and utriculus of one or both ears. The bony labyrinth is normal; the mice are not deaf and do not circle. Mutant mice have prolonged bleeding times and a platelet storage pool deficiency (SPD) associated with abnormalities of the dense granules of the blood platelets. The combination of pigment, otolith, and SPD abnormalities also occurs in two other mouse mutants, pallid and mocha (Ap3d1mh), and is also seen in human Hermansky-Pudlak syndrome. | ||
| 000506 | B6C3Fe a/a-Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 000636 | B6C3Fe a/a-Lmx1adr-J/J | Cryopreserved - Ready for recovery |
| Lmx1a encodes a LIM homeodomain (LIM-hd) protein that is expressed in the roof plate along the neuraxis during CNS development. The Lmx1adr-J mutation replaces a conserved cysteine in the LIM1 domain of the protein with a tyrosine (Millonig et al. 2000). Mice homozygous for Lmx1adr-Jare identifiable at birth by a thin filament extending from the end of the tail, which drops off within a few days, and a short or blunt tail. They may also have a head bleb. When fur develops, there may be a white belly spot. Lmx1adr-J/Lmx1adr-J mice are ataxic and hyperactive and have difficulty righting themselves, and they do not reproduce (Sweet and Wahlsten 1983). They also exhibit circling behavior, are deaf, and have inner ear and vertebral malformations (Manzanares et al. 2000).
Lmx1adr-J homozygotes exhibit defects of three classes of anatomic structures: the hindbrain roof plate, neural crest derived ..... | ||
| 001280 | B6C3Fe a/a-Lse/J | Cryopreserved - Ready for recovery |
| Lse/+ pups can be identified at birth by the presence of an open auditory meatus, which in normal mice remains closed until approximately day 13, when the eyes also open. Fewer than the expected 50% affected pups are born, and about 50% of pups identified as Lse/+ fail to survive until weaning. Homozygotes either die prenatally or are indistinguishable from heterozygotes. The ears of Lse/+ mice are positioned lower and further forward than those of normal mice and are abnormally formed. These mice are not deaf. In addition to the ear abnormalities, Lse/+ mice are smaller than their normal littermates and have opaque corneas (Theiler and Sweet 1986). | ||
| 001573 | B6C3Fe a/a-MitfMi/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the MitfMi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 000181 | B6C3Fe a/a-Otogtwt/J | Cryopreserved - Ready for recovery |
| When mice homozygous for the twister spontaneous mutation (twt) are picked up by the tail, all affected mice tuck their heads. Homozygous mutant mice may show circling behavior or tilted heads and none can swim. These mice are deaf. | ||
| 002078 | B6C3Fe a/a-Pcdh15av-2J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (av) that have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames waltzer 2 Jackson homozygous mutant mice (av2J/av2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av2J/av2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3 Jackson homozygotes (av3J/av3J), like Ames waltzer Jackson homozygotes (avJ/avJ), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 000230 | B6C3Fe a/a-Tcirg1oc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the osteosclerotic spontaneous mutation (oc) can be recognized at about 10 days by failure of eruption of the incisors, clubbed feet, and circling behavior. Homozygous mutant mice may also have a kinked tail. They grow normally for about the first 10 days of life, then lose weight or at least fail to gain. | ||
| 000063 | B6C3Fe a/a-sy/J | Cryopreserved - Ready for recovery |
| Most mice homozygous for the shaker-with-syndactylism mutation (sy) die within the first month, and none have lived to breed. Homozygous mutant mice may be syndactylous on all four feet; the forefeet may often be normal and possibly one or both hindfeet very occasionally so. The remainder of the skeleton shows many slight anomalies in addition to small size. The shafts of the long bones are considerably thinner than normal, and there are differences in shape of the sacral vertebrae and the scapula. Abnormal behavior appears during the first week. It consists of head-tossing and some circling, and the affected mice are always deaf. Abnormalities of the labyrinth can be seen at E13. | ||
| 000296 | B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-J) are more pigmented than the original varitint waddler mice (Mcoln3Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes of the two alleles (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying the semidominant hypodactyly spontaneous mutation (Hoxa13Hd). Heterozygous hyp ..... For more information please see the full phenotype on the strain data sheet | ||
| 003301 | B6C3FeF1 a/A-Eya1bor/J | Cryopreserved - Ready for recovery |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. The Eya1bor/Eya1bor mice are deaf and their behavior is marked by circling and head-bobbing. They lack all but the most basal one-quarter of the cochlea, and the organ of Corti is completely absent. They have foreshortened, narrower semicircular canals and in some the common crus is incomplete. Their kidneys are absent or dysmorphic with greater severity generally on the left side. Fewe ..... For more information please see the full phenotype on the strain data sheet | ||
| 000956 | B6CB-Mitfmi-rw/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. | ||
| 000288 | B6CBACa Aw-J/A-we a Mafbkr/J | Cryopreserved - Ready for recovery |
| 000551 | B6EiC3 a/A-Tbx15de-H/J | Cryopreserved - Ready for recovery |
| 000503 | B6EiC3Sn a/A-Gy/J | Cryopreserved - Ready for recovery |
| Gyro (Gy) is an X-linked dominant mutation that causes circling behavior and defects in phospate metabolism. It is allelic with the hypophosphatemia mutation (PhexHyp). Hemizygous males and heterozygous females are characterized by hypophosphatemia, rickets, circling behavior, and inner ear abnormalities. Affected males are also sterile. | ||
| 002432 | B6J x B6.C-H2-Kbm1/ByJ-Cdh23v-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the waltzer Jackson spontaneous mutation (Cdh23v-J) exhibit the circling, head-tossing, deafness, and hyperactivity typical of circling mutants. Homozygous mutant mice are very similar to other waltzer mutants (Cdh23v and Cdh23v-2J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (Cdh23v/+ Myo7ash1/+) become deaf by 3 to 6 months of age. Double heterozygotes show degeneration in the organ of Corti, stria vascularis, and spiral ganglion similar to that of Cdh23v-J homozygotes, but less severe and with much later onset. Viability and breeding ability are somewhat reduced. | ||
| 004771 | BALB/cBy-Ush1cdfcr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for either Ush1cdfcr or Ush1cdfcr-2J display head tossing and hyperactive circling. They are unable to orient themselves in water to swim at the surface. Despite these behavioral traits, these mice are able to breed and have normal life spans. Adult homozygotes have no auditory-evoked brainstem response. This complete deafness was found in an Ush1cdfcr homozygote as early as 21 days of age. Scanning electron micrographs of the organ of Corti at 3 weeks of age reveal disorganized and splayed stereocilia of outer hair cells and, less severely, of inner hair cells along with degeneration of hair cells that yields a disorganized hair cell pattern. While progressive loss of hair cells and a secondary loss of spiral ganglion cells are found and are severe by 8 months of age, no gross morphological abnormalities were discerned in whole mounts of inner ears. At 9 months of age a slight peripheral retinal degeneration is fou ..... For more information please see the full phenotype on the strain data sheet | ||
| 006274 | BALB/cByJ-Dfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the deaf ballerina mutation display circling and head tossing behavior, are deaf, and lack the corpus callosum. Heterozygous females do not breed. | ||
| 005226 | BALB/cJ-Mbpshi-J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the shiverer Jackson mutation can be identified at 12 days of age by a generalized tremor during locomotion and the severity of the phenotype progresses with age and includes a loss of coordination of the hindlimbs. Deficiency of myelin from the central nervous system has been found at 7 weeks of age, the earliest time-point assessed. | ||
| 004949 | BKS(Cg)-Grxcr1pi-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 3 Jackson mutation display bi-directional circling and head bobbing and are completely deaf by ABR assessment. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 004176 | BKS.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 003929 | BXA4/Pgn-Tmiesr-J/J | Cryopreserved - Ready for recovery |
| 006816 | BXA7/Pgn-Slc26a4pdsm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pdsm mutation display head bobbing, circling, and occasional head tilt, evident by 3 weeks of age. The inner ear defects include diminished or absent otoconia, hair cells and spiral ganglion cells, malformed tectorial membrane, a reduction in the number of cochlear turns, degeneration of the organ of Corti, and displacement of Reissner's membrane resulting in enlarged scala media. Serum chemistry and histology failed to detect any signs of hypothyroidism. | ||
| 005494 | C3.129S1(B6)-Grm1rcw/J | Cryopreserved - Ready for recovery |
| Visibly, Grm1rcw/Grm1rcw mice are identifiable by 2.5 - 3 weeks of age. Their constant wobbly gait frequently throws them off balance, but only briefly, as they show immediate and normal righting response. When walking, they often brace for balance with their fore- and hindfeet extended forward or sideways. Their heads lurch mildly and the mutants often sit on their haunches when motion falters. Their forefeet show normal grip strength when the mutant mice are pulled gently backwards over a cage cover. When picked up by the tail, they may clasp their hindfeet. However, they show sufficient hindlimb strength to prevent their falling when placed on an edge. Mutants live through adulthood, and mice of both sexes breed. Grm1rcw has been mapped between the flanking markers D10Mit49, at map position 6.3 Mb and D10Mit80, at map position 11.4 Mb. | ||
| 000638 | C3FeB6 A/Aw-J-Spnb4qv-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering-Jackson spontaneous mutation (Spnb4qv-J) are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their young. | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 000511 | C3H/HeJ-Ap3d1mh-2J/J | Cryopreserved - Ready for recovery |
| The mh-2J allele of Ap3d causes a similar yet less severe pigment dilution than that caused by the mh allele, but each causes a different neurological phenotype. These homozygotes are recognizable by a lighter coat color and decreased pigmentation in the eyes. For the Ap3dmh allele, this coat color dilution has been shown to result from smaller and fewer melanin granules in the hairs. While both alleles cause similar degrees of hyperactivity, the cochlear degeneration and accompanying head tilt is observed less frequently in the Ap3dmh-2J homozygotes and the auditory evoked brain responses in these mice are similar to wildtype. At three months of age, mice homozygous for the Ap3dmh allele have significantly increased auditory evoked potentials after the first of two paired tones. Ap3dmh-2J homozygotes also show an increased response to the first tone, but this has not been proven with stat ..... For more information please see the full phenotype on the strain data sheet | ||
| 001276 | C3H/HeJ-Atp2b2dfw/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the deaf waddler spontaneous mutation (Atp2b2dfw) are deaf, walk with a hesitant, wobbly gait, and bob their heads. Both sexes are fertile. | ||
| 000627 | C3H/HeJ-KitW-x/J | Cryopreserved - Ready for recovery |
| 003532 | C3HeB.129S7-Kcna1tm1Tem/J | Cryopreserved - Ready for recovery |
| Homozygous null mice display an epileptic phenotype (episodic eye blinking, twitching of vibrissae, forelimb paddling, arrested motion, hyperstartle response) beginning during the third postnatal week. Quantitative RNase protection analysis on brain tissue indicates that in heterozygous mice the Kcna1 transcript is reduced to approximately half that observed in wild-type littermates. No transcripts were detected in homozygous mice. Approximately 50% of the homozygous mice die between the third and fifth weeks of life. Mice surviving this period survive for varying periods, depending on genetic background; congenic C3HeB/FeJ mice usually die at 6-8 weeks; hybrid N:NIHS-BC mice have been maintained for over 12 months during which they continue to display spontaneous seizures. A similar phenotype with spontaneous seizures has been observed in mice having 129/Sv, C3HeB/FeJ, C57BL/6 X 129/Sv, and 129/Sv X N:NIHS-BC backgrounds. | ||
| 001434 | C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Zeb1Tw/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the twirler mutation (Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1rE-so) and extra toes-Jackson (Gli3St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E ..... For more information please see the full phenotype on the strain data sheet | ||
| 002588 | C3HeB/FeJ-Eya1bor/J | Cryopreserved - Ready for recovery |
| The human Branchio-Oto-Renal Syndrome is generally a dominant disorder with incomplete penetrance and variable expressivity resulting from null mutations in the EYA1 gene. The mouse Eya1bor allele is primarily a recessive hypomorphic mutation. Nevertheless, homozygous mice with this hypomorphic allele offer a good model for Branchio-Oto-Renal Syndrome. The phenotype of Eya1bor/Eya1bor mice parallels that of the human Branchio-Oto-Renal Syndrome and both are thought to result from reduced gene dosage. During mapping crosses using CAST/Ei and C3H/HeJ, it was found that genetic background impacts both the kidney and inner ear phenotypes, and modifier genes in humans also may impact the severity of Branchio-Oto-Renal-Syndrome. | ||
| 004406 | C3HeB/FeJ-Pou3f4del-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pou3f4del-J display head shaking and circling behavior by three weeks of age. Homozygous females and males hemizygous for this X-linked mutation have profound deafness, although heterozygous females do not. They have cochlear hypoplasia, a reduced number of cochlear turns, failure to fully form the bony structure of the modiolus, and detachment of the stria vascularis. | ||
| 000847 | C3Sn.B6-KitW-39J/J | Cryopreserved - Ready for recovery |
| 001547 | C3Sn.Cg-Cm/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the coloboma spontaneous mutation (Cm) show abnormal posture, head shaking or bobbing, and circling. Heterozygous mutant mice are extremely hyperactive, locomotor activity being three times that of normal mice. | ||
| 001380 | C3Sn.Cg-KitlSl-con/J | Cryopreserved - Ready for recovery |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 004764 | C57BL/6J-Cdh23v-8J/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-8J entry. | ||
| 004819 | C57BL/6J-Cdh23v-9J/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-9J entry. | ||
| 003129 | C57BL/6J-Epha4rb-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Epha4rb-2J allele can be visibly identified by 2.5 - 3 weeks of age by a constant hopping gait of the hind limbs; the forelimbs may show a hopping gait or move normally. When picked up by the tail mutants clasp their hindlimbs and show reduced ability to hold on to an edge; forelimbs show normal strength. More severely affected homozygous mutant mice also lean frequently to either side, a phenotype not reported in mice homozygous for the rb allele of Epha4. Homozygous females may deliver 2-3 pups per litter but often exhibit poor nurturing. | ||
| 004820 | C57BL/6J-Kcne12J/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcne12J entry. | ||
| 004703 | C57BL/6J-Kcnq2Nmf134/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq2Nmf134 entry. | ||
| 000166 | C57BL/6J-KitW-17J/J | Cryopreserved - Ready for recovery |
| 000167 | C57BL/6J-KitW-18J/J | Cryopreserved - Ready for recovery |
| 000169 | C57BL/6J-KitW-20J/J | Cryopreserved - Ready for recovery |
| 000117 | C57BL/6J-KitW-34J/J | Cryopreserved - Ready for recovery |
| 000128 | C57BL/6J-KitW-35J/J | Cryopreserved - Ready for recovery |
| 000134 | C57BL/6J-KitW-37J/J | Cryopreserved - Ready for recovery |
| 000062 | C57BL/6J-KitW-39J/J | Cryopreserved - Ready for recovery |
| 000121 | C57BL/6J-KitW-40J/J | Cryopreserved - Ready for recovery |
| 000119 | C57BL/6J-KitW-41J/J | Cryopreserved - Ready for recovery |
| 000127 | C57BL/6J-KitW-42J/J | Cryopreserved - Ready for recovery |
| 000129 | C57BL/6J-KitW-43J/J | Cryopreserved - Ready for recovery |
| 000990 | C57BL/6J-KitW-55J/J | Cryopreserved - Ready for recovery |
| 001179 | C57BL/6J-KitW-62J/J | Cryopreserved - Ready for recovery |
| 003252 | C57BL/6J-KitlSl-20J/J | Cryopreserved - Ready for recovery |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. | ||
| 002611 | C57BL/6J-Mitfmi-bws/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. | ||
| 005749 | C57BL/6J-Myo6sv-3J/J | Cryopreserved - Ready for recovery |
| 005468 | C57BL/6J-Myo7ash1-11J/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Myo7ash1-11J entry. | ||
| 000531 | C57BL/6J-Otx1jv/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Jackson waltzer mutation run in circles and shake their heads. The lateral semicircular canal and its cristae are absent, and the sacculus and utriculus may be morphologically abnormal. However, hearing is unaffected. This pheontype is similar to that reported for the Otx1tm1Asim targeted mutation and complementation testing with this targeted mutation showed jv to be an allele of Otx1. (Note that C57BL/6J is homozygous for ahl, the age related hearing loss 1 mutation, which on this strain background causes progressive hearing loss with onset after 10 months of age.) Homozygotes can swim. | ||
| 002072 | C57BL/6J-Pcdh15av-3J/J | Cryopreserved - Ready for recovery |
| There have been several remutations to Ames waltzer (av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames wa ltzer 2J homozygous mutant mice (av2J/av2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av2J/av2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (av3J/av3J), like Ames waltzer-J (avJ/avJ), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 003484 | C57BL/6J-Pou4f3ddl/J | Cryopreserved - Ready for recovery |
| 000219 | C57BL/6J-Slc30a4lm/J | Cryopreserved - Ready for recovery |
| Female mice homozygous for the lethal milk mutation (Slc30a4lm, formerly Znt4lm) produce milk that is lethal to mice nursed during the first week of life and detrimental to mice nursed thereafter. The lethal and detrimental effects are due to a deficiency of zinc in the milk. If foster nursed on normal dams, lethal milk homozygotes survive and become reproductively mature. Zinc supplementation of the drinking water of dams enables them to nurse their young successfully. All homozygous mutant mice lack utricular otoliths and this defect is not prevented by zinc supplementation. They have varying loss of saccular otoliths and show mild behavioral abnormalities related to the otolith defect. Homozygotes over eight months of age show progressive hair loss, dermatitis, and skin lesions, symptoms of zinc deficiency. | ||
| 000563 | C57BL/6J-Sobpjc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Jackson circler spontaneous mutation (Sobpjc) show erratic circling behavior which becomes more pronounced with age. Homozygous mutant mice are very active, bobbing up and down and flexing head and trunk ventrally towards the tail and mice can swim. Mice can be identified at weaning by a characteristic flexing behavior when suspended by tail. | ||
| 001028 | C57BL/6J-Spnb4qv-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering 3 Jackson spontaneous mutation (Spnb4qv-3J) are very similar to mice homozygous for the quivering-Jackson mutation (Spnb4qv-J). Homozygous quivering mutant mice are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are st ..... For more information please see the full phenotype on the strain data sheet | ||
| 000543 | C57BL/6J-Tmiesr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spinner spontaneous (Tmiesr) show the typical head tossing, circling, deafness, and hyperactivity of the shaker and waltzer mutants. Abnormal behavior in homozygous mutant mice can be recognized as early as 7 days. Inner ear abnormalities consist of degeneration of the organ of Corti and spiral ganglion, reduction in size of the stria vascularis of the cochlea, and degeneration of the saccular macula. Both sexes are fertile, but females are not good mothers. | ||
| 004811 | C57BL/6J-nmf110/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf110 entry. | ||
| 004812 | C57BL/6J-nmf111/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf111 entry. | ||
| 004747 | C57BL/6J-nmf118/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf118 entry. | ||
| 004818 | C57BL/6J-nmf172/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf172 entry. | ||
| 004831 | C57BL/6J-nmf219/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf219 entry. | ||
| 004656 | C57BL/6J-nmf88/J | Cryopreserved - Ready for recovery |
| nmf88 mutants have an increased propensity for seizure triggered by PTZ or transcorneal stimulation. For further details see the Neuroscience Mutagenesis Facility web page for the nmf88 entry. | ||
| 003711 | CAST.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 010826 | CB.129S-Tectatm1.1Ogha/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygous mice have a thickened and shortened tectorial membrane, which covers only the first of the three rows of the cochlear outer hair cells. In homozygotes the membrane is thicker, appears to be detached from the sensory epithelium, loosely connected to the spiral limbus and elevated from the organ of Corti. Heterozygous and homozygous mice exhibit, respectively, reduced and absent forward transduction, partial and severe hearing loss, partial and severe disruption of the fibrils surrounding the edges of the tectorial membrane. Both genotypes exhibit enhanced reverse transduction. | ||
| 006169 | CBA.Cg-Tmc1dn/AjgJ | Cryopreserved - Ready for recovery |
| Homozygotes for this spontaneous mutation exhibit degeneration in the spiral ganglion neurons as well as the organ of Corti and the saccular macula. Mice are deaf throughout life. This strain may be used to research inherited deafness. | ||
| 002457 | CBA/J-wl3J/J | Cryopreserved - Ready for recovery |
| 000965 | CBACa.C3-KitW-x/J | Cryopreserved - Ready for recovery |
| 005696 | CBACaJ;129S-Chrna9tm1Bedv/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable and fertile and have normal balance, movement, cochlear duct morphology, and gross development and position of the olivo-cochlear (OC) bundle. However, most outer hair cells are innervated by one large OC efferent fiber terminal instead of multiple smaller terminals as in wildtype. OC terminal plexus in close apposition to the inner hair somata are absent in homozygotes. Null mice fail to show electrophysiological cochlear responses during efferent fiber activation. This mutant may be suitable for use in studies related to auditory-related studies of the inner ear, including the cochlea, organ of Corti, and hair cells as well as acetylcholine receptor/neurotransmitter or olfactory research. | ||
| 000805 | CBy.RF-Tshrhyt/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hypothyroid spontaneous mutation (Tshrhyt) are characterized by growth retardation, low thyroid hormone levels, elevated thyroid stimulating hormone (TSH) and hypoplastic thyroid glands. Homozygous mice of both sexes are infertile but fertility as well as growth can be restored by treatment with thyroid hormone. The mice do not respond to exogenous TSH. Homozygous mutant mice also display audiotory defects characterized by morphologic abnormalities of the stereocilia on both inner and outer hair cell systems | ||
| 002894 | CByJ.A-Atp2b2dfw-2J/J | Cryopreserved - Ready for recovery |
| The deaf waddler 2J allele (Atp2b2dfw-2J) arose spontaneously in a congenic substrain of BALB/cByJ mice, CByJ.A-fsn/J. Homozygous mutant mice are viable, but neither sex will breed. They are recognizable by 12-14 days of age by their hesitant, wobbly gait and head bobbing behavior. Homozygotes also develop a slight body tremor and become increasingly lethargic. Homozygous mutant mice are profoundly deaf, exhibiting no discernible auditory brainstem responses (ABR) to stimuli up to 100 dB. Heterozygous Atp2b2dfw-2J mutant mice also show age-dependent changes in ABR and progressive hearing loss as a result of a modifier allele (ahl) present in BALB/cByJ mice. | ||
| 005016 | CByJ;B6-Cdh23v-10J/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23v-10J entry. | ||
| 000293 | CHMU/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the congenital hydrocephalus (Foxc1ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Mutedmu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths ..... For more information please see the full phenotype on the strain data sheet | ||
| 004223 | CHa.SWV(C3Fe)-Mbpshi/J | Cryopreserved - Ready for recovery |
| 004641 | DBA/2J-Grxcr1pi-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pirouette 2 Jackson mutation display bi-directional circling and head bobbing and are completely deaf by ABR assessment. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue. | ||
| 000252 | DC/LeJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004). | ||
| 000092 | FL/1Re-KitW/J | Cryopreserved - Ready for recovery |
| Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 000619 | FS/EiJ | Cryopreserved - Ready for recovery |
| The FS/Ei strain was originally used as a linkage testing stock for gene mapping. It is homozygous for several visible recessive mutations including brown (Tyrp1b), pink-eyed dilution (Oca2p), chinchilla (Tyrc-ch), frizzy (fr), and the neurological mutation shaker 1 (Myo7ash1). It is also homozygous for a couple allelic variants that can be easily typed (Mod2b and Hbbd). Mice homozygous for the shaker 1 show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist ..... For more information please see the full phenotype on the strain data sheet | ||
| 000259 | JE/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the jerker spontaneous mutation (Espnje) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes ar ..... For more information please see the full phenotype on the strain data sheet | ||
| 000262 | LS/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the lethal spotting mutation (Edn3ls) resemble piebald mice (Ednrbs/Ednrbs) mice. Homozygous mutant mice exhibit considerable white spotting and like homozygotes for the piebald-lethal allele (Ednrbs-l) usually develop megacolon. Lethal spotting mutant mice usually die in the third week of life from the megacolon abnormality, which is associated with deficiency of intrinsic ganglion cells in the lower colon. A few homozygotes may survive and breed. This strain is also homozygous for the black and tan coat color mutation (at). | ||
| 002757 | MK;B6-Slc12a2sy-ns/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker with no syndactylism spontaneous mutation (Slc12a2sy-ns) is allelic with the original radiaton-induced shaker-with-syndactylism mutation (sy). Homozygous mutant mice exhibit deafness and balance defects but have a normal foot morphology. Two other spontaneous alleles of sy, fused phalanges and fused phalanges 2 Jackson, do not affect hearing or behavior. Tests for allelism among mice with four different mutant alleles at the shaker-with-syndactylism locus (sy, syfp, syfp-2J, and Slc12a2sy-ns) indicate that sy is a deletion including at least two genes associated with distinct phenotypes. Mice homozygous for sy have syndactylous feet and other skeletal malformations, are deaf, and exhibit abnormal behavior characteristic of vestibular dysfunction. Complementation test results indicate that sy, syfp and syfp-2J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000993 | NZB/BlNJ-KitW-59J/J | Cryopreserved - Ready for recovery |
| 005052 | PN/nBSwUmabJ | Cryopreserved - Ready for recovery |
| PN/nBSwUmabJ mice develop a predominantly female lupus-like syndrome with age (Walker et al., 1978). Characteristics of the systemic lupus erythemoatosus syndrome include: abnormalities in B and T cell function, hypergammaglobulinemia, antibody production against multiple autoantigens, severe systemic perivasculitis and vasculitis, and immune complex-mediated glomerulonephritis (Walker et al.,1978, Luzina et al., 1999, Davidson et al., 1982, Handwerger et al.,1999). Perivascular and vascular infiltrates are composed of unusual phenotypic markers characteristic of both T and B cells (Luzina et al, 1999). By three months of age 88-100% of mice have IgG autoantibodies (Handwerger et al., 1999). Death usually occurs earlier in females as a result of glomerulonephritis and arteritis. The disease progression is accelerated in the female offspring of NZB and PN F1 crosses (Walker et al., 1986). PN/nBSwUmabJ mice develop hearing loss and otic capsule sclerosis demonstrating some paralle ..... For more information please see the full phenotype on the strain data sheet | ||
| 000682 | RF/J | Cryopreserved - Ready for recovery |
| Derived from an unknown stock at the Rockefeller Institute, RF/J are commonly used in research in genetics, immunology, oncology and virology. This strain displays a high cancer incidence including leukemia (reportedly between 40 and 66%) and reticulum cell sarcomas (approximately 50%). Mice also have a high incidence of spontaneous glomerular hyalinisation and glomerulosclerosis developing between eight and twenty months. | ||
| 000268 | RSV/LeJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002747 | SENCARB/PtJ | Cryopreserved - Ready for recovery |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 000271 | SH1/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 1 spontaneous mutation (Myo7ash1) show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist of degeneration of the organ of Corti, the spiral ganglion, and the stria vascularis in the cochlea, and of the saccular macula and the vestibular ganglion in the vestibular labyrinth. | ||
| 002335 | SKH2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa ..... For more information please see the full phenotype on the strain data sheet | ||
| 000308 | SSL/LeJ | Cryopreserved - Ready for recovery |
| This inbred strain carries both the piebald (Ednrbs) and piebald lethal (Ednrbs-l) alleles. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. Homozygous piebald lethal mice are almost completely white with dark eyes and only an occasional small pigmented spot on the head or rump. Piebald-piebald lethal heterozygotes (Ednrbs/Ednrbs-l) mice resemble piebald mice in the degree of spotting. The piebald mutations disrupt the development of melanocytes derived from the neural crest. All piebald lethal homozygotes develop megacolon with a lack of enteric ganglion cells in the posterior end of the colon. On the SSL/Le background, although many Ednrbs-l homozygotes die between 2 and 4 weeks of age, significant numbers survive and may breed. The incidence of megacolon is reduced in piebald and piebald-piebald lethal ..... For more information please see the full phenotype on the strain data sheet | ||
| 002267 | STOCK Bdnftm1Jae/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Bdnftm1Jae mutation show about 1/2 normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 007674 | STOCK Esrrbtm1.1Nat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nr3b2CKO allele possess loxP sites flanking exon 2 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exon containing the initiator methionine codon and encoding the N-terminal 132 amino acids (including part of the DNA-binding domain) deleted in the cre-expressing tissue(s). Of note, if the conditional Nr3b2CKO is deleted by Cre recombinase in the placenta and embryo, embryonic lethality will result (placental defect). If the conditional Nr3b2CKO is deleted by Cre recombinase only in the embryo, the resulting mice exhibit an inner ear defect (decreased endolymph production) resulting in deafness and defective balance. These Nr3b2CKO mutant mice may be useful in generating conditional mutations to study disorders of hearing and balance, inner ear development (such as endolymph-producing epithelia withi ..... For more information please see the full phenotype on the strain data sheet | ||
| 000979 | STOCK KitlSl-16J/J | Cryopreserved - Ready for recovery |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. | ||
| 001253 | STOCK MitfMi-wh +/+ Wnt7apx/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7apx) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet | ||
| 000109 | STOCK Myo15sh2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 spontaneous mutation (Myo15sh2) are viable and fertile, showing only a slight reduction in both compared to wildtype mice. Homozygous mutant mice display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. Homozygotes appear to be deaf from the beginning, and the saccular macula is abnormal at birth. The stria vascularis appears normal by light microscopy at 2 weeks, but begins to show degenerative changes shortly thereafter. Many of the cells contain electron-dense inclusions filled with a fine granular material. At 2.5 months, the type I hair cells of the cristae ampullares and maculae utriculi contain rod-shaped inclusion bodies composed of actin filaments. The visible phenotype of the shaker-2 Jackson (Myo15sh2-J, Stock No. 002048<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002919 | STOCK Myo7ash1-7J/J | Cryopreserved - Ready for recovery |
| Myo7ash1-7J homozygotes exhibit circling behavior, a slight head tilt and side-to-side head bob. They develop progressive hearing loss, becoming totally deaf by 60 days of age. Heterozygotes are normal. (Samples et al., 2000). Mutations of the human ortholog of Myo7a, MYO7A, have been characterized in pedigrees of patients having Usher syndrome type 1 (USH1), an autosomal recessive disorder characterized by profound deafness, vestibular dysfunction and progressive retinitis pigmentosa (Weil et al., 1995; Weston et al., 1996; Adato et al., 1997; Levy et al., 1997; Liu et al., 1998; Espinos et al., 1998; Cuevas et al., 1998, 1999; Janecke et al., 1999). MYO7A mutations have also been identified in patients with autosomal dominant non-syndromic deafness (Liu et al., 1997) and autosomal recessive isolated deafness (Liu et al., 1997; Weil et al., 1997). | ||
| 000302 | STOCK a/a MitfMi-wh +/+ Itpr1opt/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalities of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the opisthotonus spontaneous mutation (Itpr1opt) display a characteristic upward arching of head and tail. Homozygous mutant mice can be recognized at about 10 days of age by their loss of balance when standing or moving. Typical behavior of 15 to 20 day old homozygotes consists of falling over and struggling to get up. Agitation and s ..... For more information please see the full phenotype on the strain data sheet | ||
| 000279 | STOCK gr +/+ Ap3d1mh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the mocha spontaneous mutation (Ap3d1mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1mh allele have si ..... For more information please see the full phenotype on the strain data sheet | ||
| 000312 | STOCK stb + a/+ Fignfi a/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fidget spontaneous mutation (Fignfi) toss their heads from side to side and tend to run in circles. Homozygous fidgit mice are hypersensitive to sound in early life, but later lose hearing ability. Corneal lesions are common, and hind foot polydactylism occurs. The bony labyrinth is quite defective. Other abnormalities including small eyes, absence of lachrymal glands, dislocation of the hip, and displaced parafloccular lobes of the cerebellum. Viability of homozygotes is usually less than normal and fertility is poor. The STOCK is also carrying the stubby spontaneous mutation (stb). Homozygous stubby mice are recognizable at 4 or 5 days by a domed head and thick short tail. Adult stubby mice have shorter heads, bodies, and legs compared to wildtype mice. Most females are fertile but males do not breed. Male mice do produce normal numbers of motile sperm. Cartilage histology is within normal limits, but chondrogenesis stops earlier than ..... For more information please see the full phenotype on the strain data sheet | ||
| 003304 | STOCK Rb(16.17)7Bnr-Myo15sh2-2J/J | Cryopreserved - Ready for recovery |
| 000275 | V/LeJ | Cryopreserved - Ready for recovery |
| This strain was originally used as a linkage stock for gene mapping. It is homozygous for several visible recessive mutations all located on different chromosomes including nonagouti (a), fuzzy (fz), leaden (Mlphln), and piebald (Ednrbs) and is segregating for the neurological mutation, waltzer (Cdh23v). Homozygous waltzer mice show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. Homozygous piebald mice have dark eyes. The white areas of the coat are completely lacking in melanocytes and there is a reduction in the number of melanocytes in the choroid layer of the eye. | ||
| 000161 | WB.D2-KitlSl-d/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 000933 | YBR/EiJ | Cryopreserved - Ready for recovery |
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