Search Criteria: Strain Type is "Spontaneous Mutation"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full phenotype on the strain data sheet | ||
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full phenotype on the strain data sheet | ||
| 001800 | FVB/NJ | Level 1 |
| FVB/NJ was inbred for the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ mice are commonly used for transgenic injection. Compared to many other inbred strains, FVB/NJ is highly susceptible to asthma-like airway responsiveness with significant generation of antigen-specific IgE. Despite having the H2q MHC haplotype, FVB/NJ are resistant to collagen-induced arthritis. This resistance stems from coding polymorphisms in Tcra-V11.1 and a genomic deletion of some Tcrb-V genes that includes Tcrb-V8.2. FVB/NJ have higher than average activity, anxiety, and basal body temperature, low stress-induced hyperthermia, and are homozygous for the Pde6brd1 allele, which results in early onset retinal degeneration. Although FVB/N typically do not develop spontaneous tumors, they are highly susceptible to chemic
..... For more information please see the full phenotype on the strain data sheet | ||
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 001162 | B6(C)-H2-Ab1bm12/KhEgJ | Level 2 |
| 000058 | B6(Cg)-Tyrc-2J/J | Level 2 |
| Mice homozygous for Tyrc-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyrc-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004). | ||
| 000632 | B6.V-Lepob/J | Level 2 |
| Mice homozygous for the obese spontaneous mutation, (Lepob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase in body weight, and probably results from it. Homozygotes have an ab
..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol
..... For more information please see the full phenotype on the strain data sheet | ||
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 2 |
| The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmdmdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmdmdx mutants do not express dystrophin and therefore have been
..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 001913 | B6.CB17-Prkdcscid/SzJ | Level 3 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 000482 | B6.MRL-Faslpr/J | Level 3 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full phenotype on the strain data sheet | ||
| 005557 | NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ | Level 3 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34+ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr
..... For more information please see the full phenotype on the strain data sheet | ||
| 002019 | NU/J | Level 3 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when
..... For more information please see the full phenotype on the strain data sheet | ||
| 100409 | B6129PF1/J-Aw-J/Aw | Level 4 |
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. The Cryaa
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| 000051 | C57BL/6J-Aw-J/J | Level 4 |
| Mice are agouti (hairs are black with a subapical yellow band) with a cream or white belly. Females may be used as foster mothers for ovary transplantation of mutations maintained in a/a strains because Aw-J is dominant to the nonagouti a. Since a to Aw is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin. | ||
| 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. | ||
| 000629 | C57BL/6J-Lystbg-J/J | Level 4 |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn
..... 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). 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. | ||
| 000711 | CByJ.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 000485 | MRL/MpJ-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-lpr/lpr mouse but not the MRL normal (Hewicker 1990). Onset and severity of symptoms associated with the Faslpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 000395 | 129S1/Sv-Vsx2or-J/J | Repository- Live |
| 008456 | 129S1/SvImJ-Myo6sv-4J/J | Repository- Live |
| 006246 | A/J-sunk/J | Repository- Live |
| 005136 | A/WySnJ-ctl/J | Repository- Live |
| Mice homozygous for the ctl mutation are easily recognizable at birth by their curly or bent tails. | ||
| 008657 | AKR/J-agil2J/J | Repository- Live |
| 004684 | B6(129P2) Nos2tm1Lau-chtl/J | Repository- Live |
| This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock. | ||
| 005559 | B6(129S4)-Hps6ru-7J/J | Repository- Live |
| 005379 | B6(A)-Rpe65rd12/J | Repository- Live |
| 008288 | B6(Cg)-Cdh23v-11J/J | Repository- Live |
| 003916 | B6(Cg)-Col2a1sedc/J | Repository- Live |
| Newborn homozygotes are smaller than normal, have a shortened trunk, and often display head bobbing. Decreased body weight persists into adulthood, and the noses, trunks, tails, skulls, and long bones of adults are shortened relative to those of normal siblings. Abnormal epiphyses, with dysplasia of the vertebrae, femora, and tibias are found. Although light microscopy failed to detect any abnormalities in the inner ear, the head bobbing characteristic accompanying this mutation is usually associated with inner ear defects. Auditory brainstem response threshold analysis of 10-15 week old homozygotes does show hearing impairment. Clefts develop between the inner and outer aspects of the inner nuclear layer of the retina (retinoschisis). | ||
| 005071 | B6(Cg)-DctSlt-lt3J/J | Repository- Live |
| DctSlt-lt3J heterozygous mice are diluted to a dark brown and homozygous mice are diluted to a light brown. | ||
| 006111 | B6(Cg)-Ush1gjs-2J/J | Repository- Live |
| 004640 | B6(MOR)-Tmhshscy/J | Repository- Live |
| Mice homozygous for the Tmhshscy mutation circle rapidly, shake their heads from side to side, fail to swim, and are congenitally deaf. Although hair cells appear normal at birth, they degenerate. At 4 months of age, degeneration of the organ of Corti is also found, more pronounced in the basal region of the cochlea than the apex, with loss of inner and outer hair cells and decreased spiral ganglia (Longo-Guess et al., 2005). | ||
| 005717 | B6(NOD) H2g7-Sostdc1shk/J | Repository- Live |
| 005624 | B6(V) Lepob-whe/J | Repository- Live |
| 008129 | B6(V)-Bhrd/J | Repository- Live |
| 006860 | B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Repository- Live |
| Mice homozygous for the targeted mutation and heterozygous for the Ins2Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants
..... For more information please see the full phenotype on the strain data sheet | ||
| 008451 | B6.129P(Cg)-Ptprca Cx3cr1tm1Litt/LittJ | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprca) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul
..... For more information please see the full phenotype on the strain data sheet | ||
| 000783 | B6.A-Ush1gjs/J | Repository- Live |
| Mice homozygous for the Ush1gjs allele are deaf, circle, and toss their heads from side to side. They are viable and fertile but due to their circling gait females may trample their pups and thus should not be used for breeding. No auditory brain response was detected from homozygotes at 14, 21, and 30 days of age. At 10-14 days of age the stereocilia of the outer and macular hair cells are disarrayed or missing although no abnormal phenotype is evident in inner hair cells, or in the gross anatomy of the cochlea or vestibule. The steriocilia degeneration in outer hair cells continues but the inner hair cells remain normal at 30-47 days of age. (Dickie and Deol, 1967; Kitamura et al., 1992.) | ||
| 007227 | B6.B10ScN-Tlr4lps-del/JthJ | Repository- Live |
| This spontaneous mutation is a 7 kb deletion in the Tlr4 gene, which results in absence of both mRNA and protein and thus exhibits a defective response to LPS stimulation. The functionally similar Tlr4Lps-d mutation found in C3H/HeJ mice is a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4lps-n, occurs in most other C3H and C57BL/10 substrains and most mouse strains. This strain may be used to study the Toll signalling pathway and susceptibility to Gram-negative bacterial infection. | ||
| 000537 | B6.BR-Agtpbp1pcd/J | Repository- Live |
| Mice homozygous for the Purkinje cell degeneration spontaneous mutation (Agtpbp1pcd) show a moderate ataxia beginning at 3 to 4 weeks. Homozygous mutant mice are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic nuclei begin to appear in the photoreceptor cells between 18 and 25 days, and the outer rod segments become disorganized. Degeneration of the photor
..... For more information please see the full phenotype on the strain data sheet | ||
| 008140 | B6.C(Cg)-Atcayji/BurJ | Repository- Live |
| ji homozygotes can first be identified at approximately 12 days of age by a leaning, zig-zag gait when they attempt to run and by the difficulty they have righting themselves when placed on their backs. Disease progression is rapid such that within two more days mutants are found to crouch on their heels in a squatting position and can not run without falling. Within three to four days of the first symptoms, tetany is seen during exertion or excitement. This is initially most pronounced in the forelegs, which the mice beat up and down during these two- to three-second spasms. Failure to gain weight is seen by the third week of life and it is unclear whether this results from an inability to take in food. The severity and frequency of tetany increases, and during the fourth week weight loss and increased weakness precede death. The mean age of death is approximately 31 days. Tetrahydrobiopterin levels in the brain and GTP cyclohydrolase activity in the liver are lower in ji homoz
..... For more information please see the full phenotype on the strain data sheet | ||
| 006557 | B6.C3-Gusbmps-2J/BrkJ | Repository- Live |
| Mice homozygous for the Gusmps-2J allele exhibit a phenotype similar to Gusmps homozygotes including skeletal deformities, lysosomal storage disease and elevated levels of the lysosomal enzymes alpha-galactosidase and beta-hexosaminidase (Gwynn et al., 1998). Like the Gusmps heterozygote, Gusmps-2J heterozygotes have a 26-85% reduction in beta-glucuronidase activity. depending on tissue type (Gwynn et al., 1998, Birkenmeier et al., 1989). Homozygotes of both alleles have beta-glucuronidase activity levels at 1% of the control level. Unlike the Gusmps homozygote, Gusmps-2J homozygotes on the C3H background live longer, are fertile and can raise litters to weaning age (Gwynn et al., 1998). In addition to a difference in the nature of the mutations between these two alleles, it is also likely that the phenotypic differences are the result of strain background. C3H/HeOuJ mice carry a
..... For more information please see the full phenotype on the strain data sheet | ||
| 006562 | B6.CBy(Cg)-Gusbmps Gpi1a-m1J/BrkJ | Repository- Live |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 008000 | B6.CBy-Dscamdel17/RwbJ | Repository- Live |
| Mice homozygous for this spontaneous mutation become severely uncoordinated by postnatal day 3, developing spontaneous seizures and kyphosis. On a mixed BALB/cBy and C57BL/6 background some homozygotes survive, are fertile and have a normal lifespan. On the C57BL/6 background, homozygotes exhibit a more severe phenotype and die shortly after birth. With the exception of the caudal folium of the cerebellum, the central nervous system appears normal on a gross level, however, the retinal ganglion cell layer and inner plexiform layer exhibit disorganization by postnatal day 4. Retinal amacrine cells display defects in the arborization of processes and spacing of cell bodies. This mutant mouse strain may useful in studies of the retina and the mechanism of neuronal self-avoidance. | ||
| 004297 | B6.CXB1-Pde6brd10/J | Repository- Live |
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Repository- Live |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 006124 | B6.Cg-Myo6sv-2J/J | Repository- Live |
| 004643 | B6.Cg-Nr2e3rd7/J | Repository- Live |
| Nr2e3 is a retinal transcription factor important in the developmental pathways of photoreceptor cells. In mice homozygous for Nr2e3rd7, evenly distributed white spots cover the retina and have been detected by Fundus examination as early as 16.5 days of age. Whorls and rosettes in the outer nuclear layer can first be detected at 12.5 days of age, before the eyes open. These whorls likely underlie the appearance of the white spots on the retina and the white spots and whorls are both present at one month of age then are reduced in number by 5 months, and disappear by 16 months. Electroretinographs give normal signals until 5 months of age when both rod and cone signals begin to show a progressive reduction. Attenuated retinal vessels and mottled pigment are found by 16 months of age, and the outer nuclear layer is only half normal thickness subsequent to progressive loss of cones and rods. Immunohistochemical assessment revealed that the whorls are filled
..... For more information please see the full phenotype on the strain data sheet | ||
| 000528 | B6.Cg-PhexHyp/J | Repository- Live |
| Hypophosphatemia (PhexHyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (PhexGy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males. | ||
| 005089 | B6.Cg-Qkqk-2J/J | Repository- Live |
| Qkqk-2J homozygotes display rapid tremors by approximately 2 weeks of age. Histological examination at 3 weeks of age reveals holes in the striatum of the cortex and cerebellum and in the myelin of the spinal cord. Vision and hearing appear normal. | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Repository- Live |
| On an albino background Tg(Tyr)3412ARpw permits the identification of gender as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother.
This strain is also homozygous for Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not female brain (Dewing et al., 20
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| 006428 | B6.Cg-hyrh/J | Repository- Live |
| Mice homozygous for this spontaneous mutation have smaller bodies and develop hydrocephaly and rhinitis, dying by 3 weeks of age. | ||
| 002504 | B6.D2-Pmp22Tr-J/J | Repository- Live |
| Mice heterozygous for the trembler-Jackson spontaneous mutation (Pmp22Tr-J) are similar to heterozygotes carrying the original trembler mutation (Pmp22Tr). However, the behavior and neuropathology of trembler-Jackson heterozygotes is less severe. The tremor phenotype cannot be reliably recognized before 20 to 25 days. There are no obvious seizures and only a mild gait abnormality. In the PNS, the myelin deficiency is considerably less severe than that of trembler mice. Homozygous trembler-Jackson mice are recognizable by 8 days of age after which they become progressively disabled. Homozygous mutant mice are unable to walk normally and can right themselves only with great difficulty; most are dead by 18 days. It should be noted that although trembler homozygotes are more severely demyelinated than trembler-Jackson homozygotes, the trembler mice live a normal lifespan while trembler-Jackson mice die prior to weaning. Survival of trembler homozygotes
..... For more information please see the full phenotype on the strain data sheet | ||
| 003923 | B6.HRS(BKS)-Cpefat/J | Repository- Live |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BL/6J genetic background (N10) become noticeably obese by 14-15 weeks of age. There is also some sexual dimorphism; female homozygous mutant mice develop obesity at a later age than males. Cpefat mice actually weigh less than wildtype controls prior to weaning age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance. Cpefat mice appear healthier on the C57BL/6J genetic background, avoiding the hereditary hydronephrosis present in C57BLKS/J and a lower incidence of malocclusion. | ||
| 004521 | B6.PL-Nppclbab/J | Repository- Live |
| 008723 | B6.WB-trls2J/J | Repository- Live |
| 000524 | B6.WK-Lama2dy-2J/J | Repository- Live |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full phenotype on the strain data sheet | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/J | Repository- Live |
| 005250 | B6;129S2-Relnrl-4J/J | Repository- Live |
| 003506 | B6;C-Npr3lgj/J | Repository- Live |
| 004200 | B6;CBACa Aw-J/A-Npr2cn-2J/J | Repository- Live |
| Mice carrying the Npr2cn-2J display mutation short thick femurs, round heads, disorganized growth plates, and relatively normal vertebrae; A one month old female exhibited the same phenotype as above but also had splayed ribs. | ||
| 005956 | B6;D1Lac-Scd1ab-2J/J | Repository- Live |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in
..... For more information please see the full phenotype on the strain data sheet | ||
| 000235 | B6C3Fe a/a-Relnrl/J | Repository- Live |
| Mice homozygous for the reeler (Relnrl) mutation exhibit an ataxic gait, dystonic posture and tremors starting around 2 weeks of age. These mutants are incapable of maintaining their hindquarters upright and often fall over during locomotor activity. Moreover, viability and fertility are greatly reduced, especially when the gene is carried on an inbred genetic background. Heterozygotes are visually indistinguishable from wildtype controls. Neuropathies characteristic of Relnrl/Relnrl mutants include a failure of neuronal layer formation in laminated brain regions during development. Neuronal positioning is abnormal within cerebellar, cerebral and hippocampal cortices. The behavioral phenotype is primarily attributed to the severe hypoplasia of the cerebellum, which lacks foliation. Here, there are reduced numbers of granule and Purkinje cells and these cells are aberrantly dispersed among the layers. In the Reln-deficient neo
..... For more information please see the full phenotype on the strain data sheet | ||
| 000501 | B6CBACa Aw-J/A-Aifm1Hq/J | Repository- Live |
| Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11
..... For more information please see the full phenotype on the strain data sheet | ||
| 001201 | B6CBACaF1/J-Aw-J/A | Repository- Live |
| 006449 | B6Ei.P-fold/J | Repository- Live |
| 006450 | B6EiC3 a/A-Vss/J | Repository- Live |
| 000391 | B6EiC3Sn a/A-Pax6Sey-Dey/J | Repository- Live |
| Mice homozygous for the spontaneous semidominant Dickie's small eye mutation(Pax6Sey-Dey) die during embryogenesis. Heterozygous mutant mice are characterized by an overall small body size, small eyes with coloboma, small or lacking lens with cataract, abnormal folding of the retina and reduction of the pigment layer. The anterior chamber is usually missing. Mutations in the Pax6 gene lead to an impairment of axonal growth and differentiation, and delay migration of preneuronal cells. Optic nerve cross-sectional area and fiber count are decreased in these mutant mice, but probably indirectly as a consequence of reduced neural retina size. Formation of lens and of nasal cavity placodes are dependent on normal Pax6 expression. | ||
| 003237 | BALB/cByJ-Agtpbp1pcd-3J/J | Repository- Live |
| Mice homozygous for the Purkinje cell degeneration 3 Jackson spontaneous mutation (pcd3J) have an external and histological phenotype that is very similar to the original Purkinje cell degeneration mutation (pcd). Homozygous pcd mutant mice show a moderate ataxia beginning at 3 to 4 weeks, are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic
..... For more information please see the full phenotype on the strain data sheet | ||
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/J | Repository- Live |
| Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminipherous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp. | ||
| 001592 | BALB/cByJ-Lpin1fld/J | Repository- Live |
| The original fld (fatty liver dystrophy) mutation arose spontaneously at The Jackson Laboratory in the Animal Resources BALB/cByJ colony in 1981, and was maintained by sibling mating for 47 generations, then backcrossed once in 2001 to a male BALB/cByJ via homozygous ovarian transplant, then sibling mating resumed. Homozygotes can be identified soon after birth by an enlarged, pale liver and smaller overall body size. Although the hepatic steatosis resolves to normal at wean age, a neurological phenotype manifests by day 14 as a tremor and an unsteady gait which is most pronounced in the rear legs (Sweet et al. 1988). Both phenotypes stem from improper cellular processing of lipid. fld/fld mice are smaller than their normal littermates by three days of age and remain smaller throughout life. Hair growth is retarded and abnormal resulting in a ruffled, unkempt appearance in the adult. Homozygotes experience increased mortality between 19 and 35 days of age. A
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| 002169 | BALB/cByJ-mshi/J | Repository- Live |
| Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (mshi) are characterized by reduced testis size and sterility. The testes are highly disorganized and appear to have a block in the regulation of male germ cell proliferation. Reproduction is normal in homozygous mutant female mice. In addition to the male reproductive defects this mutation also affects histocompatibility in both sexes. Most homozygous mutant mice reject sex-matched skin grafts from BALB/cBy mice. | ||
| 008292 | BALB/cJ-Agtpbp1pcd-8J/J | Repository- Live |
| 002167 | BALB/cJ-Cst6ichq/J | Repository- Live |
| 005226 | BALB/cJ-Mbpshi-J/J | Repository- Live |
| 006019 | BALB/cJ-ssl/J | Repository- Live |
| 003092 | BALB/cNctr-Npc1m1N/J | Repository- Live |
| Mice homozygous for the recessive NIH allele of the Niemann Pick type C1 gene (Npc1m1N) show a dual deficiency of sphingomyelinase and glucocerebrosidase activity. The overall phenotype resembles the sphingomyelinosis condition seen in mice homozygous for the sphingomyelinosis allele (Npc1spm, Stock No. 002760). Sphingomyelinosis mutant mice begin to lose weight and to show tremor and ataxic gait at about 7 weeks of age. Weight loss continues and tremor and ataxia become more severe until death at about 12 to 14 weeks of age. The liver and spleen are also enlarged and Purkinje cells in the cerebellum are severely depleted. Sphingomyelin and free cholesterol are markedly elevated in liver and spleen but not in brain. Sphingomyelinosis closely resembles that of human Niemann-Pick Type C disease patients. | ||
| 004824 | BTBR.V(B6)-Lepob/WiscJ | Repository- Live |
| Mice homozygous for the obese spontaneous mutation, (Lepob commonly referred to as ob or ob/ob) exhibit obesity hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with mice carrying the diabetes mutation (Leprdb
..... For more information please see the full phenotype on the strain data sheet | ||
| 003613 | BXD32/TyJ-Galctwi-5J/J | Repository- Live |
| The twitcher 5 Jackson homozygotes on this BXD32/TyJ background have a much earlier onset than the original twitcher mutation assessed on a mixed B6;CE background. A moderate tremor and smaller body size can be detected by 14 to 16 days of age, most homozygotes die by 21 days of age, and the remainder die by 30 days of age. | ||
| 000480 | C3.MRL-Faslpr/J | Repository- Live |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 008425 | C3FeLe.B6-a Trl/J | Repository- Live |
| Mice heterozygous for the trembler-like mutation have an abnormal gait and tremors by approximately three weeks of age. Males are poor breeders. | ||
| 004626 | C3H/HeDiSnJ-lew/J | Repository- Live |
| 001276 | C3H/HeJ-Atp2b2dfw/J | Repository- Live |
| Mice homozygous for the deaf waddler spontaneous mutation (Atp2b2dfw) are deaf, walk with a hesitant, wobbly gait, and bob their heads. Both sexes are fertile. | ||
| 004965 | C3H/HeJ-Clic5jbg/J | Repository- Live |
| 004806 | C3H/HeJ-Mfs/J | Repository- Live |
| 004780 | C3H/HeJ-agil/J | Repository- Live |
| Mice homozygous for this recessive mutation are recognized by 15 days of age by their shaky, unsteady, wobbly gait. Mutants die around three weeks of age. The agitans-like mutation maps to Chromosome 14 between D14Mit39 and D14Mit115 which are near the neurological mouse mutation agitans (ag). The agitans mutants exhibit a similar phenotype. | ||
| 006247 | C3H/HeJ-sevr/J | Repository- Live |
| 004476 | C3H/HeJ-snol/J | Repository- Live |
| The snol homozygous mutant phenotype includes a short nose, odd face and body shape, and kinked tail. Most mutants also get malocclusion and two homozygous mutants tested at 49 days of age exhibited intermediate hearing loss ( about 25 dB above normal). The odd shape of the face can be used to distinguish the Homozygotes by 14 days of age. snol has been mapped to Chromosome 4. The most likely gene order places the mutation between D4Mit12 and D4Mit203 in 92 tested meioses. A short nosed mutation, snubnose (sno), maps in this location, but could not be tested for allelism because it is believed to be extinct. The spina bifida occulta reported in sno homozygotes is not seen in snol homozygotes. | ||
| 003525 | C3H/HeOuJ-Gusbmps-2J/BrkJ | Repository- Live |
| Mice homozygous for the Gusmps-2J allele exhibit a phenotype similar to Gusmps homozygotes including skeletal deformities, lysosomal storage disease and elevated levels of the lysosomal enzymes alpha-galactosidase and beta-hexosaminidase (Gwynn et al., 1998). Like the Gusmps heterozygote, Gusmps-2J heterozygotes have a 26-85% reduction in beta-glucuronidase activity. depending on tissue type (Gwynn et al., 1998, Birkenmeier et al., 1989). Homozygotes of both alleles have beta-glucuronidase activity levels at 1% of the control level. Unlike the Gusmps homozygote, Gusmps-2J homozygotes live longer, are fertile and can raise litters to weaning age (Gwynn et al., 1998). In addition to a difference in the nature of the mutations between these two alleles, it is also likely that the phenotypic differences are the result of strain background. C3H/HeOuJ mice carry a different set of
..... For more information please see the full phenotype on the strain data sheet | ||
| 004683 | C3H/HeSnJ-Slc12a6gaxp/J | Repository- Live |
| Giant axonopathy (gaxp) is an autosomal recessive mutation that arose spontaneously in the Mouse Mutant Resource colony at The Jackson Laboratory. It occurred in a strain bearing another mutation on the C3H/HeDiSnJ background. Homozygous mutants exhibit ataxia of the hind legs with a slight side - to - side wobble. Histopathologic studies showed pale staining, vacuolated structures measuring between 20 and 150 micra in deep cerebellar nuclei, pons, lateral vestibular nuclei and dorsal root and trigeminal ganglia. Ultrastructurally these structures were often bounded by a few layers of myelin, suggesting that they are swollen axons. gaxp has been mapped to Chromosome 2. The most likely gene order places the mutation between D2Mit128 and D2Mit102 in 174 meioses tested. | ||
| 004406 | C3HeB/FeJ-Pou3f4del-J/J | Repository- Live |
| 003752 | C57BL/10ScNJ | Repository- Live |
| The breeder pair of C57BL/10ScN mice, obtained from NIH, that were the progenitors of all mice of this strain at The Jackson Laboratory were tested by PCR analysis for the spontaneous Il12rb2 mutation described by Poltorak et al. (J. Immunol. 167:2106-2111, 2001) and found to carry only the wild type Il12rb2 allele. C57BL/10ScN mice have a deletion of the Tlr4 gene that results in absence of both mRNA and protein and thus in defective response to LPS stimulation. Tlr4lps-del differs from the Tlr4Lps-d mutation of C3H/HeJ mice, a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4lps-n, occurs in most other C3H and C57BL/10 substrains and most other mouse strains. | ||
| 003548 | C57BL/6-Ins2Akita/J | Repository- Live |
| Mice heterozygous for the Akita spontaneous mutation (Ins2Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes. Aged mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as 12 weeks after the onset of hyperglycemia. Retinal complications include increased vascular permeability, alterations in the morphology of astrocytes and microglia, increased apoptosis and thining of the inner layers of the retina. (Barber AJ, et al., 2005) The mean lifespan of diabetic male mice on the C57BL/NJcl background (305 days) was significantly shorter than that of nondiabetic males in anothe
..... For more information please see the full phenotype on the strain data sheet | ||
| 005349 | C57BL/6J Tyrc-2J-awag/J | Repository- Live |
| awag homozygotes have a distinct tremor when walking. When lifted by the tail these mutant mice do not splay their hind legs out as normal mice do, but instead hold their legs in a bowlegged umbrella manner and arch their backs. Both sexes breed and live a normal life span. | ||
| 002552 | C57BL/6J-Cdh23v-2J/J | Repository- Live |
| Mice homozygous for the waltzer 2J spontaneous mutation (Cdh23v-2J) show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Homozygous mutant mice are very similar to the other waltzer mutants (Cdh23v and Cdh23v-J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (v/+ Myo7ash1/+) are deaf beginning at 3 to 6 months. Double heterozygotes have changes similar to those of the homozygotes in the organ of Corti, stria vascularis, and spiral ganglion, but less severe and with much later onset. Viability and breeding ability are somewhat reduced. | ||
| 000533 | C57BL/6J-Ghrhrlit/J | Repository- Live |
| Mice homozygous for the little spontaneous mutation (Ghrhrlit) are characterized by a deficiency in pituitary growth hormone and prolactin and growth retardation. Male mice have reduced fertility and female mice show a delay in lactation. | ||
| 007711 | C57BL/6J-Hps3coa-8J/J | Repository- Live |
| 002134 | C57BL/6J-Mitfmi-vit/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitfmi-vit are only mildly affected compared to other Mitf alleles. Homozygous mutant mice have a lighter initial coat color than normal with extensive white spotting. After eight weeks of age, the mice producing increasing numbers of white hairs with each hair cycles resembling human vitiligo. Homozygotes exhibit uneven pigmentation of the retina and slow, progressive photoreceptor cell loss, eventually leading to blindness. | ||
| 000531 | C57BL/6J-Otx1jv/J | Repository- Live |
| Mice homozygous for the Jackson waltzer mutation run in circles and shake their heads. The lateral semicircular canal and its cristae are absent, and the sacculus and utriculus may be morphologically abnormal. However, hearing is unaffected. This pheontype is similar to that reported for the Otx1tm1Asim targeted mutation and complementation testing with this targeted mutation showed jv to be an allele of Otx1. (Note that C57BL/6J is homozygous for ahl, the age related hearing loss 1 mutation, which on this strain background causes progressive hearing loss with onset after 10 months of age.) Homozygotes can swim. | ||
| 000565 | C57BL/6J-Pax3Sp-d/J | Repository- Live |
| Mice homozygous for the splotch-delayed spontaneous mutation (Pax3Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3Sp, Stock No. 002469). Splotch-delayed homozygous embryos survive to birth, compared to splotch mutant embryos that die at E13 due to neural tube defects. Homozygous splotch-delayed mutant embryos display caudal rachischisis only. Heterozygous splotch-delayed have a white belly spot. Delayed splotch is a point mutation within the paired domain of Pax3. This impairs DNA binding of this domain and also, suprisingly, of the homeodomain, not directly affected in the mutant gene. | ||
| 002469 | C57BL/6J-Pax3Sp/J | Repository- Live |
| Mice homozygous for the splotch spontaneous mutation (Pax3Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. Splotch is a point mutation within intron 3 of the paired homeobox 3 (Pax3) gene on mouse Chromosome 1. The mutation interferes with normal splicing of intron 3 and leads to at least 4 aberrantly spliced mRNAs with exon 4 deleted. The Pax3Sp mutation also impairs homodimerization of the protein, a function associated with the octapeptide-encoding central segment of the gene. There are multiple alleles at this locus including splotch-delayed (Pax3Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. | ||
| 002072 | C57BL/6J-Pcdh15av-3J/J | Repository- Live |
| There have been several remutations to Ames waltzer (av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames wa ltzer 2J homozygous mutant mice (av2J/av2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av2J/av2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (av3J/av3J), like Ames waltzer-J (avJ/avJ), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate. | ||
| 000811 | C57BL/6J-Ptpn6me-v/J | Repository- Live |
| Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo
..... For more information please see the full phenotype on the strain data sheet | ||
| 007892 | C57BL/6J-Relnrl-7J/J | Repository- Live |
| 005135 | C57BL/6J-Sls/J | Repository- Live |
| 000563 | C57BL/6J-Sobpjc/J | Repository- Live |
| Mice homozygous for the Jackson circler spontaneous mutation (Sobpjc) show erratic circling behavior which becomes more pronounced with age. Homozygous mutant mice are very active, bobbing up and down and flexing head and trunk ventrally towards the tail and mice can swim. Mice can be identified at weaning by a characteristic flexing behavior when suspended by tail. | ||
| 008522 | C57BL/6J-Spnb4qv-11J/J | Repository- Live |
| 004246 | C57BL/6J-sbse/J | Repository- Live |
| 007599 | C57BL/KaLawRij-Sharpincpdm/RijSunJ | Repository- Live |
| Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. Mice appear runted and life span is shortened. In addition to dermatitis, homozygotes exhibit multi-organ inflammation with eosinophilia, defective TH1 cytokine production, splenomegaly, absent Peyer's patches (adult), diminished serum immunoglobulins, and an absence of B cell follicles, follicular dendritic cells, and germinal centers in secondary lymph organs. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation, and secondary lymphoid organ deveopment. | ||
| 000516 | C57BLKS-Rpl24Bst/J | Repository- Live |
| Belly spot and tail (Rpl24Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1
..... For more information please see the full phenotype on the strain data sheet | ||
| 004625 | C57BLKS/J-Car8wdl/J | Repository- Live |
| wdl homozygotes display a side-to-side wobble in their gait as early as two weeks of age and this persists throughout life. Despite this, they can swim in a straight line. | ||
| 006448 | C;A-Bolt/J | Repository- Live |
| 008521 | C;B6-Spnb4qv-10J/J | Repository- Live |
| 006169 | CBA.Cg-Tmc1dn/AjgJ | Repository- Live |
| 001876 | CBA/KlJms-Faslpr-cg/J | Repository- Live |
| Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Faslpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Faslpr-cg complemented both Faslpr and the Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr. Like Faslpr and Faslgld homozygotes, CBA/KlJms-Faslpr-cg homozygotes produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr homozygotes. | ||
| 006130 | CBACa.Cg-ScribCrc/RachJ | Repository- Live |
| Mice homozygous for this spontaneous mutation develop severe neural tube defects and die at birth. In it's most severe form, the neural tube fails to initiate Closure 1 (craniorachischichisis). Heterozygotes, predominantly males, often exhibit a looping or kinked tail. This strain may used to research neural tube defects. | ||
| 000805 | CBy.RF-Tshrhyt/J | Repository- Live |
| Mice homozygous for the hypothyroid spontaneous mutation (Tshrhyt) are characterized by growth retardation, low thyroid hormone levels, elevated thyroid stimulating hormone (TSH) and hypoplastic thyroid glands. Homozygous mice of both sexes are infertile but fertility as well as growth can be restored by treatment with thyroid hormone. The mice do not respond to exogenous TSH. Homozygous mutant mice also display audiotory defects characterized by morphologic abnormalities of the stereocilia on both inner and outer hair cell systems | ||
| 002718 | CByJ.Cg-hop/J | Repository- Live |
| Mice homozygous for the hop-sterile spontaneous mutation (hop) are viable, females are fertile but males are sterile. Homozygous mutant mice walk with a characteristic hopping gait using the hindlegs simultaneously. There is preaxial polydactyly of both fore- and hindfeet. Defects in spermatogenesis result in abnormal sperm tail development. Tailed sperm are completely absent from the lumen of the testicular tubules. The second meiotic division is frequently abnormal or incomplete, often leaving four centrioles per cell. These centrioles usually fail to form flagella, and tail development is arrested. | ||
| 000657 | CE/J | Repository- Live |
| CE/J mice are resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breeding the female can ameliorate this trait.<
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| 001998 | CFW-Em/J | Repository- Live |
| 002932 | CPt.C3-Faslgld/J | Repository- Live |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 003777 | CXB5/By-Sil1wz/J | Repository- Live |
| 002799 | CZECHI/EiJ | Repository- Live |
| This strain has a coat color mutation which results in heightened agouti yellow pigment. This mutation has not yet been characterized in detail. | ||
| 007562 | D2.B6-Ins2Akita/MatbJ | Repository- Live |
| DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.
Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as
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| 006057 | DBA/2J-sky/J | Repository- Live |
| 006867 | FVB.B6-Ins2Akita/MlnJ | Repository- Live |
| FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type offs
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..... For more information please see the full phenotype on the strain data sheet | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The phenotype of this congenic "FVB-db" strain varies from that previously published on other genetic backgrounds. Specifically, obese FVB-db mice show long-term hyperglycemia that is primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite escalating insulin secretion and a massive increase in pancreatic beta-cell mass. Obese FVB-db mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. Whereas the original C57BLKS/J-db mice are hyperglycemic due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of FVB-db appears to be due to severe insulin resistance with continual increases in insulin secretory capacity from beta-cell mass expansion. As the phenotype varies by genetic background, these mutant mice, along with db mutants on other genetic backgrounds (see Stock No. 000642, For more information please see the full phenotype on the strain data sheet | ||
| 000804 | HPG/BmJ | Repository- Live |
| Mice homozygous for the hypogonadal mutation (Gnrh1hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement. | ||
| 008296 | KK(Cg)-fsq/J | Repository- Live |
| At approximately two months of age, flying squirrel homozygotes stiffen throughout their trunk and limbs, particularly on the ventral side of the body, and when picked up take on a rigid spread out posture. As a result they walk with a slight stagger. Homozygotes are not fertile but do live to adulthood. | ||
| 006058 | LPT;C3-dkd/J | Repository- Live |
| 006825 | MRL/MpJ-Faslpr/2J | Repository- Live |
| The current colony (as of fall 2006) of MRL/MpJ-Faslpr/J has experienced a progressive loss of lymphoproliferative phenotype over the past several years, as reported by some of our customers and as observed by our technical staff. This loss of phenotype has been manifested by reduced enlargement of brachial and mesenteric lymph nodes, and poor splenomegaly. Also, the life spans of the mice in the current colony have also been found to be much longer than the historically observed and reported 17 weeks for females and 22 weeks for males. However, genotyping continues to show that all the mice in the colony remain homozygous for the Faslpr mutation, and the SNP profile in the region of the mutation on Chromosome 19 has not changed.
In an effort to regenerate the desired phenotype, we recovered mice from our embryo archive cryopreserved in 1993. The sixteen-week old cryo-recovered mice have lymph nodes that were 4.5 (females) to 10.1 times (male) la
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| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Repository- Live |
| NOD congenic mice homozygous for the Faslgld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 007840 | NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ | Repository- Live |
| Tg(Ins2-CD86)12B7 mice homozygous for the Prkdcscid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdcscid homozygous mice lack functional T cells and B cells, and do not become diabetic.
In the absence of the Prkdcscid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d
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| 006605 | NOD.Cg-Prkdcscid Emv30b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Repository- Live |
| Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets. | ||
| 005053 | NOD.Cg-Prkdcscid Gusbmps/SndsJ | Repository- Live |
| Mice homozygous for the mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 008254 | NOD/ShiLtJ-Npr3lgj-4J/J | Repository- Live |
| 004774 | NOD/ShiLtJ-wly/J | Repository- Live |
| Mice develop curly hair by 4 weeks of age; whiskers are normal (straight). Giant hair follicles in anagen and a paucity of subdermal fat were found in histology of the skin at 5 weeks of age. | ||
| 005354 | RB156Bnr/Ei rul-Gulosfx-2J/J | Repository- Live |
| The phenotype of the sfx2J remutation is identifiable at 4-5 weeks of age when the mutants appear smaller than their control littermates and begin to hobble about their cage. Between 5 and 8 weeks of age the mutants develop rear limb paralysis and many die by 8 weeks of age. The phenotypic characteristics of this mutation are similar to the original mutation spontaneous fracture (Gulosfx ) except for the eye phenotype described below that is inherent in the background strain on which the sfx2J mutation arose. Mice homozygous for the sfx2J remutation also had cataracts and rosettes and wavy outer nuclear layer of retinas. The eyes of a female mutant were checked using an opthalmascope and it was found to have cataracts on both eyes (as the strain background has characteristically). It has not yet been determined if the rosettes and wavy outer nuclear layer of the retinas is also characteristic of the background s
..... For more information please see the full phenotype on the strain data sheet | ||
| 005362 | RB156Bnr/Ei-rul/J | Repository- Live |
| The phenotype of this mutation can be identified at about 10 days of age by a ruffled looking coat, which is different than the smooth coat of control littermates. The hair of mutant mice is sparse and has some curling. The ruffled looking coat is maintained throughout the animal's lifespan, unlike the caracul and caracul-like mutants who lose some of their curly coat with age. Mice homozygous for the ruffled mutation have a normal lifespan and both sexes breed normally. | ||
| 005415 | RHJ/LeJ-stpm/J | Repository- Live |
| The phenotype of this mutation can be identified by a curly coat, which is different from the smooth coat of control littermates. At 3 weeks of age, mice homozygous for this new mutation have very curly coats and slightly curved vibrissae. In several weeks time the curly coat disappears but the hair retains a rough texture, and the vibrissae then appear normal. Heterozygous mice have normal smooth coats and straight whiskers. | ||
| 000268 | RSV/LeJ | Repository- Live |
| 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
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000644 | SEA/GnJ | Repository- Live |
| 002759 | SM;NZB-Fbxw4Dac/J | Repository- Live |
| 003392 | STOCK Crb1rd8/J | Repository- Live |
| 001618 | STOCK Oca2p/Oca2p Prop1df/J | Repository- Live |
| Mice homozygous for the Ames dwarf spontaneous mutation (Prop1df) resemble mice homozygous for the Snell's dwarf mutation (Pit1dw). Homozygous Ames dwarf mutant mice show growth retardation after the first postnatal week, and weight at 2 months is only about one-half normal. Females and most males are sterile. There is no detectable growth hormone or prolactin. Ames dwarf mice have a secondary immune deficiency presumably resulting from the lack of growth hormone. | ||
| 006128 | STOCK Otofdeaf5Jcs/Kjn | Repository- Live |
| 003818 | STOCK bdd/J | Repository- Live |
| At 3 weeks of age homozygotes are smaller than their unaffected littermates and have horseshoe shaped hips. A paralysis-like dragging of the hind limbs appears with age and by 1 year of age prolapsed discs are found in the spinal cord although no muscle loss or neurological damage is found in the legs. | ||
| 006857 | STOCK ne/J | Repository- Live |
| 005040 | STOCK Tg(Pfkl)224Yg/J-Dll3pu-J/J | Repository- Live |
| This recessive remutation to Dll3pu results in mice with shortened vertebral spines, splayed ribs, and kinked tails. Common clinical characteristics include compression of the cervical, thoracic and lumbar vertebrae plus extreme variability in size, shape, and irregular fusion of tail vertebrae. | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 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 | ||
| 000641 | 129P1/ReJ-Lama2dy/J | Repository-Cryopreserved |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full phenotype on the strain data sheet | ||
| 000709 | 129P3/J-Leprdb-3J/J | Repository-Cryopreserved |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 000212 | 129P4.Cg-Axin1Fu/J | Repository-Cryopreserved |
| 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.) | ||