Search Criteria: Research Area is "Developmental Biology Research: Growth Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000687 | SM/J | Level 4 |
| SM/J mice carry a number of rare polymorphic alleles and are often matched to LG/J (Stock No. 000675), A/J (Stock No. 000646) or NZB/BINJ (Stock No. 000684) for quantitative trait locus analysis. These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. SM/J mice exhibit a hyperresponsiveness to B cell mitogens (Clark et al. 1981, Engel et al. 1981). A point mutation in Neu1 is responsible for a partial deficiency of lysosomal neuraminadase and may explain the altered immune response (Rottier et al. 1998). Small in size at birth and through weaning, SM/J mice attain a normal body weight as they age. | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
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| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 007859 | 129S1/Sv-Sufutm1Aeb/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 10. No gene product (protein) is detected by Western blot analysis. Truncated gene product (mRNA) is detected by Northern blot analysis. Homozygous embryos at 9 to 9.5 embryonic day exhibit growth retardation, incomplete embryonic turning, abnormal somite development, abnormal heart looping (due to abnormal left-right axial patterning) and open neural tubes. This mutant mouse strain may be useful in studies of the Hedgehog signaling pathway and embryonic development. | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil
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| 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). | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Repository- Live |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa
..... For more information please see the full descriiption on the strain data sheet | ||
| 006257 | B6.129-Aldh5a1tm1Kmg/J | Repository- Live |
| Homozygous mutation of this gene results in reduced body weight, ataxia, seizures, gliosis of the hippocampus, and eventual status epilepticus. From 19-26 days of age, repetitive tonic-clonic seizures results in more than 95% mortality. Biochemical assays shows complete ablation of the endogenous enzymatic activity in the brains, livers, hearts, and kidneys of homozygous mutant mice. Homozygotes have increased levels of GHB and GABA in liver and brain tissues, as well as in urine. Phenotype can be rescued to varying degrees utilizing a number of both pharmacotherapeutic and gene therapeutic approaches. Although heterozygous mice have approximately 50% of the endogenous enzyme activity compared to wildtype mice, they are viable and fertile. Mice with this targeted mutation may be useful in studying succinate semialdehyde dehydrogenase (SSADH) deficiency and to explore the effect of GABA and GHB accumulation on central nervous system development and function. | ||
| 004912 | B6.129P2-Akt1tm1Mbb/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and do not display any gross behavioral abnormalities. Homozygotes exhibit lower fertility. Female homozygotes do not nurse well; up to 50% perinatal mortality can occur. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of mouse embryonic fibroblasts. Homozygotes are only 80% of wildtype body weight at birth, and remain small. This mutant mouse strain may be useful in related to organismal growth. | ||
| 005644 | B6.129X-Gusbtm3Sly/J | Repository- Live |
| Homozygous mice are viable but infertile. Fertility can be restored with enzyme replacement therapy. Less than 1% residual enzyme activity is observed. Homozygous mice are indistinguishable from wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at three months with a moderate increase in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild-type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is less severe than that observed in a similarly constructed mutant (Stock No. 005643) which bears a E536A point mutation. This strain represents a model of human GUS def
..... For more information please see the full descriiption on the strain data sheet | ||
| 007181 | B6.129X1-Notch1tm2Rko/GridJ | Repository- Live |
| Mice homozygous for this "floxed" Notch1 allele (fN1) are viable and fertile. These mice possess loxP sites on either side of exon 1 of the targeted gene. When bred to mice with a Cre recombinase gene, exon 1 of the targeted gene is deleted in the cre expressing tissue(s). These conditional knockout mice may be useful in generating tissue-specific mutants for studying the development of a wide range of tissues: for example, when crossed to a strain expressing Cre recombinase primarily in the nervous system (see Stock No. 003771), this mutant strain may be useful in studies of apoptosis in neural development.
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 modi
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| 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 descriiption 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 descriiption 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. | ||
| 007083 | B6.Cg-Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction
..... For more information please see the full descriiption on the strain data sheet | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3sf/Y mice do not develop scurfy
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| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/J | Repository- Live |
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in studying cellular signal
..... For more information please see the full descriiption on the strain data sheet | ||
| 007200 | B6;129S4-Arid5bGt(ROSA)75Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth, occur at lower than Mendelian ratio (16%) and 46% die within 3 weeks of age. Homozygotes are fertile when they survive to adulthood. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit kidney defects (abnormally high blood urea nitrogen level, mutant kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli), and abnormalities in palate bone fusion. These Arid5b-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Repository- Live |
| 25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 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 descriiption on the strain data sheet | ||
| 006019 | BALB/cJ-ssl/J | Repository- Live |
| 007810 | C.129-Stat5btm1Hwd/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern and immunoblot analysis of liver, spleen, mammary gland, thymus, kidney or skeletal muscle from homozygous animals. Levels of the closely related Stat5a gene products (mRNA and protein) are unaffected in thymus and spleen. At 4 - 5 weeks of age, male homozygotes are smaller in size and have a reduced body weight (27% lighter than wildtype controls) when compared to wildtype. Female homozygotes exhibit spontaneous abortion between day 8 and 17 of pregnancy and have impaired lactation. Pups (independent of genotype) born to heterozygous females have higher perinatal death than pups born to wildtype females. Some homozygotes have pale and enlarged livers. Homozygotes have less adipose tissue than wildtype controls, exhibit abnormal gene expression in liver, reduced insuli
..... For more information please see the full descriiption on the strain data sheet | ||
| 004626 | C3H/HeDiSnJ-lew/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 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. | ||
| 004246 | C57BL/6J-sbse/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 000643 | DW/J Mlphln Pou1f1dw/J | Repository- Live |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 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. | ||
| 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). | ||
| 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). | ||
| 000644 | SEA/GnJ | Repository- Live |
| 004585 | STOCK Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction
..... For more information please see the full descriiption on the strain data sheet | ||
| 006951 | STOCK Notch1tm2Rko/GridJ | Repository- Live |
| Mice homozygous for this "floxed" Notch1 allele (fN1) are viable and fertile. In the targeted allele, loxP sites were placed flanking exon 1 of the targeted gene. When these floxed mice are bred to mice expressing Cre recombinase, exon 1 of the targeted gene is deleted in cre-expressing tissue(s) in the cre-positive, homozygous floxed offspring. These conditional knockout mice may be useful in generating tissue-specific mutants for studying the development of a wide range of tissues: for example, when crossed to a strain expressing Cre recombinase primarily in the nervous system (see Stock No. 003771), this mutant strain may be useful in studies of apoptosis in neural development. | ||
| 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. | ||
| 001743 | STOCK dwg/J | Repository- Live |
| Mice homozgyous for the dwarf grey spontaneous mutation (dwg) are viable but do not breed. Homozygous mutant mice have grey coats, are smaller than littermates, and develop cataracts by 3-4 weeks of age. Additional characteristics include increased numbers of osteoclasts, reduced bone mass, reduced red pulp area of the spleen, and slightly reduced thyroxin levels. | ||
| 003100 | STOCK dwgBayer/J | Repository- Live |
| The dwarf-Bayer mutation (dwgBayer) occurred spontaneously in an embryonic stem cell line during genetic targeting of the insulin receptor gene. The phenotype of the mice resemble drawf grey (dwg, Stock No. 001743) and subsequent characterization determined that the two mutations are allelic. Homozygous mutant mice are grey and smaller in size than wildtype littermates. | ||
| 005865 | STOCK Tg(YACW408A5)1952Ricc/J | Repository- Live |
| Hemizygous offspring from wild type mothers and transgenic fathers are viable, fertile, and normal in size. The imprinted methylation pattern on this transgene is dependent on maternal or paternal transgene inheritance, and is faithful to normal patterns with the following exceptions; defective methylation of Tssc4 and improper imprinting of Tssc4 and Ascl2. Fetal growth restriction is observed following maternal, but not paternal, transmission of the transgene. This phenotype is a characteristic of maternal duplication of chromosome 11p15.5. In addition, this mouse may also be useful in studying Beckwith-Wiedemann syndrome, imprinting/methylation mechanisms, and differentially methylated regions. | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Repository-Cryopreserved |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 005098 | A.B6 Tyr+-Spnb4qv-7J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Spnb4qv-7J entry. | ||
| 003485 | A/J-frg/J | Repository-Cryopreserved |
| Mice homozygous for the froggy mutation have a smaller body size and a shortened face with wide set eyes. | ||
| 000004 | ABP/LeJ | Repository-Cryopreserved |
| Mice homozygous for the Tgfawa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth.
Mice homozygous for the recessive Adamts20bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported findin
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| 000251 | AEJ.Cg-ae +/a Gdf5bp-H/J | Repository-Cryopreserved |
| 001013 | B10.D2/nSnJ-Myo5ad-n/J | Repository-Cryopreserved |
| Mice homozygous for the dilute-neurological spontaneous mutation (Myo5ad-n) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal mutant mice (Myo5ad-l, Stock No. 000253). | ||
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Repository-Cryopreserved |
| 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. 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 disease
..... For more information please see the full descriiption on the strain data sheet | ||
| 002831 | B6.129-Ahrtm1Bra/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 005951 | B6.129-Dgat2tm1Rvf/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation have a perinatal lethal phenotype, most fail to survive past 6 hours after birth due to dehydration, skin barrier abnormalities, hypothermia and energy deficiencies. Reduced levels of gene product (mRNA) are detected by RT-PCR analysis of brown adipose tissue and livers of neonate homozygous mutants. Growth retardation is observed in homozygous embryos after embryonic day 12.5. Newborn homozygotes are hypoglycemic and lipopenic, exhibiting reduced plasma triglyceride, free fatty acid and glucose levels and have almost no white fat tissue. Within a few hours of birth, the skin of homozygotes becomes dry and cracked. Homozygous mutants rapidly lose weight due to dehydration caused by impaired permeability barrier function. Histological analysis of skin tissue from homozygotes reveals abnormally thin epidermis and compact orthohyperkeratosis of the stratum corneum. Homozygotes surviving between 8 and 24 hours develop tail necrosis. Hetero
..... For more information please see the full descriiption on the strain data sheet | ||
| 003537 | B6.129-Kif3atm1Gsn/J | Repository-Cryopreserved |
| Ciliary formation appears to be crucial in developing left-right asymmetry in early mouse embryonic development. One of the necessary cilia components is the Kif3a gene product. Homozygous Kif3a knockout mice die at 10 days postcoitum, exhibit randomized establishment of left-right asymmetry and display numerous structural abnormalities. Cardiac looping is randomized, often retarded. Growth is severely retarded with caudal truncation. A neural tube closure defect is also apparent. Scanning electron microscopy indicates the absence of embryonic cilia. A small percentage of heterozygotes exhibit morphological abnormalities. | ||
| 004098 | B6.129-Klc1tm1Gsn/J | Repository-Cryopreserved |
| The donating investigator indicates that mice that are homozygous for the targeted allele on a C57BL/6 genetic background exhibit significant perinatal mortality (60%). Mortality seems not to be a factor on a mixed B6;129 background. Surviving mice are noticeably smaller than wildtype mice. Mice surviving to adulthood breed poorly, possibly due to less than adequate nurturing capabilities. Minor amounts of a functionless, truncated protein product can be detected. Motor defects are evident, as are alterations in intracellular localization of kinesin-I and COP-I components. | ||
| 004361 | B6.129-Xrcc5tm1Nus/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, but are 40-60% the size of normal mice. No Xrcc5 protein product is detected. The growth deficiency phenotype is exhibited as early as E15.5. Organ weights, excepting lymphoid organs, are proportional to total body weight. Histological analysis shows decreased size of spleen, lymph nodes and thymus. T cell and B cell development is arrested at early precursor stages and a deficiency in V(D)J rearrangement is exhibited. B cell maturation stops at the B220+CD43+ stage. Only CD4-CD8- cells are found in the thymus. Primary embryonic fibroblasts (MEFs) have slower growth and early loss of proliferating cells. Early appearance of non-dividing cells in MEF cultures suggest early onset senescence. Karyotypes reveal increased chromosomal aberrations. Breaks or translocations occur in 83% of metaphases, polyploidy in 15%. Although cells from the mutant mice display chromosomal instability, these mice do not display ea
..... For more information please see the full descriiption on the strain data sheet | ||
| 005601 | B6.129S-Atxn1tm1Hzo/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable but have a reduced lifespan (34-40 weeks). The allele consists of a 154 CAG trinucleotide repeat unit placed within exon 8 of the targeted endogenous mouse locus. Modified transcripts and protein can be detected in brain tissue. By 8 weeks of age, mutant mice exhibit noticeable growth retardation. Progressive neurological degeneration initiates by 9 weeks of age, when mutant mice begin to exhibit a clasping phenotype when held by the tail. By 20 weeks of age muscle wasting, ataxia and an abnormal gait are observed. A lack of motor coordination is detected via an accelerating rotarod test by 5 to 7 weeks. Cognitive defects include poor spatial learning performance and reduced Pavlovian conditioned fear response (impaired memory). Hippocampal basal synaptic function is impaired. Immunohistochemical and immunofluorescent analysis of brain tissue reveals neuronal intranuclear inclusions by 6 weeks of age. Older animals exhibit
..... For more information please see the full descriiption on the strain data sheet | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 006566 | B6.129S6-Ppt1tm1Hof/SopJ | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunoassay. Palmitoyl-protein thioesterase activity in the brain of the mutant is reduced to background levels. Although healthy at birth, by age four to five months, mutant mice display lack of grooming and an abnormal gait that progresses to hind limb paralysis. By six to eight months of age mutant mice have a low body weight and display an abnormal clasping behavior. Aggressive behavior results in fighting and dermatitis due to bite wounds. By seven months of age, mortality is 50% with very few mice surviving beyond ten months of age. Myoclonic jerks and seizures manifest at age three to four months. Strong rapid hind limb seizures ("popcorn" seizures) that propel mice several feet also occur. Brain size of the mutant mice is reduced. Histologically, mutant brains show neuronal loss and apoptosis in
..... For more information please see the full descriiption on the strain data sheet | ||
| 003336 | B6.129S7-Cdkn1ctm1Sje/J | Repository-Cryopreserved |
| Mice lacking the Cdkn1c gene have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochrondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; lens cell hyperproliferation and apoptosis. The targeted gene is imprinted. The phenotype differs depending on whether the targeted allele is transmitted from the dam or the sire; maternal inheritance of the null allele is lethal. This is a model for the human Beckwith-Wiedemann syndrome. | ||
| 005536 | B6.129S7-Dp(11Cops3-Zfp179)1Jrl/J | Repository-Cryopreserved |
| Homozygous mutant mice are viable and fertile. Studies employing heterozygous mutant mice (where the duplication exists only on one chromosome) indicate that mutant mice weigh less than their wildtype litter mates. Spleens are noted to be slightly smaller than those from wild type mice. Mutant mice also exhibit impaired contextual fear conditioning. Male heterozygotes have been shown to be hyperactive in open field analysis. This mutant mouse may be useful in studies exploring the consequences of duplications involving the SMS critical interval. (Mice bearing the reciprocal deficiency mutation are also available; see Stock: 005535) | ||
| 005643 | B6.129X-Gusbtm1Sly/J | Repository-Cryopreserved |
| Homozygous mice are viable but have reduced neonatal survival. Homozygotes are infertile, but fertility can be restored with enzyme replacement therapy. No residual enzyme activity is observed. Homozygous mice are indistinguishable from heterozygous and wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at wean and increasing in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild-type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, spleen, neurons, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is more severe than that observed in a similarly constructed mutant (Stock No. 005644) which bears a L175F point
..... For more information please see the full descriiption on the strain data sheet | ||
| 004863 | B6.129X1-Snap25tm1Mcw/J | Repository-Cryopreserved |
| Homozygous mutant mice die at birth from respiratory failure. At embryonic day 17.5 to 18.5 homozygous embryos appear smaller and do not display spontaneous movement or sensorimotor reflexes. Dilated vascular channels in subcutaneous tissues give the embryos an external blotchy appearance. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue from homozygous animals. Histological analysis of fetal diaphragm tissue reveals a dispersed pattern of innervation and fewer layers of muscle fibers. Thin, disarrayed intercostal and anterior chestwall muscles are also observed. Spontaneous miniature endplate potential (mEPP) activity is detected in the diaphragm phrenic nerve, but no evoked endplate potentials (EPP), evoked neurotransmitter release or muscle contraction is detected with stimulation of the neuromuscular junction (NMJ). Mutant NMJs exhibit larger endplate diameters and lower levels of acetylcholinesterase. Tetrodotoxin (TTX) resistant m
..... For more information please see the full descriiption on the strain data sheet | ||
| 006559 | B6.C-H2bm1/ByBir-Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000256 | B6.C-H2bm1/ByBir-Gusbmps/J | Repository-Cryopreserved |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000056 | B6.Cg-Bmp5se/J | Repository-Cryopreserved |
| 006407 | B6.Cg-Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. These mice have the H2b haplotype typical of inbred C57BL/6 mice. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 002086 | B6.Cg-Gusbmps Tg(Gussx)1Wat/J | Repository-Cryopreserved |
| Androgen induction of Gus is faster but lower in M. saxicola than in Mus musculus. However, growth hormone induces Gus upregulation in Mus musculus but has no affect on Gus induction in Mus saxicola. When transferred to a Mus musculus background in the absence of endogenous Gus the Mus saxicola derived Gus (Gussx) also showed no growth hormone enhancement of induction supporting the idea that an evolutionary change in regulatory sequence underlies this variation in response. These mice do not exhibit the phenotypic characteristics of Gusmps homozygotes indicating rescue by Gussx. (Niermann and Watson, 1999; Paigen 1989.) | ||
| 000285 | B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J | Repository-Cryopreserved |
| Mice homozygous for the staggerer spontaneous mutation (Rorasg) show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex of homozygous mutant mice is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The remaining granule cells migrate inward from the external layer prematurely and then degenerate. Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur. Staggerer mutant mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells. Kopmels et al. have reported a hyperproduction of IL1 biological activity and mRNA from LPS stimulated spleen cells of Rorasg/Rorasg mice on the C57BL/6J background relative to wild type siblings.
In this congenic strain the staggerer mutation is maintain
..... | ||
| 001623 | B6.D2-Car2n/J | Repository-Cryopreserved |
| In human, CAR2 deficiencies can result in osteopetrosis, renal tubular acidosis, impaired growth, cerebral calcification, and mental retardation. Mice homozygous for Car2<n> do not display cerebral calcification or osteopetrosis, although medial calcification of small arteries has been found in several organs, most notably the male genital tract. The phenotype of these mice includes renal tubular acidosis, doubled urine output, increased urine pH and Cl-, decreased blood pH and HCO-3, phosphatemia, lower plasma bicarbonate, and a smaller body size. Despite smaller body weight, the kidneys are of normal size and plasma potassium and creatinine levels are normal. Type A and B intercalated cells of the kidney are severely depleted. Car2n homozygotes have reduced susceptibility to audiogenic and chemogenic seizures and hippocampal slices from homozygotes are more resistant to hypoxia than are those of wild type controls. Increase
..... For more information please see the full descriiption on the strain data sheet | ||
| 000772 | B6.DW-Pou1f1dw/J | Repository-Cryopreserved |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 001271 | B6.RBF-Nek1kat/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 002727 | B6;129-Ahrtm1Bra/J | Repository-Cryopreserved |
| Mice homozygous for the Ahrtm1Bra targeted mutation are viable and fertile. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 004264 | B6;129-Cycstm1Wlm/J | Repository-Cryopreserved |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 004313 | B6;129-Ppt1tm1Hof/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunoassay. Palmitoyl-protein thioesterase activity in the brain of the mutant is reduced to background levels. Although healthy at birth, by age four to five months, mutant mice display lack of grooming and an abnormal gait that progresses to hind limb paralysis. By six to eight months of age mutant mice have a low body weight and display an abnormal clasping behavior. Aggressive behavior results in fighting and dermatitis due to bite wounds. By seven months of age, mortality is 50% with very few mice surviving beyond ten months of age. Myoclonic jerks and seizures manifest at age three to four months. Strong rapid hind limb seizures ("popcorn" seizures) that propel mice several feet also occur. Brain size of the mutant mice is reduced. Histologically, mutant brains show neuronal loss and apoptosis in
..... For more information please see the full descriiption on the strain data sheet | ||
| 007947 | B6;129P2-He/J | Repository-Cryopreserved |
| 002265 | B6;129S2-Bcl2tm1Sjk/J | Repository-Cryopreserved |
| Mice homozygous for the Bcl2tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle. | ||
| 002537 | B6;129S2-Ccnd1tm1Wbg/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a
..... For more information please see the full descriiption on the strain data sheet | ||
| 002494 | B6;129S2-Cgatm1Sac/J | Repository-Cryopreserved |
| Mice homozygous for the Cgatm1Sac targeted mutation are viable but both sexes are infertile. They lack TSH, LH, and FSH. Homozygous mutant mice are hypogonadal and exhibit severe hypothyroidism resulting in dwarfism. Development of the thyroid gland was arrested in late gestation. However, gonadotropin releasing hormone (GNRH) neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development are normal. Mice heterozygous for the Cgatm1Sac targeted mutation appear normal. | ||
| 007208 | B6;129S4-Axud1Gt(ROSA)80Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Axud1-mutant allele are viable and fertile, with some incidence of perinatal lethality before two weeks of age (the Donating Investigator reports 18% of homozygotes die by two weeks of age). Homozygotes have abnormalities in palate bone fusion. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. These Axud1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 002850 | B6;129S4-Nfkbiatm1Bal/J | Repository-Cryopreserved |
| Mice homozygous for the Nfkbiatm1Bal mutation are runted, and have granulocytosis as well as abnormalities in epithelial keratinization. Neonates die at around 8 days of age. | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These Zfp640-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 002788 | B6;129S7-Fsttm1Zuk/J | Repository-Cryopreserved |
| Homozygous mice die within hours after birth due to a failure to breathe. They are smaller in size than normal wildtype siblings and show craniofacial, musculoskeletal, and skin defects. | ||
| 005520 | B6;CByJ-Cacna1atg-6J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cacna1atg-6J entry. | ||
| 005654 | B6C3-Del(16Cbr1-ORF9)1Rhr/J | Repository-Cryopreserved |
| These mice are monosomic for the mouse chromosome segment MMU16. The deleted segment contains mouse orthologs of 33 conserved and minimally conserved genes in the human Down's syndrome critical region (DSCR). The borders of the deletion are defined by the carbonyl reductase 1 (Cbr1) gene and a site adjacent to the myxovirus (influenza virus) resistance 2 (Mx2) locus. Monosomic mice are viable, fertile and are significantly smaller than wildtype (euploid) littermates from birth to adulthood. This mouse may be useful in studies of Down syndrome and further exploring the ploidy of DSCR/MMU16. | ||
| 001035 | B6C3Fe a/a-Napahyh/J | Repository-Cryopreserved |
| Although no overt phenotype is appearant in newborn hyh mice, they have dilated lateral ventricles. By 2 weeks of age, an outward phenotype of a domed head and a hop gait is apparent. Dissection and histological examination reveal "hydrocephalus of lateral and third ventricles and of the caudal aspects of the cerebreal aquiduct" increasing in severity with age (Bronson et al., 1990). Homozygotes have a decreased lifespan usually dying before 2 months of age. Some homozygotes will live for several months, but usually will not breed. | ||
| 000278 | B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J | Repository-Cryopreserved |
| 000205 | B6C3Fe a/a-Papss2bm/J | Repository-Cryopreserved |
| 004317 | BALB/cBy-Gulosfx/J | Repository-Cryopreserved |
| The sfx phenotype is not apparent until shortly after weaning age. By 26-30 days of age, homozygotes display decreased mobility, diminished weight gain, and more scruffy appearance than their heterozygous or wildtype siblings. Dissection reveals smaller spleen and thymus and increased kidney and brain weights. A reduction in bone mass is accompanied by a paucity of mature osteoblasts on bone surfaces, a subtle reduction of chrondrocytes in epiphyseal-plate columns, growth plate arrest in long bones, and other architectural abnormalities. Bone analysis shows sponteneous fractures both in large bones and smaller ones such as metacarpals. Serum analysis shows a decrease in calcium, inorganic phosphate, alkaline phosphatase, osteocalcin, and insulin-like growth factor 1. These homozygotes also have a reduction in the number of both the red and white blood cells. Homozygotes are fragile and must be handled with great care. (Beamer et al., 2000.) | ||
| 002088 | BALB/cByJ-Herc2J/J | Repository-Cryopreserved |
| Herc2J, Jackson; spontaneous; recessive: Arose spontaneously on a BALB/cJ background. Homozygous mutants are smaller than littermates and have a subtle tremor that is recognizable by 2.5 to 3 weeks of age. The visible tremor is not progressive with age. Males are functionally sterile and have reduced sperm numbers and sperm abnormalities similar to those seen in mice with the pink-eyed dilution deletion alleles, Herc2p-bs, Herc2p-6H, and Herc2p-25H. In vitro fertilization was not attempted. Females have poor fertility but ovaries are functional when transplanted into histocompatible hosts. Ovaries may exhibit fewer and smaller copora lutea based on limited sample. Herc2J was allele tested with Herc2p-6H/Herc2p-cp and with Herc2PJ/Herc2P-bs and found to be allelic with Herc2p-6H and Herc2p-bs
..... For more information please see the full descriiption on the strain data sheet | ||
| 000652 | BDP/J | Repository-Cryopreserved |
| 003478 | C.129P2-Cbx2tm1Cim/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation show greatly retarded growth, premature death, homeotic transformations of the axial skeleton, sternal and limb malformations and arrested T cell development. Null mice show an aggravation of the skeletal malformations when treated to retinoic acid at embryonic day 7.5. | ||
| 000200 | C3FeB6 A/Aw-J-Ankank/J | Repository-Cryopreserved |
| The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting i
..... For more information please see the full descriiption on the strain data sheet | ||
| 001904 | C3H-Atcayji-hes/J | Repository-Cryopreserved |
| Mice homozygous for the hesitant spontaneous mutation (Atcayji-hes) can be recognized at 14 days of age by their slightly smaller size and hesitant walking motion. From 3 weeks of age on, the hindlimbs of homozygous mutant mice hesitate after lifting and then are placed flat on the surface and stiffly extended causing the posterior to rise. No body tremors, spasticity, or muscle degeneration is observed. Homozygotes of both sexes are fertile, although fertility in males may be reduced. | ||
| 003401 | C3H/HeJ-Lpin1fld-2J/J | Repository-Cryopreserved |
| Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot analysis of sciatic nerve from two-to-three month old fld/fld mice showed a 7-13-fold reduction in myelin P0, a vast increase in apoE, an increase in GAP-43, and no detectable myelin P2. It was also noted that a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000510 | C3H/HeJ-Pou1f1dw-J/J | Repository-Cryopreserved |
| Mice homozygous mice for the dwarf Jackson spontaneous mutation (Pou1f1dw-J) have a phenotype very similar to mice homozygous for the original dwarf mutation (Pou1f1dw). Homozygous mutant mice are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 001431 | C3H/HeSn-ocd/J | Repository-Cryopreserved |
| 002333 | C3H/HeSnJ-gri/J | Repository-Cryopreserved |
| On an agouti background gri homozygotes resemble Tyrc-ch homozygotes. There is a graying of the coat due to a lighter than normal phaeomelanin band. There is no change in eye color. gri homozygotes are slightly smaller than their unaffected littermates. Homozygous females breed well, but homozygous males often do not breed. Testis biopsies failed to identify any sperm abnormalities. The gri mutation does not cause a clotting disorder. (Davisson et al., 2000.) | ||
| 000233 | C3Wf.Cg-Hmga2pg/BmJ | Repository-Cryopreserved |
| Mice homozygous for the pygmy mutation (Hmga2pg) are recognizably smaller at birth, growth rate is slow, and adults weigh about one-third as much as normal mice. They are healthy and active; some are sterile, but fertility may be almost normal on genetic backgrounds favoring large size. Pituitary, thyroid, and adrenals appear normal; Normal somatomedin activity; Normal serum levels of GH and PRL, but below normal concentrations in the pituitary; Unresponsive to administration of growth hormone. | ||
| 001496 | C57BL/6J-Bmp5se-4J/J | Repository-Cryopreserved |
| 005322 | C57BL/6J-Gusbmps-3J/J | Repository-Cryopreserved |
| 000529 | C57BL/6J-Lbric-J/J | Repository-Cryopreserved |
| Lbric-J/Lbric-J homozygotes can be identified at 2 weeks of age due to sparse fur and at 3-4 weeks of age scales develop on the tail and, to a lesser degree, on the trunk. These mutants are smaller than their wild type siblings. The mutants develop mild epidermal hyperplasia with orthokeratotic hyperkeratosis and dilation of the piliary canals. Homozygotes have an increased incidence of syndactyly and hydrocephaly, and a high prenatal mortality rate. Aberrant morphology of nuclear heterochromatin occurs in lymphocytes, neutrophils, eosinophils, intestinal epithelium, and cerebellar granule cells. Electron microscopy reveals clumps of heterochromatin at the periphery of the nucleus within splenic lymphocytes. These mice are a model for Pelger-Huet anomaly, which is associated with mutations in LBR, although the skin pathology is specific to the mouse mutation. (Eicher, 1976; Hoffmann et al., 2002; Shultz et al., 2003.) | ||
| 002854 | C57BL/6J-Nek1kat-2J/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 000219 | C57BL/6J-Slc30a4lm/J | Repository-Cryopreserved |
| 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. | ||
| 004765 | C57BL/6J-nmf148/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf148 entry. | ||
| 004416 | D2(B6Ei)-twit/J | Repository-Cryopreserved |
| Mice homozygous for this recessive mutation are recognizable by 2.5 - 3 weeks of age by their smaller body size, gaunt torso, frailty, and constant quivering which is most obvious from the nose to the abdominal-thoracic area. Mutants also show poor ability to hold onto an edge with either their fore- or hindlimbs. Adult mutants may chatter excessively. Some homozygous mutants die before weaning; others survive through adulthood but they are unreliable breeders. twithas been mapped between the flanking markers D14Mit44 and D14Mit175 in the B band of Chr 14 at 22.9 Mb and 27.9 Mb, respectively. | ||
| 006003 | D2.129P2(Cg)-Cbx2tm1Cim/Ei | Repository-Cryopreserved |
| 002838 | DBA/1LacJ-Dsg4lah-J/J | Repository-Cryopreserved |
| Mice homozygous for the Dsg4lah-J mutation completely lack vibrissae and develop only very short hair that resembles peach fuzz. This is lost by a few months of age, leaving these mice bald. They are runted from birth throughout life. These mice have hyperplasia in the interfollicular epidermis that leads to thickened skin, and their skin wrinkles as they age. Transmission electron micrographs of epidermis from Dsg4lah-J homozygotes reveals acantholysis with small, poorly formed, and dislodged desmosomes. Rather than the normal gradual transition of keratinocytes from proliferation to differentiation in the lower hair follicle, the lanceolate hair mice show a premature, abrupt switch. Above the melanogenic zone a swelling forms that subsequently is pushed out by continued growth of the hair shaft to become the distal tip of the hair. Lanceolate hair mice take their name from the resulting lance-head shape of the hair. The less severely affect
..... For more information please see the full descriiption on the strain data sheet | ||
| 002337 | DBA/2J-pdw/J | Repository-Cryopreserved |
| Mice homozygous for the recessive proportional dwarf (pdw) mutation can be identified by 25 days of age, having shortened limbs, tail, head, and body. Abnormalities were not detected in growth plates and skeletal mineralization patterns. Some pre-wean mortality has been reported. Both female and male homozygotes are fertile. (Sweet et al., 1992.) | ||
| 000253 | DLS/LeJ | Repository-Cryopreserved |
| Mice homozygous for the dilute-lethal spontaneous mutation (Myo5ad-l) display a severe neuromuscular disorder characterized by convulsions and opisthotonus. Homozygous mutant mice usually die by approximately 3 weeks of age. Dilute lethal homozygotes lack smooth endoplasmic reticulum in the dendritic spine of Purkinje cells causing an absence of intracellular calcium. Loss of this intracellular calcium may be the cause of dilute-lethal neurological symptoms. Homozygous dilute-neurological mutant mice (Myo5ad-n, Stock No. 001013) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal homozygotes. In this DLS/Le inbred strain the dilute-lethal mutation is maintained in repulsion with short ear (Bmpse), closely linked mutations on Chromosome 9. | ||
| 000681 | DW.C3-Mlph+ Pou1f1+/J | Repository-Cryopreserved |
| This DW/J congenic strain is wildtype for both the leaden (+Mlph-ln) and dwarf ( +Pit1-dw) mutations and thus serves as a control strain for DW/J-Pit1dw/+ Mlphln/Mlphln, Stock No. 000643. | ||
| 001595 | DW/J-Acdacd/J | Repository-Cryopreserved |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic
..... For more information please see the full descriiption on the strain data sheet | ||
| 002935 | FVB.129S2(B6)-Ccnd1tm1Wbg/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000572 | JIGR/DnJ | Repository-Cryopreserved |
| JIGR/Dn is maintained with jittery (Atcayji) and grizzled (gr) in repulsion.
Atcayji 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 approxi
..... | ||
| 000270 | SEC/1GnLeJ | Repository-Cryopreserved |
| 001880 | STOCK Gusbmps Tg(GUSB)4Sly/BirJ | Repository-Cryopreserved |
| 006241 | STOCK Hhiptm1Amc/J | Repository-Cryopreserved |
| Mice heterozygous for this targeted mutation are viable and fertile. Homozygotes die from respiratory failure shortly after birth. Expression of the "knocked-in" lacZ gene is detected in a pattern similar to the endogenous transcript (in lung, skeleton, stomach, duodenum, spleen, and pancreas), and serves as a faithful reporter for Hedgehog (Hh) signaling. Because Hh and fibroblast growth factor (Fgf) signaling are abnormal, homozygous mice have defects in many Hh target tissues. Although the primary lung buds form in homozygotes, lung branching morphogenesis is defect beginning at 10.5 days postcoitus (dpc), and fails to generate a complete respiratory tree. The single left lobe also is significantly reduced, and total lung size at birth is diminished 67-75% compared to wildtype. In addition, homozygous mice have delayed mineralization of the endochondral skeleton, as well as impaired pancreas morphogenesis, islet formation and endocrine cell proliferation. These mutant mice ma
..... For more information please see the full descriiption on the strain data sheet | ||
| 003318 | STOCK Shhtm1Amc/J | Repository-Cryopreserved |
| Mice homozygous for the Shhtm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.
When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e
..... | ||
| 003119 | STOCK Sp4tm1Ssp/J | Repository-Cryopreserved |
| 001433 | STOCK a skt/J | Repository-Cryopreserved |
| Mice homozygous for the skt mutation are smaller than their wild-type siblings and have a kinky tail with only the caudal vertebrae affected. | ||
| 000279 | STOCK gr +/+ Ap3d1mh/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 000312 | STOCK stb + a/+ Fignfi a/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 000596 | STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J | Repository-Cryopreserved |
| 001788 | STOCK Tg(Fabp1-GH1)10Bir/J | Repository-Cryopreserved |
| 001400 | STOCK Tg(Fabp1-GH1)5Bir/J | Repository-Cryopreserved |
| 001515 | STOCK Tg(Fabp1-GH1)7Bir/J | Repository-Cryopreserved |
| 001878 | STOCK Tg(IFABP-GH)11Bir/J | Repository-Cryopreserved |
| 001879 | STOCK Tg(IFABP-GH)12Bir/J | Repository-Cryopreserved |
| 001909 | STOCK Tg(IFABP-GH)15Bir/J | Repository-Cryopreserved |
| Obligate hemizygous F1 offspring from founder 54 carried approximately 60 copies of the transgene in tandem head-to-tail arrangement in a single insertion site. Expression of the reporter gene, human growth hormone, is appropriately restricted to the intestine where the duodenum and proximal jejunum show expression levels normal for intestinal fatty acid binding protein, but the distal small intestine shows reduced expression. Resultant serum human growth hormone levels were 6-38 ng/ml which is approximately 1000 times lower than in mice carrying a transgene with an extended I-FABP promoter which includes nucleotides -1178 to +28. Use of the extended (-1178 to +28) promoter also results in a more normal expression in the distal small intestine. (Sweetser et al., 1988.) | ||
(127 stocks) Back to Top
IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002577 | B6;CB17-Ghrhrlit Prkdcscid/Bm | Research Strain |
| 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 description on the strain data sheet | ||
| 005013 | C57BL/6J-GarsNmf249/J | Research Strain |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for GarsNmf249 entry. | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
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