Search Criteria: Research Area is "Reproductive Biology Research: Fertility Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000697 | B6.BKS(D)-Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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 four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. Adipose tissue transplants in Lepob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight mainte ..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-Dock7m +/+ 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 | ||
| 002468 | KK.Cg-Ay/J | Level 3 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and ..... For more information please see the full phenotype on the strain data sheet | ||
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 014634 | 129(B6)-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. . Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013762). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 013762 | 129-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 007915 | 129S.FVB-Tg(Amh-cre)8815Reb/J | Repository- Live |
| Mice harboring the Amh-cre transgene are viable and fertile, with expression of Cre recombinase directed by the testis Sertoli cell-specific promoter elements of the anti-Mullerian hormone (Amh) gene. Cre-recombinase activity is reported in testis Sertoli cells during male sexual development as early as E14.5, with no evidence for cre expression detected in other tissues examined. When Amh-cre transgenic males are bred with female mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence specifically in testis Sertoli cells. These Amh-cre transgenic mice may be useful in generating conditional knockouts in testis Sertoli cells for studying male embryonic sexual differentiation and the regulation of spermatogenesis. | ||
| 002753 | 129S6/SvEvTac-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for the Atmtm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice. | ||
| 001809 | B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J | Repository- Live |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 013702 | B6.129(Cg)-Cep290tm1.1Jgg/J | Repository- Live |
| Homozygous Cep290 (centrosomal protein 290) targeted mutation neonates are runted and display retinal degeneration. Normal body weight is attained 1-2 months after birth. Both male and female homozygotes are sterile. This strain may be useful in studies of retinal degeneration, cilia/flagella development and fertility. | ||
| 007741 | B6.129-Arg1tm1Rki/J | Repository- Live |
| Homozygous AI-mutant mice completely lack hepatic arginase (AI) activity, exhibit hyperagrininemia, severe symptoms of hyperammonemia (ncluding decerebrate posture, lethargy, and high-frequency tremor of the extremities, particularly the tail) and die between 10-14 days after birth. Neural stem cells (NCSs) isolated from homozygous mice exhibit abnormal proliferation and differentiation. In addition, haploid germ cells carrying the disrupted AI allele may be less fit/less effective in forming zygotes compared to wild-type spermatozoa. Heterozygotes are viable and fertile. These AI-mutant mice may be useful in studying metabolic defects of arginase I deficiency, urea cycle (excretion of excess nitrogen), and neuronal development and function. | ||
| 014607 | B6.129-Mkkstm1Vcs/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exon 3 of the McKusick-Kaufman syndrome protein (Mkks or Bbs6) gene, abolishing gene function. Homozygous females are viable and fertile, while homozygous males are infertile due to lack of flagellated sperm. These mice are also smaller at birth than littermates. Mutations in Mkks have been known to cause McKusick-Kaufman syndrome (MKS) and Bardet-Biedl syndrome (BBS). MKS is a disorder characterized by post-axial polydactyly, congenital heart defects and hydrometrocolpos, while BBS is a pleiotropic disorder characterized by retinal and photoreceptor degeneration, obesity, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. Mkks-/- mice lack MKKS expression in brain, lung, heart, kidney, eye, liver, spleen, testes, and muscle. They develop age-related blindness due to retinal degeneration, are obese, and have elevated blood pressure. These mice may be useful for ..... For more information please see the full phenotype on the strain data sheet | ||
| 008289 | B6.129P2(C)-Ptprjtm1.2Weis/J | Repository- Live |
| Gene targeting was used to remove a transmembrane domain from the targeted protein. Homozygotes exhibit a partial peripheral B cell development block at the first transitional stage (T1), although total T or B cell numbers in the spleen and lymph node are unchanged. Truncated product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. A secreted protein without known physiologic consequences is detected in serum from homozygous animals, but no surface protein is detected on cells of hematopoietic lineage, including T cells, B cells, and myeloid cells. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities; homozygotes are not fertile. This strain may be useful in studies of immune responses. | ||
| 004744 | B6.129P2-Esr1tm1Ksk/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable and normal in size and appearence. Female mice exhibit ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. In males, below normal testis weight is associated with a diminished sperm count (10% of normal). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished. | ||
| 004745 | B6.129P2-Esr2tm1Unc/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical abnormalities. Stop codons inserted into exon 3 result in the production of truncated transcripts that are unlikely to be translated into a functional protein. Immunostaining of ovary tissue derived from homozygous females fails to detect protein product. Homozygous females are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation (6 compared to 33.7 in wildtype controls). Male homozygotes are fertile and present no marked abnormalities other than epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system. | ||
| 013584 | B6.129P2-Hspa2tm1Dix/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are infertile, homozygous female mice are fertile. No gene product (mRNA) is detected by Northern blot analysis of testis tissue from homozygous male animals. Immunohistochemical examination of seminiferous tubules does not detect protein gene product. Homozygous males have testes that weigh significantly less than testes from controls. Spermatogenesis in homozygotes is arrested in prophase of meiosis I with a reduced number of postmeitotic spermatids in seminiferous tubules, many with abnormal morphology, and no spermatozoa in the epididymis. Apoptosis of germ cells (late pachytene spermatocytes) in the testes is greatly increased in mutants. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background. | ||
| 012909 | B6.129P2-Klf9tm1Yfk/J | Repository- Live |
| Coding sequence of the Klf9 (Kruppel-like factor 9; also known as BTEB) gene is replaced by lacZ in these targeted mutation mice. Homozygotes show reduced activity levels in rotorod and contextual fear-conditioning tests. They also show a subtle increase in anxiety-like behavior. During development, dentate granule neurons lacking expression of this gene show delayed maturation. Homozygous females exhibit sub-fertility and slightly delayed labor. Homozygous pups are generally smaller at birth but catch up in weight by the time of weaning. This strain may be useful in studies of reproduction, development and behavior. | ||
| 016222 | B6.129S(Cg)-Id2tm1.1(cre/ERT2)Blh/ZhuJ | Repository- Live |
| The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreERT2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring.
No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... | ||
| 010945 | B6.129S2-Pms2tm1Lisk/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, but show an increased incidence of sarcomas and lymphomas. Sperm, tail and tumor cells from homozygous mice exhibit microsatellite instability. Male mice on the mixed C57BL/6 and 129S2 background are infertile with reduced numbers of spermatozoa. Spermatozoa exhibit misshapen heads, truncated, irregular flagella. This strain may be useful in the studies of spermatogenesis, cancer and DNA mismatch repair. | ||
| 009641 | B6.129S4-Adcyap1tm1Clw/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, but experience high postnatal mortality between postnatal week 1 and 2 due to thermoregulatory defect. The Donating Investigator reports that postnatal survival is improved if temperature is kept at 82.5 F. Homozygous males are fertile, homozygous females are subfertile. No gene product (protein) is detected by RIA (radioimmunoassay) analysis of hypothalamus, cerebral cortex, kidney, and stomach tissues in homozygotes. Homozygotes exhibit sustained hyperactivity, shortened circadian period and abnormal circadian phase shifting with 50% reduction in the magnitude of light cued phase shift. Homozygous mice lack the light stimulation increase of sympathetic nerve activity and plasma corticosterone that is observed in wildtype mice. Testicular aging is delayed in 15-month old male homozygotes; reactive oxygen species generation and apoptosis in the testis is reduced. Young male homozygotes (4 month old) exhibit decreased steroi ..... For more information please see the full phenotype on the strain data sheet | ||
| 002781 | B6.129S4-Cdkn1btm1Mlf/J | Repository- Live |
| Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous (nullizygous) adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens. | ||
| 008519 | B6.129S4-Nos1tm2Plh/J | Repository- Live |
| In this targeted mutation exon 6, which encodes the heme-binding domain, is deleted. Mice that are homozygous for the targeted mutation are viable only when maintained on a liquid diet and are not fertile. Some truncated gene product (mRNA) containing exon 2 but completely lacking exon 6 is detected by RR-PCR of brain. Nitric oxide synthase activity is only 0.3% of wildtype levels in the brain. Homozygotes have smaller total body and gonad weight and develop pyloric stenosis. Female homozygotes have fewer ovarian corpora lutea and increased hypothalmic gonadotropin-releasing hormone and circulating luteinizing hormone. Homozygous males have decreased follicle stimulating hormone levels and do not display mating behavior. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of hypothalamo-pituitary axis and neuroendocrine regulation of ..... For more information please see the full phenotype on the strain data sheet | ||
| 008101 | B6.129S6(FVB)-Ptgs2tm1.1Fun/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis.
This mutant mouse strain may be useful in studies of ..... For more information please see the full phenotype on the strain data sheet | ||
| 008536 | B6.129S6-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for this targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma. Homozygotes are infertile. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice. This mutant mouse strain may be useful in studies of ataxia telangiectasia, neurodevelopment and thymic lymphoma. This mutation was originally characterized on the 129S6/SvEvTac background. 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 modif ..... | ||
| 014633 | B6.129S6-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygotes are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013761). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 013761 | B6.129S6-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
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| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of ..... For more information please see the full phenotype 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 (Foxn1nu/Foxn1nu) ..... | ||
| 013716 | B6.Cg-Lhfpl2vgim/GrsrJ | Repository- Live |
| 008596 | B6.Cg-Tg(Prnp-Abca1)EHol/J | Repository- Live |
| These transgenic mice express the mouse Abca1 (ATP-binding cassette, sub-family A (ABC1), member 1) gene under the control of the mouse Prnp (prion protein) promoter. These founder line E mice have a 6-fold increase in expression of ABCA1 in the cortex over wild-type levels. Trangene expression is high in total brain tissue, kidney, testis and muscle as detected by Western blot analysis. Transgenic mice exhibit reduced apoE levels: 40% of wild-type levels in the hippocampus, approximately half of wild-type levels in cerebrospinal fluid (CSF). The apoE protein that is overexpressed has altered biochemical properties and is not as soluble as that found in controls. Lipoprotein particles from the CSF that contain apoE protein are larger in size than wild-type, indicating that the transgenic apoE particles are more lipidated.
Male transgenic mice have atropied testes, defective spermatogenesis and are infertile. The strain can be maintained by mating hemizygous femal ..... | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 004847 | B6;129-Gt(ROSA)26Sortm1(cre/ERT)Nat/J | Repository- Live |
| These R26CreER mutant mice have a tamoxifen-inducible Cre-mediated recombination system driven by the endogenous mouse Gt(ROSA)26Sor promoter. The mutant allele consists of a fusion product involving Cre recombinase and an altered version of the mouse estrogen receptor ligand binding domain. The mutant ligand binding domain does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the CRE/ESR1 protein can only gain access to the nuclear compartment to mediate recombination after exposure to tamoxifen. Tamoxifen administration will also induce Cre recombination in the developing embryos of treated mothers. When crossed with a strain containing a loxP site-flanked sequence of interest, this mutant is useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnor ..... For more information please see the full phenotype on the strain data sheet | ||
| 006401 | B6;129P-Trpa1tm1Kykw/J | Repository- Live |
| Homozygous mice are viable and fertile. The donating investigator reports a dramatic loss of fecundity after 5-6 months of age. The targeting vector contains an endoplasmic reticulum (ER) retention signal (KDEL), which is reported to sequester the potential truncated mRNA product in the ER. The vector also contains an IRES-PLAP reporter gene, allowing extracellular antibody staining/chromogenic development tracking of cells normally expressing the endogenous gene. Homozygous mice display behavioral deficits in response to mustard oil, cold, and punctate mechanical stimuli. These mice have a normal startle reflex to loud noise, a normal sense of balance, a normal auditory brainstem response, and normal transduction currents in vestibular hair cells. These mutants may be useful in neurobiological studies involving dorsal root ganglion neurons and cells of the inner ear, as well as for auditory, temperature, or chemical irritant trials. | ||
| 014635 | B6;129S-Nr1h2tm1Djm/J | Repository- Live |
| In this strain, maintained on a mixed C57BL/6 x 129S6 background, a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013763). These mice may be useful for studying lipid and cholesterol metabolism, and the regulation of the immune r ..... For more information please see the full phenotype on the strain data sheet | ||
| 009358 | B6;129S2-Lats1tm1Tx/J | Repository- Live |
| Homozygous animals exhibit a lack of mammary gland development, infertility and growth retardation. Accompanying these defects are hyperplastic changes in the pituitary and decreased serum hormone levels. The reproductive hormone defects of homozygotes are reminiscent of isolated luteinizing hormone (LH)-hypogonadotropic hypogonadism and corpus luteum insufficiency in humans. Furthermore, Homozygous mice develop soft tissue sarcomas (some by 4-10 months of age) and ovarian stromal cell tumors (by 3 months of age) and are highly sensitive to carcinogenic treatments. Data demonstrates a role for this gene in mammalian tumorigenesis and specific endocrine dysfunction. | ||
| 003379 | B6;129S2-Scarb1tm1Kri/J | Repository- Live |
| The class B, type I scavenger receptor (Srb1 or Scarb1) is a cell surface HDL receptor that can recognize the apolipoproteins on the surface of the HDL particle. It plays a key role in determining the levels of plasma lipoprotein cholesterol (primarily HDL) and the accumulation of cholesterol stores in the adrenal gland.In this strain plasma cholesterol (primarily HDL) concentrations increase by 31% in heterozygotes and 125% in homozygotes, as compared to wild type controls. Also, cholesterol levels in adrenal tissue in heterozygous and homozygous mutants decrease by 42% and 72% respectively, relative to wild type controls. The plasma concentration of Apoa-I, the major protein in HDL, is unchanged in mutant animals, relative to wild type controls.Homozygous females are infertile; homozygous males are fertile. Please note that the donating investigator reports that the number of homozygotes resulting from a cross between heterozygotes is significantly lower than what the expected Mendel ..... For more information please see the full phenotype on the strain data sheet | ||
| 008752 | B6;129S4-Nhlh2tm1Irk/J | Repository- Live |
| Male mice homozygous for this targeted mutation exhibit bilateral cryptochism, hypogonadism, azoospermia, low testosterone and follicle stimulating hormone levels and lack instinctual male sexual behavior. Homozygous females are hypogondal unless raised in the presence of male mice, have estrous cycle defects, and reduced fertility. No gene product (mRNA) is detected by Northern blot analysis of embryos. Initially, homozygous male mice, 4 to 7 weeks of age, have a reduced weight compared to wildtype controls. By 12 weeks of age, homozygous males are significantly heavier than wildtype, and mutants progressively increase weight with age. Female homozygotes 5 to 6 weeks of age have normal body weight, however by 7 weeks of age they are significantly heavier than wildtype controls. The increased body weight is due to increased adipose tissue, with the exception of female homozygotes more than 52 weeks of age that exhibit increased lean body mass. Male heterozygotes and homozygotes, ..... For more information please see the full phenotype on the strain data sheet | ||
| 013763 | B6;129S6-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 008219 | B6;129S7-Zpbptm1Zuk/J | Repository- Live |
| Female mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous males are infertile due to severe abnormal spermatozoa morphology and diminished sperm motility. Heterozygous males exhibit terato-asthenozoospermia (increase in the percentage of abnormal sperm) and globozoospermia, but are fertile with normal fecundity. Electron microscopic examination of sperm reveals ultrastructural abnormalties. No gene product (mRNA or protein) is detected by Northern or Western blot analysis or testicular tissue and sperm. This mutant mouse strain may be useful in studies of acrosomal biogenesis and spermiogenesis. | ||
| 012711 | B6;129X1-Dkkl1tm1.1Mldp/J | Repository- Live |
| In this strain, exons 2-4 of the endogenous mouse Dickkopf-Like 1 (Dkkl1) gene are removed, abolishing gene function. Homozygous mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. While homozygous females have no fertility problems, homozygous males have reduced fertilization efficiency. In these mice, DKKL1 expression was absent in developing trophectoderm and spermatocytes, and in the acrosome of mature sperm. This absence of expression did not result in infertility as it is not required for development of sperm or fertility in vivo. These mice may be useful for studying spermatogenesis and fertility. | ||
| 000314 | B6CBACa Aw-J/A-EdaTa/J-XO | Repository- Live |
| XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles. | ||
| 001923 | B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J | Repository- Live |
| The Tim mutation (translocation induced circling mutation) was induced by ethylene oxide in a mutagenesis experiment. The mutation was induced simultaneously with a reciprocal translocation between Chrs 4 and 17. Because the mutation has so far been inseparable from the translocation, it may be that one of the translocation breakpoints has disrupted a gene on Chr 4 or 17. Heterozygotes exhibit circling, head tossing, poor limb coordination, and corneal clouding. The affected mice are usually smaller than wildtype littermates. Inner ear studies have not been done. The mutants swim poorly but can orient themselves in the water. One mutated copy of the gene is dominant over two normal alleles because segmentally trisomic mice with two normal Chrs 4 and 17 and the small 417 translocation product have the behavioral abnormalitites. Breeding is generally poor. | ||
| 002169 | BALB/cByJ-Mtap7mshi/J | Repository- Live |
| Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (Mtap7mshi) 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. | ||
| 008172 | BKS(HRS)-Ddr2slie/JngJ | Repository- Live |
| Mice homozygous for this mutation appear normal at birth. By weaning, they exhibit a reduced body mass, gain weight slower and display minor craniofacial abnormalities such as protruding eyes and a shortened snout. Bone mineral content, but not density is reduced in homozygotes. Plasma glucose levels are significantly increased while blood urea nitrogen levels are decreased in homozygotes. By six weeks, it can be seen that homozygous females lack a corpora lutea. By four months, homozygous males exhibit atrophy of spermatogonia, Sertoli and Leydig cells. This mutant mouse strain has characteristics similar to human Levi type dwarfism and may be useful in studies related to dwarfism and infertility. | ||
| 008340 | BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ | Repository- Live |
| These double mutant mice harbor both the Leprdb spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS-/- C57BLKS/J db/db, eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 016093 | C.129S4(B6)-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Repository- Live |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent dur ..... For more information please see the full phenotype on the strain data sheet | ||
| 013080 | C57BL/6-Actbtm3.1(Sirt1)Npa/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, exhibit delayed reproduction and lower body weight. No homozygotes are produced from heterozygous crosses. Fewer than expected heterozygotes are produced from heterozygote X wildtype crosses. Overexpression of gene product (protein) is detected by Western blot analysis of white adipose tissue, brown adipose tissue, MEFs, skull calvaria cells and brain tissue. Overexpression of the protein is not detected in liver or muscle tissue. Fusion gene product (mRNA) is detected in white adipose tissue by Northern blot analysis. Beta-actin protein expression is equivalent to wildtype levels. Heterozygote knock-in mice have reduced fat mass (epididymal fat pad weight), circulating free fatty acids, leptin, adiponectin and total cholesterol. Food consumption, glucose tolerance and metabolic rate (with associated higher oxygen consumption) are increased in the mutant mice. In fasted conditions, heterozygotes have lower circul ..... For more information please see the full phenotype on the strain data sheet | ||
| 009062 | C57BL/6-Magel2tm1Stw/J | Repository- Live |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 004246 | C57BL/6J-sbse/J | Repository- Live |
| 010543 | C;129-Hsf1tm1Ijb/J | Repository- Live |
| Mice that are heterozygous for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A truncated gene product (mRNA) is detected by Northern blot analysis of embryonic cells. No gene product (protein) is detected by Western blot analysis of non-treated and heat shocked cells or brain, testis, heart and liver tissue. The prenatal lethal phenotype of homozygous mice is more severe on the 129 background than on BALB/c, C57BL/6, or ICR backgrounds. Surviving homozygotes have slowed growth with body weights approximately 78% of normal at eight weeks of age. Homozygotes exhibit abnormal chorioallantoic placenta (thinned spongiotrophoblast layer). Homozygous females are infertile due to impaired meiosis and zygotic cell division. Homozygotes are more resistant to experimentally induced skin tumors and exhibit a lower tumor burden than wild-type controls. Cultured MEFs from homozygotes are less sensitive to glucose depriv ..... For more information please see the full phenotype on the strain data sheet | ||
| 010822 | CByJ(Cg)-dde/GrsrJ | Repository- Live |
| dde homozygotes have disproportionate dwarfing evident at birth by shortened limbs, although the axial skeleton appears normal. The back feet have fused toes. Retinal dysplasia presents as white lines in the retina and electroretinaograms show abnormal rod and cone function. Males are sterile and females are poor breeders and poor mothers, often requiring foster mothers to rear the pups. The lifespan of homozygotes varies with some dying shortly after wean and others surviving to approximately one year of age. Ailments identified in homozygotes include emphysema, stomach polyp, apoptitic cells of the tesis, thyroid cysts, holes in the thoracid chord white matter, and holes in the skeletal muscle fibers in the leg. While it has been proposed that dde may offer a model for Walker-Wardburg syndrome, this has not yet been proven. | ||
| 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. | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The congenic "FVB-db" strain differs from that previously published on other genetic backgrounds in that it presents a marked obesity/diabetes phenotype intermediate between the severe uncompensated hyperglycemia observed in C57BLKS/J and DBA2/J backgrounds and the mild, compensated syndrome reported on the C57BL/6J and 129/J backgrounds. The literature reports that obese FVB-db mice of both sexes show long-term hyperglycemia primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite continued extreme hyperinsulinemia correlated with a marked pancreatic cell hypertrophy and hyperplasia. These phenotypes have been replicated in the stock at The Jackson Laboratory. However, the diabetic nephropathy (glomerulosclerosis) reported in the literature was not evident in the stock imported to JAX at the age evaluated (24 weeks).
As the phenotype varies by genetic background, these mutant mice, along with db mutants on other ge ..... | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002105 | NZO/HlLtJ | Repository- Live |
| NZO mice of both sexes exhibit high birth weights and are significantly heavier at weaning age, Severe obesity (including both visceral and subcuatneous fat depots) develops even when mice are maintained on a standard diet containing 4.5% fat. Both males and females of the NZO/Hl substrain exhibit impaired glucose tolerance (IGT), but subsequent type 2 maturity onset (NIDDM) diabetes development is limited to males, with a phenotype penetrance of 50% or less. NZO/Hl mice also show anti-insulin receptor antibodies, a defect in leptin transport, and hypertension. The genetic lesion appears to be within the islets of Langerhans as transfer of pancreatic islets from normal mice returns body weights and blood glucose levels to within normal range. Ovarian granulosa cell tumors, lymphomas, duodenal, and lung tumors have also been noted to occur in NZO mice at an elevated frequency. F1 hybrids of NON/ShiLt and NZO/Hl provide a new model of obesity-induced diabetes. Male (NON/ShiLt x NZO/Hl)F1 ..... For more information please see the full phenotype on the strain data sheet | ||
| 001384 | PANCEVO/EiJ | Repository- Live |
| 004660 | PWD/PhJ | Repository- Live |
| PWD/PhJ is an inbred mouse strain of the subspecies Mus musculus musculus. M. m. musculus is estimated to have diverged approximately 1 million years ago from M. m. domesticus, the subspecies from which derives most of the genome of practically every laboratory mouse strain. However, the extent of polymorphism for randomly selected microsatellite markers between the two subspecies (70-80%) is nearly as great as between M. m. domesticus and Mus spretus (84%), which diverged about 3 million years ago (Montagutelli et al. 1991; Gergorova and Forejt 2000). PWD/Ph mice exhibit differences from mice of common laboratory strains for a number of complex phenotypic characteristics, including body mass, distribution of adipose tissue, serum concentrations of intermediary metabolites, susceptibility to type I diabetes and various behavioral traits (Gregorova and Forejt 2000). Male, but not female, F1 hybrid offspring of crosses between mice of most lab ..... | ||
| 003715 | PWK/PhJ | Repository- Live |
| 001146 | SPRET/EiJ | Repository- Live |
| The wild-derived inbred strain SPRET/Ei is often used in crosses with common inbred strains to create highly polymorphic panels for genetic mapping. SPRET/Ei mice are resistant to high doses of tumor necrosis factor alpha (TNFa) (Staelens et al 2002). Mice from a C57BL/6 x SPRET/Ei F1 cross were protected from TNFa-induced arthritis and partially protected against induced allergic asthma (Staelens et al 2004). SPRET/Ei may be useful in understanding certain inflammatory diseases. | ||
| 006873 | STOCK Cebpbtm1Vpo/J | Repository- Live |
| Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg ..... For more information please see the full phenotype on the strain data sheet | ||
| 014179 | STOCK Mov10l1tm1.1Eno/J | Repository- Live |
| These mice possess loxP sites on either side of exon 20, which encodes a helicase domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 20 deleted in the cre-expressing tissue(s).
When bred to a strain with widespread expression of Cre recombinase, this mutant mouse strain may be useful in studies of retrotransposon activiation in male germ cells. Global homozygous deletion results in male infertility due to apoptosis of pachytene spermatocytes. | ||
| 007658 | STOCK Npr2tm1Gar/J | Repository- Live |
| Homozygous females are not fertile due to the failure of their reproductive tract development. Homozygous males are also infertile; although spermatogenesis and accessory structures appear unaffected, abnormalities in the neuronal control of penile erection have been found. Null mice are notably smaller than their wildtype and heterozygous littermates several days after birth. Heterozygous mice show a slight reduction in naso-anal length. A dramatic impairment of endochondral ossification and an attenuation of longitudinal vertebra or limb-bone growth are also seen in null animals. They show self-clasping and priapism, suggesting neuronal disorders, but no histological abnormalities are seen in the brain or spinal cord. Survival is reduced. Lethal tonic-clonic seizure attacks have been observed. mRNA is not detected in the brain, growth-plate cartilage, or primary cultures of dermal fibroblasts as determined by Northern blot analysis. This strain may be useful in studies of bo ..... For more information please see the full phenotype on the strain data sheet | ||
| 008208 | STOCK Tg(Stra8-cre)1Reb/J | Repository- Live |
| Homozygous Stra8-cre transgenic mice are viable and fertile, with expression of an optimized variant of Cre recombinase (iCre) directed by the 1.4 kb mouse Stra8 (stimulated by retinoic acid gene 8) genomic promoter fragment. Postnatal Cre-recombinase expression is first observed in testes at postnatal day (P)3 (early-stage spermatogonia), increases out to P7 (pre-leptotene-stage spermatocytes), and is not detected in other tissues examined (including ovaries). In addition, no cre expression is reported in male or female embryos. When Stra8-cre transgenic males are bred with female mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence, specifically during these stages of spermatogenesis. These Stra8-cre transgenic mice may be useful in generating conditional knockouts in postnatal, premeiotic, male germ cells for studying spermatogenesis. | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J-KitlSl/KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet | ||
| 003122 | 129-Cdkn1btm1Mlf/J | Cryopreserved - Ready for recovery |
| Mice deficient in p27kip are viable, but are larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous mutant, Cdkn1b-null adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung following exposure to gamma irradiation or chemical carcinogens. | ||
| 003451 | 129-Smad3tm1Par/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was fo ..... For more information please see the full phenotype on the strain data sheet | ||
| 000709 | 129P3/J-Leprdb-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days 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. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 007659 | 129S-Atp8b3tm1Gar/J | Cryopreserved - Ready for recovery |
| Both male and female homozygotes are fertile, but the average litter sizes from homozygous males are slightly smaller than observed with wildtype males. Sperm morphology and motility are unaffected, but tests show that phosphatidylserine (PS) already exists in the outer membrane leaflet before sperm capacitation. When the zona pellucida (ZP) is removed from eggs, fertilization rates are normal; although when the extracellular matrix is intact, fewer spermatozoa bind tightly or penetrate the ZP, and fewer undergo acrosome reactions. Homozygous mice do not express protein as determined by Western blot analysis of testis tissues and immunostaining of mature spermatozoa. This published information is based on studies of mixed background C57BL/6 and 129S6 background animals; the line offered here is on a pure 129S6 background. This strain may be useful in studies of male fertility. | ||
| 006820 | 129S-Catsper3tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 006821 | 129S-Catsper4tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 004511 | 129S-Tnp1tm1Mlm/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected in testicular homogenates. Levels of transition nuclear protein 2 and protamine 2 precursor are elevated. Homozygous female mice are fertile. Homozygous male mice are subfertile, approximately 60% are infertile, and display diminished sperm motility, sperm tail abnormalities and sperm chromatin abnormalities. Electron microscopy analysis of spermatids reveals both abnormal large rod-like chromatin condensation units as well as normal fine fibrillar chromatin morphology. This mutant mouse strain may be useful in studies of male infertility and/or subfertility. | ||
| 004514 | 129S-Tnp2tm1Mzh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis. Homozygous female mice are fertile. Homozygous male mice are subfertile, producing small litters. Sperm retention in seminiferous tubules of mutant mice is due to increased sperm tail abnormalities. Transition protein 1 and precursor and partially processed protamine 2 levels are elevated in testis tissue. Electron microscopy analysis of mutant testis tissue reveals abnormal cylindrical focal chromatin condensation morphology in spermatids and incomplete chromatin condensation with lacunae and granularity in late stage spermatids and epididymal sperm. Increased uptake of DNA intercalating dyes by mutant sperm nuclei and susceptibility of mutant sperm DNA to acid denaturation is indicative of DNA strand breakage. This mutant mouse strain may be useful in studies ..... For more information please see the full phenotype on the strain data sheet | ||
| 010750 | 129S.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts). Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010751 | 129S.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. | ||
| 010752 | 129S.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002323 | 129S4/SvJae-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 008109 | 129S4/SvJae-Shank1tm1Shng/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant mice show altered postsynaptic density (PSD) protein composition (depletion of Shank-associated proteins guanylate kinase-associated protein (GKAP) and homer homolog 1 (HOMER)), reduced size of dendritic spines, smaller and thinner PSD's, and weaker basal synaptic transmission in the brain. Synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), and late-phase LTP (L-LTP) is normal. Behaviorally, they have increased anxiety-related behavior and impaired contextual fear memory. Homozygous targeted mutant mice have enhanced performance in a spatial learning task, however long-term memory retention is impaired. This strain may be useful in studies of cognitive processes, a feature that may be relevant to human autism spectrum disorders. | ||
| 005730 | 129S6.CB(B6)-Del(1)1Brk Gpi1b/Gpi1c/BrkMdfJ | Cryopreserved - Ready for recovery |
| Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood. | ||
| 002722 | 129S6/SvEv-Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 000385 | 129S;AKR-bs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spontaneous blind sterile mutation (bs) are characterized by bilateral nuclear cataracts, smaller than normal eyes, and glossy coats. Female mutant mice are fertile but males are sterile. Cataracts are visible in 16 day embryos and continue to adulthood. Adult male mice copulate normally but have smaller than normal testes. Defects in spermatogenesis lead to a reduced number of sperm and those that are formed completely lack acrosomes. | ||
| 008671 | A.129S6-Atmtm1Awb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma. Homozygotes are infertile. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice. This mutant mouse strain may be useful in studies of ataxia telangiectasia, neurodevelopment and thymic lymphoma. This mutation was originally characterized on the 129S6/SvEvTac background. 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 modif ..... | ||
| 000277 | ATEB/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the atrichosis spontaneous mutation (at) are characterized by sparsely distributed hair, especially on the trunk. The amount of hair varies, but affected mice can be easily recognized at 8 to 10 days old. Both sexes are sterile and have very small gonads with few germ cells. There is a great deficiency of primary spermatogonia in the testes. A quantitative study of maturation of ovarian oocytes showed that the proportion of resident oocytes recruited into the first wave of growth was much higher than in phenotypically normal heterozygous controls (J.J. Eppig, personal communication). This strain is also segregating for the eye blebs spontaneous mutation (Grip1eb). | ||
| 006102 | B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J | Cryopreserved - Ready for recovery |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Cryopreserved - Ready for recovery |
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 005543 | B6(129)-Duox2thyd/J | Cryopreserved - Ready for recovery |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet | ||
| 000552 | B6-Aw-J-EdaTa-6J.Cg-Sxr | Cryopreserved - Ready for recovery |
| 001730 | B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J | Cryopreserved - Ready for recovery |
| 010726 | B6.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts. Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010727 | B6.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. This strain may be useful as a model for Bardet-Biedl syndrome. | ||
| 010728 | B6.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. This strain may be useful as a model for some features of Bardet-Biedl syndrome. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 008235 | B6.129P2-Abcg5tm1Plo/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this adenosine triphosphate-binding cassette (ABC) half-transporter G5 mutant allele (Abcg5-/-) are viable and severely subfertile; the donating investigator reports that males have significantly reduced fertility and females are almost non-fertile. No gene product (mRNA) from the mutant allele is detected in homozygous liver extracts. The expression of beta-galactosidase (lacZ) from the targeted gene is not characterized to date (July 2008). Abcg5-deficient mice exhibit sitosterolemia (high plasma plant sterol concentrations) and macrothrombocytopenia (enlarged platelets caused by defective megakaryocyte development) associated with a near 70% reduction in total number of platelets. Specifically, when allowed ad libitum access to PicoLab Rodent Diet 5053 chow, homozygous mice exhibit strongly elevated plasma levels of β-sitosterol (37-fold) and campesterol (7.7-fold); with further increased levels upon addition of the synthetic ..... For more information please see the full phenotype on the strain data sheet | ||
| 003142 | B6.129P2-Prlrtm1Cnp/J | Cryopreserved - Ready for recovery |
| There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants. | ||
| 005423 | B6.129S-Terttm1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. No telomerase activity is detected by telomeric repeat amplification (TRAP) assay analysis of testis cells. Mice homozygous for the targeted mutation lack telomerase activity and exhibit telomere shortening. Homozygous intercrossing for multiple generations causes telomere instability (shortening) and infertility. This mutant mouse strain may be useful in studies of telomerase function. | ||
| 004621 | B6.129S1-Il11ra1tm1Wehi/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No transcripts are detected in kidney, testis or bone marrow. Bone marrow cells derived from homozygous mice fail to display the synergistic growth reaction usually observed in response to the combined treatment with interleukin-11 and interleukin-3 or stem cell factor in hematopoietic assays. Homozygous females are infertile due to defective decidualization the process necessary for successful implantation whereby the uterine stroma transforms into a specialized tissue known as decidua. Fertilty of homozygous males is normal. This mutant mouse strain may be useful in studies related to hematopoiesis and female reproduction. | ||
| 003808 | B6.129S2(Cg)-Prltm1Hmn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the null Prl allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null females have an irregular estrous cycle and are completely infertile. Homozygous null males and heterozygous females exhibit no fertility problems. The targeted insertion of a neomycin resistance gene into exon 4 results in a truncated Prl transcript that produces an 11 kDa prolactin protein that lacks any detectable bioactivity. Mammary gland development is marked by an absence of terminal or lateral lobulation. The disruption of the prolactin gene appears to have no effects on the hematopoietic system. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 002442 | B6.129S4-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 008108 | B6.129S4-Shank1tm1Shng/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant mice show altered postsynaptic density (PSD) protein composition (depletion of Shank-associated proteins guanylate kinase-associated protein (GKAP) and homer homolog 1 (HOMER)), reduced size of dendritic spines, smaller and thinner PSD's, and weaker basal synaptic transmission in the brain. Synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), and late-phase LTP (L-LTP) is normal. Behaviorally, they have increased anxiety-related behavior and impaired contextual fear memory. Homozygous targeted mutant mice have enhanced performance in a spatial learning task, however long-term memory retention is impaired. This strain may be useful in studies of cognitive processes, a feature that may be relevant to human autism spectrum disorders. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 009640 | B6.129S4-Viptm1Clw/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by immunohistochemical analysis of homozygotes. Homozygous females are subfertile, 15-20% of homozygous females can have litters. Homozygotes exhibit impaired circadian rhythm generation, muscle weakness, increased motor activity and increased induced airway hyperresponsiveness and inflammation. In constant darkness, homozygotes initially display shortened circadian period. Some homozygotes develop arrhythmic circadian periods after extended darkness. Heterozygotes also display abnormal circadian rhythm. Homozygotes have both gross and microscopic anatomical abnormalities of the gastrointestinal tract. 10-15% of homozygotes die of stenosis of the gut before one year of age. Male homozygotes exhibit moderate right ventricular (RV) hypertension, RV hypertrophy, thickened and remodeled pulmonary arteries, perivascular inflammation of smaller pulmonary vessels and airways, red ..... For more information please see the full phenotype on the strain data sheet | ||
| 004038 | B6.129S4-Zp3tm1Dean/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Zp3 gene are viable, normal in size and do not display any gross physical or behavioral abnormalities. No Zp3 gene product (mRNA or protein) is detected. Homozygous females are not fertile; they lack a zona pellucida and exhibit a disorganized corona radiata. Heterozygous females are fertile. Homozygous males appear normal in all respects and are fertile. | ||
| 011021 | B6.129S6-Bmftm1Rjd/J | Cryopreserved - Ready for recovery |
| Homozygous Bmf (BCL2 modifying factor) targeted mutant mice lack expression of its protein which bears only the pro-apoptotic BH3 domain. Expression in brain, spleen, thymus and lymph node tissues is eliminated. Female homozygotes exhibit an imperforate vagina and hydrometrocolpos (22% penetrance). Male and female mice exhibit increased numbers of B cells. | ||
| 004267 | B6.129S6-Dnmt3ltm1Bes/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, normal in size, do not display any gross physical or behavioral abnormalities, but are sterile. Adult homozygous males display severe hypogonadism, Sertoli-cell-only phenotype and apoptotic death of spermatocytes prior to pachytene with loss of spermatogonia progressing to nonsyndromic azoospermia in later adulthood. Extreme abnormalities of meitotic pairing occur. There is a failure to methylate transposons in prospermatogonia with expression of very high levels of both LTR and non-LTR transposons in spermatogonia and spermatocytes. Homozygous females have normal oogenesis. Heterozygous progeny of homozygous females do not develop past 9.5 day post coitum, with pericardial edema with exencephaly and other neural tube defects. Maternally imprinted gene sequence that is usually heavily methylated in control oocytes is undermethylated in mutant mice oocytes. Paternally imprinted gene sequence is not effected and global genome ..... For more information please see the full phenotype on the strain data sheet | ||
| 002723 | B6.129S6-Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 002188 | B6.129S7-Amhtm1Bhr/J | Cryopreserved - Ready for recovery |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. Homozygous females are fertile. | ||
| 005535 | B6.129S7-Del(11Cops3-Rnf112)1Jrl/J | Cryopreserved - Ready for recovery |
| These mutant mice possess an engineered deletion spanning approximately 3 Mb on mouse Chromosome 11. The region involved encompasses a chromosomal segement that shares conserved synteny with the Smith-Magenis syndrome (SMS) critical interval on human Chromosome 17. Mice carrying one copy of the deletion prove to be viable while mice homozygous for the deletion are embryonic lethal. Heterozygous males suffer from reduced fertility, exhibiting reduced sperm counts and an increase in sperm structural abnormalities. Mutant mice weigh less than their wild type littermates at birth but rapidly gain weight such that by 4 months of age, they exceed wild type weight and eventually become obese (60 grams by 8 months of age). Mutant mice exhibit craniofacial abnormalities characterized by overall shorter skulls with broader, shorter snouts and nasal bones. Mutants also produce abnormal electroencephalograms (EEG) with tonic clonic-type seizures being observed in 22% of the mice tested. Behavioral ..... For more information please see the full phenotype on the strain data sheet | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38 ..... For more information please see the full phenotype on the strain data sheet | ||
| 002099 | B6.129X1-Fostm1Pa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fostm1Pa mutation show reduced placental and fetal weights, lack teeth, and have a significant pre-weaning loss of viability. Survivors grow at a normal rate until about 11 days of age when they begin to develop a severe osteopetrosis. They may live as long as 5-7 months. Homozygous mice have delayed or absent gametogenesis and show lymphopenia. They also exhibit behavioral abnormalities, including hyperactivity and diminished response to external stimuli. | ||
| 009680 | B6.B-Vps54wr/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this spontaneous mutation on the C57BL/6 background are viable, but infertile and die prematurely. The average lifespan is 3 months, although this can be increased if littermates are present in the cage, the Donating Investigator reports. Homozygotes exhibit progressive locomotor impairment with corresponding motor neuron and muscular degeneration. Homozygous males have defective spermiogenesis and are sterile. Homozygotes of both sexes have reduced serum estrogen. Mitochondria in motor neurons are abnormal. This mutant mouse strain may be useful in studies of Spinal Muscular Atrophy, Distal Hereditary Motor Neuronopathy and Amyotrophic Lateral Sclerosis 1. | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Cryopreserved - Ready for recovery |
| 000560 | B6.C-H7b/By KitW-50J/J | Cryopreserved - Ready for recovery |
| 000122 | B6.C3-KitW-44J/J | Cryopreserved - Ready for recovery |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full phenotype on the strain data sheet | ||
| 002624 | B6.C3-Lmx1adr-6J/J | Cryopreserved - Ready for recovery |
| 000100 | B6.C3-Zbtb16lu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the luxoid mutation exhibit preaxial polydactly or oligodactly of the hindfeet, preaxial polydactly of the forefeet, tail kinks, tibial hemimelia and occasionally radial hemimelia. Heterozygotes exhibit preaxial polydactly or hyperphalangy of the hindfeet. An increased number of vertebra, ribs and sternebrae are found in homozygotes and to a lesser extent in heterozygotes (Forsthoefel, 1958). Male mice are infertile with a complete lack of spermatogonia after six weeks (Johnson et al., 1971). By eight months, many seminiferous tubules are agametic, lacking one or more germ cell generations (Buaas et al., 2004). Histological and FACS analysis demonstrate that luxoid homozygotes have progressive germ-cell loss starting as early as eight days (Buaas et al., 2004). This mutant mouse strain may be useful in studies related to male infertility or contraception, limb or skeletal abnormalities, and stem cell research. | ||
| 000991 | B6.C58-KitW-57J/J | Cryopreserved - Ready for recovery |
| 008608 | B6.Cg-Dmc1tm1Jcs/JcsJ | Cryopreserved - Ready for recovery |
| While mice heterozygous for this meiosis-specific RecA homolog (Dmc1) mutation are viable and fertile, homozygotes are viable but sterile due to arrest of gametogenesis in the first meiotic prophase (prophase I). No RNA message from the targeted gene is observed in homozygous testis. Homozygous males have reduced testis size and no mature spermatozoa in the epididymis; spermatocytes undergo meiotic arrest from defective double strand break repair and extensive chromosome asynapsis. Homozygous females exhibit defective oogenesis due to similar aberrations occurring at the pachytene stage or earlier and thus have small, malformed ovaries with complete depletion of oocytes and follicles by adulthood. These Dmc1-mutant mice may be useful in studying gametogenesis and meiosis (including double strand breaks, chromosome asynapsis, DNA repair mechanisms, homologous recombination, and the pachytene checkpoint). | ||
| 000699 | B6.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed, and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency, and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabe ..... For more information please see the full phenotype on the strain data sheet | ||
| 000133 | B6.Cg-KitW-24J/J | Cryopreserved - Ready for recovery |
| 000139 | B6.Cg-KitW-25J/J | Cryopreserved - Ready for recovery |
| 000164 | B6.Cg-KitW/J | Cryopreserved - Ready for recovery |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 000194 | B6.Cg-Lx KitW-v/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/ | ||
| 000567 | B6.Cg-T2J +/+ Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation. | ||
| 004039 | B6.Cg-Zp1tm1Dean/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Zp1 gene are viable, normal in size and do not display any gross physical or behavioral abnormalities. No Zp1 gene product (mRNA or protein) is detected. The zona pellucida matrix from homozygous females appears loosely organized resulting in structural abnormalities and perturbation of normal folliculogenesis. Consequently, litters borne from homozygous females are significantly smaller. | ||
| 006098 | B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous females are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for NFAT, an inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These mice may be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation. | ||
| 000171 | B6.D2-KitW-45J/J | Cryopreserved - Ready for recovery |
| 001563 | B6.D2-KitW-73J/J | Cryopreserved - Ready for recovery |
| 000772 | B6.DW-Pou1f1dw/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 001177 | B6.LP-KitW-49J/J | Cryopreserved - Ready for recovery |
| 001271 | B6.RBF(C3Fe)-Nek1kat/J | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 007733 | B6;129-4930579C15Riktm1Gar/J | Cryopreserved - Ready for recovery |
| Female mice that are homozygous for the targeted mutation are healthy and fully fertile. Male homozygous mice do not display any gross physical or behavioral abnormalities, however they are subfertile. No RNA message is detected by Northern blot analysis of testis tissue from homozygotes. The mechanism for sub-fertility is unknown. This mutant strain may be useful in the study of sperm biology. | ||
| 002784 | B6;129-Dhhtm1Amc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are sterile due to arrested spermatogenesis at the late meiosis, primary spermatocyte stage. Female homozygotes are fertile. No gene product (mRNA) was detectable by semiquantitative RT-PCR analysis of peripheral nerve. Embryonic testis development is impaired. By six weeks of age, the mass of testes from homozygous males is 90% smaller than testes from heterozygous males. Histological examination reveals a diminished number of germ cells and no mature sperm in the testis or epididymis. Peripheral nerves from mutant mice appear flattened with structurally disorganized protective sheaths. The perineural cells, glia and mesenchymal cells, develop defective tight junctions, causing the perineurium to be permeable. This mutant mouse strain may be useful in studies related to male sterility and regulation of peripheral nerve de ..... For more information please see the full phenotype on the strain data sheet | ||
| 002201 | B6;129-Gja1tm1Kdr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gja1tm1Kdr targeted mutation die at birth. The cause of death is a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. The cardiac abnormality involves a delay in the normal looping of the ascending limb of the heart tube, which includes the right ventricle and the outflow tract. This predisposes homozygous mutant mice to malformations of the subpulmonary outflow tract and tricuspid valve. The mutation also predisposes mice to lens cataracts and causes a severe reduction of germ cell numbers in homozygous mutant mice of both sexes. Both neonatal and adult mice heterozygous for the Gja1tm1Kdr targeted mutation have slower ventricular epicardial conduction of paced beats in the heart. | ||
| 006088 | B6;129-Mcl1tm3Sjk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator indicates that homozygous males have severely reduced fertility for unknown reasons, while females have normal fertility. Endogenous protein expression is unaffected by the inserted loxP sequences. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying global, temporal, or tissue-specific deletion of the endogenous gene, particularly in studies of immune function, including apoptosis, B and T cell development, and bone marrow cell differentiation. When bred to a strain with the targeted null allele (Stock No. 006072) and a strain with a Cd19 null allele and expressing Cre recombinase during th ..... | ||
| 011076 | B6;129-Ndptm1.1Nat/J | Cryopreserved - Ready for recovery |
| The human placental alkaline phosphatase (AP) reporter was introduced upstream of the Ndp (Norrie disease (pseudoglioma) (human)) locus start codon. The coding region is intact but it is not apparently expressed and as a result, the retinal hypovascularization defect caused by this allele is as severe as that seen with a conventional null allele. Retinas exhibit retarded vascular growth and sparse vascular coverage. Histochemical staining for AP in males shows homogenous staining throughout the retina at postnatal day 4 (P4), P7 and in adulthood. AP expression in females is mosaic as a result of X chromosome inactivation, and may be useful in visualizing individual cell morphologies. This strain may be useful in studies of vascular growth, remodeling, maintenance, and disease. | ||
| 004362 | B6;129-Scarb1tm1Kri Apoetm1Unc/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous for both targeted alleles are viable, normal in size and do not display any gross physical or behavioral abnormalities. All double mutants die between 5 to 8 weeks following birth, exhibiting hypercholesterolemia and significantly lower body weights compared to control mice. Mice display an altered appearance several days before death, displaying ruffled fur, an abnormal gate and sometimes labored breathing. Hearts from double mutants are enlarged, exhibit evidence of myocardial infarction and are functionally impaired. Histological examination reveals extensive coronary artery disease characterized by atherosclerotic plaques with evidence of cholesterol clefts and fibrin deposition. As with other Scarb1 homozygous null mutants, females are infertile while the fertility of homozygous males remains intact. This double mutant mouse strain offers a model that may be a useful tool in studies related to coronary heart disease. | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 008042 | B6;129P2-Adam2tm1Dgm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this fertilin β (Adam2) mutant allele are viable with no gross phenotypic abnormalities reported. Both precursor and processed fertilin β proteins were absent from spermatogenic cells and mature sperm isolated from homozygous males. While homozygous females are fertile with normal egg activation, homozygous males exhibit sperm deficiencies in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida, rendering them infertile. These fertilin β (Adam2) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the cyritestin (Adam3)-deficient strain (see Stock No. 00 ..... For more information please see the full phenotype on the strain data sheet | ||
| 008043 | B6;129P2-Adam3tm1Pmkf/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this cyritestin (Adam3) mutant allele are viable with no gross phenotypic abnormalities reported. No protein product is detected from the targeted gene in sperm isolated from homozygous males. While homozygous females are fertile, homozygous males exhibit sperm deficiencies in adhesion to the egg zona pellucida and to the egg plasma membrane rendering them infertile. These cyritestin (Adam3) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the fertilin β (Adam2)-deficient strain (see Stock No. 008042). | ||
| 010719 | B6;129P2-Prdm9tm1Ymat/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes are viable but sterile. No gene product (mRNA or protein) is detected by RT-PCR analysis of testes from homozygotes. Male homozygotes display decreased testis weight and incomplete spermatogenesis (arrest at the pachytene stage). Female homozygotes exhibit reduced germ cell number in neonatal ovaries and no forming follicles. Homozygotes have abnormal homologous chromosome pairing, impaired double strand break repair and defective sex body (XY body) formation. This mutant mouse strain may be useful in studies of meiotic arrest, infertility, and double-stranded break repair. | ||
| 008370 | B6;129S-Cstf2ttm1Ccma/J | Cryopreserved - Ready for recovery |
| Male mice that are homozygous for this targeted mutation are infertile due to defective spermatogenesis, similar to oligoasthenoteratozoospermia. Homozygous females are fertile. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of testes tissue. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Lesions in developing sperm appear in stage-XII secondary spermatocytes and progressively worsen with spermatogenesis. Epididymal spermatozoa exhibit variable morphology. This mutant mouse strain may be useful in studies of polyadenylation and translational regulation of protein synthesis during gametogenesis. | ||
| 004153 | B6;129S-Mtap7Gt(ROSABetageo)1Sor/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous for the gene-trapped Mtap7 allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although trace amounts of a presumably nonfunctional transcript can be detected in testis tissue, no protein product is immunodetectable. Male homozygotes are sterile. Expression of the reporter gene (B-galactosidase from the Bgeo fusion gene) employed by the gene trap vector indicates that the Mtap7 promoter directs expression in various tissues with highest levels seen in the seminiferous tubules. During the first wave of spermatogenesis at 5 weeks of age, deformed spermatids can be observed. Abnormalities are attributed to aberrant microtubule organization. Microtubule aberrations are also observed in Sertoli cells. Gradual loss of germ cells occurs. At three months of age, the testes of homozygous mutants are less than one-third the size of those of heterozygous littermates. | ||
| 004715 | B6;129S1-Wnt7atm1Amc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, but sterile. A truncated mRNA transcript is detected during embryogenesis. Homozygotes exhibit ventralization of dorsal limb mesoderm tissues. The variable phenotype includes thickening of dorsal limb dermus, loss of dorsal hair on digits and abnormal or missing posterior distal digits. Abnormalities are more severe distally than proximally. Homozygous female mice have functioning ovaries, but are sterile due to abnormal development of the oviduct and uterus. Although homozygous male mice have normal spermatogenesis, Mullerian ducts do not regress resulting in blocked sperm passage. Mutant mice have reduced synapsin I levels and delayed synaptogenesis between cerebellar granule cells and mossy fiber neurons. This mutant mouse strain may be useful in studies related to dorsal-ventral and anterior-posterior patterning and axonal remodeling. | ||
| 002494 | B6;129S2-Cgatm1Sac/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002495 | B6;129S4-Col1a1tm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and develop to young adulthood without obvious differences from wildtype mice. As the mice age they develop fibrosis in the dermis characterized by a thickening and roughening of the skin, which is similar to that seen in human scleroderma. Homozygous females develop postpartum abnormalities of the uterus caused by a failure of collagen resorption. They have slightly reduced litter sizes and significantly fewer litters than normal wildtype mice. A secondary collagenase cleavage site was found in the mutant protein that could be cleaved by rat collagenase but not by human collagenase. | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis. | ||
| 007656 | B6;129S6-Catsper2tm1Gar/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable. Males, but not females, are completely infertile. The targeted mutation fails to significantly alter sperm production, protein tyrosine phosphorylation associated with capacitation, induction of the acrosome reaction, forward velocity or percentage of motility. Sperm cells fail to acquire hyperactivated motility associated with penetration of the extracellular matrix of the egg. SDS/PAGE and immunoblotting of total sperm protein were used to confirm the absence of gene product. This strain may be useful in studies of male fertility. | ||
| 007661 | B6;129S6-Slc9a10tm1Gar/J | Cryopreserved - Ready for recovery |
| Homozygous females are fully fertile, but males are completely infertile and have severely diminished sperm motility. Body weight, testis size, and caudal epididymal sperm counts of null male mice are no different from those of wildtype or heterozygous littermates. No apparent defects in spermatogenesis were found. The addition of ammonium chloride, which elevates intracellular pH, partially rescues the motility and fertility defects. Cyclic AMP analogues almost completely rescue the motility and infertility phenotypes. Northern blot analysis confirmed the absence of full-length mRNA in homozygous mutants, but a truncated product was found. No stable protein was detected in null mice by immunohistochemistry or western blot analysis. This strain may be useful in studies of male fertility and the molecular basis of fertilization. | ||
| 012715 | B6;129S6-Sun1tm1Mhan/J | Cryopreserved - Ready for recovery |
| Homozygous female and male Sun1 (Sad1 and UNC84 domain containing 1) targeted mutation mice are sterile due to massive apoptotic events that are induced in the gonads. The testes of homozygous males are much smaller than those of wildtype and heterozygous animals. Spermatids and spermatozoa are completely absent and only abnormal spermatocyte-like cells accumulate in some tubules. Ovaries of homozygous females are much smaller than those of their littermates and ovarian follicles are completely absent. No oocytes are detected in day 5 neonatal mice. Docking of chromosomal telomeres at the nuclear envelope is disrupted in both spermatocytes and oocytes of homozygous animals. Efficient chromosomal homolog pairing and synapsis formation in meiosis are disrupted. These mice otherwise develop normally into adults and live for more than a year with no overt differences in physical appearance compared to wildtype littermates. This strain may be useful in studies of meiosis, reproduct ..... For more information please see the full phenotype on the strain data sheet | ||
| 003277 | B6;129S7-Acvr2atm1Zuk/J | Cryopreserved - Ready for recovery |
| Activin receptor IIA deficient mice are viable. Homozygous males are fertile, while homozygous females are infertile. Follicle-stimulating hormone levels are reduced in mutant mice. Some skeletal and facial abnormalities, including micrognathia, cleft palate and defects in Meckel's cartilage are observed. These defects are reminiscent of Pierre-Robin syndrome in humans. Severe defects occasionally result in the perinatal or in utero death of a small number of homozygous mutant embryos. | ||
| 002187 | B6;129S7-Amhtm1Bhr/J | Cryopreserved - Ready for recovery |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. | ||
| 003283 | B6;129S7-Fshbtm1Zuk/J | Cryopreserved - Ready for recovery |
| Males carrying the targeted mutation are fertile, have small testes, reduced sperm number and sperm motility. Homozygous mutant females are infertile due to a preantral stage block in ovarian folliculogenesis. Heterozygotes are fertile. | ||
| 002788 | B6;129S7-Fsttm1Zuk/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002793 | B6;129S7-Srd5a1tm1Mahe/J | Cryopreserved - Ready for recovery |
| 008220 | B6;129S7-Zpbp2tm1Zuk/J | Cryopreserved - Ready for recovery |
| Female mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous males are subfertile with approximately 20% reduction in average litter size. Heterozygous males have normal fertility and fecundity. Homozygous males have slightly abnormal sperm morphology. Although sperm from homozygotes bind to oocyte zona pellucida normally, the slower in vitro fertilization rate indicates reduced zona pellucida penetration. No gene product (mRNA or protein) is detected by Northern or Western blot analysis or testicular tissue and sperm. This mutant mouse strain may be useful in studies of spermiogenesis and sperm-egg interaction. | ||
| 002293 | B6;129X1-Fostm1Pa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fostm1Pa mutation show reduced placental and fetal weights, lack teeth, and have a significant pre-weaning loss of viability. Survivors grow at a normal rate until about 11 days of age when they begin to develop a severe osteopetrosis. They may live as long as 5-7 months. Homozygous mice have delayed or absent gametogenesis and show lymphopenia. They also exhibit behavioral abnormalities, including hyperactivity and diminished response to external stimuli. | ||
| 010816 | B6;C-Ghrhrlit Prkdcscid/BmJ | Cryopreserved - Ready for recovery |
| B6;C-GhrhrlitPrkdcscid/BmJ mice are deficient in growth hormone and IGF1 and are useful for determining endocrine dependence of grafted cells and tissues (Beamer et al., 1993, Cancer Research, v53:3741; Friend et al., 2001 Growth Hormone & IGF Research, v11:84). | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut ..... For more information please see the full phenotype on the strain data sheet | ||
| 000506 | B6C3Fe a/a-Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 000221 | B6C3Fe a/a-Alx4lst-J/J | Cryopreserved - Ready for recovery |
| 002875 | B6C3Fe a/a-Hoxd13spdh/J | Cryopreserved - Ready for recovery |
| The spdh/spdh mutants have a normal body size but exhibit shortened, fused, and duplicated digits in both front and rear feet. Ossification is severely delayed and ossification centers are mis-patterned in developing metacarpal, metatarsal and phalangeal bones. Joint formation is severely disrupted in the phalanges, with forelimbs more affected compared to the hindlimbs. Reduced rates of proliferation and differentiation of mutant chondrocytes contribute to altered cartiledge/bone morphology. Although expression patterns of Hoxd13/11/12 and Hoxa13 do not seem to be disrupted, their function does seem to be disrupted, indicating HOX protein interactions are altered as a result of the spdh mutation. Additionally, the spdh mutant phenotype is much more severe than mutants carrying a targeted disruption of the spdh gene, supporting a dominant-negative effect. The preputial glands of the genital tract are absent in both male and female spdh ..... For more information please see the full phenotype on the strain data sheet | ||
| 001430 | B6C3Fe a/a-Ptch1mes/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the mesenchymal dysplasia spontaneous mutation (mes) have a shortened face, wide set eyes, excessive skin, belly spot, kinked tail, preaxial polydactyly, and thickened foot pads. Homozygous mutant mice also display mineralization of tendons and multiple skeletal defects. Both sexes are infertile. Male mice have cryptorchid testes. | ||
| 000248 | B6C3Fe a/a-Xpl/J | Cryopreserved - Ready for recovery |
| 006430 | B6Ei.129(Cg)-Figlatm1Dean/EiJ | Cryopreserved - Ready for recovery |
| Heterozygous female and homozygous male mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygous mice are infertile due to absence of primordial follicles in the ovary. No gene product (mRNA) is detected by RNase protection analysis of total ovarian RNA. This mutant mouse strain may be useful in studies of female infertility. | ||
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/GrsrJ | Cryopreserved - Ready for recovery |
| 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 seminiferous 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. | ||
| 002088 | BALB/cByJ-Herc2J/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 007971 | BALB/cJ-Ppp1r13lwa3-J/J | Cryopreserved - Ready for recovery |
| Homozygotes have a coat that is sparse but not wavy. They are born with their eyelids open and develop vascular corneas. They also develop early-onset cardiomyopathy, which leads to congestive heart failure. Female homozygotes have not successfully bred and male homozygotes have significantly reduced fertility, producing one or two litters in their lifetime at best. | ||
| 005898 | BKS(Cg)-trls/GrsrJ | Cryopreserved - Ready for recovery |
| Homozygotes can usually be identified at 14 days of age by a tremor and smaller than normal body size. Most homozygotes die around 3 weeks of age, although some have lived longer. | ||
| 000700 | BKS.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| 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 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. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic ..... For more information please see the full phenotype on the strain data sheet | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + Dock7m/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about two weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wild-type controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Leprdb +/+ Dock7m strain so it is also segregating for the diabetes (Leprdb) and misty (Dock7m) mutations. See strain description for Stock No. 000642 for more information. | ||
| 000696 | BKS.V-Lepob/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased 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 stimulati ..... For more information please see the full phenotype on the strain data sheet | ||
| 002391 | BKSChpLt.HRS-Cpefat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BLKS/J genetic background (N10) have a diabetes phenotype that is primarily restricted to males and is more severe than what is seen on the original HRS/J or C57BLKS/J (N5) genetic backgrounds. At weaning both males and female homozygous mutant mice were significantly lighter than wildtype or heterozygous littermates. Obesity develops between 6 and 8 weeks of age and mutant mice can be distinguished from wildtype littermates between 8 and 12 weeks of age. By 18 weeks fat mutant mice will reach 45-55 g and may reach 60-70 g by 6 months of age. Thus, the obesity is thus slower to develop than in the obese (Lepob) and diabetes (Leprdb) mutant mice. The excess adiposity is distributed throughout the body's fat stores, in contrast to the largely axial and inguinal fat deposition of the obese and diabetes mutant mice. Hyperinsulinemia is severe by 4 weeks of age and contin ..... For more information please see the full phenotype on the strain data sheet | ||
| 002368 | C.129S4(B6)-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 008465 | C.129S6-Atmtm1Awb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma. Homozygotes are infertile. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice. This mutant mouse strain may be useful in studies of ataxia telangiectasia, neurodevelopment and thymic lymphoma. This mutation was originally characterized on the 129S6/SvEvTac background. 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 modif ..... | ||
| 012903 | C.129S6-Tnfaip6tm1Cful/J | Cryopreserved - Ready for recovery |
| Male mice that are homozygous for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous females are viable, but infertile. No gene product (mRNA or protein) is detected by RT-PCR and Western blot analysis of embyronic fibroblasts from homozygous mice. Homozygous females have reduced ovulation (fewer oocytes recovered from the oviducts after ovulation) and impaired fertilization, resulting in infertility. Homozygotes develop proteoglycan-induced arthritis with greater severity than wildtype mice, with a larger influx of neutrophils into joints, destruction of articular cartilage, erosion of bone and ankylosis. Neutrophil infiltration is also exacerbated in thioglycollate induced peritonitis. The Y chromosome may not have been fixed to the BALB/cAnNCrl genetic background. | ||
| 005143 | C3.B6-Tg(Fabp1-Ccnd1)4Rdb/J | Cryopreserved - Ready for recovery |
| These transgenic mice express mouse cyclin D1 under the direction of the rat fatty acid binding protein 1 promoter (-596 to +21 fragment). Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Hemizygous mutant mice exhibit reduced fertility after 3 months of age. Transgenic mice overexpress cyclin D1 in the liver and epithelial cells of the small intestine and colon. A lower level of expression occurs in the kidneys. Onset of progressive liver disease begins at one month of age with hepatomegaly. Male transgenic mice exhibit more severe hepatomegaly than transgenic females. By 6 months of age, all transgenic males and half of the transgenic females display hepatocellular dysplasia. Eighty-seven percent of transgenic males and 69% of transgenic females develop hepatocellular adenoma or hepatocellular carcinoma by 15 months of age. This mutant mouse strain may be useful in studies of hepatocellular carcin ..... For more information please see the full phenotype on the strain data sheet | ||
| 000638 | C3FeB6 A/Aw-J-Spnb4qv-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering-Jackson spontaneous mutation (Spnb4qv-J) are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their young. | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 000627 | C3H/HeJ-KitW-x/J | Cryopreserved - Ready for recovery |
| 003401 | C3H/HeJ-Lpin1fld-2J/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 000510 | C3H/HeJ-Pou1f1dw-J/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002333 | C3H/HeSnJ-gri/J | Cryopreserved - Ready for recovery |
| On an agouti background gri homozygotes resemble Tyrc-ch homozygotes. There is a graying of the coat due to a lighter than normal phaeomelanin band. There is no change in eye color. gri homozygotes are slightly smaller than their unaffected littermates. Homozygous females breed well, but homozygous males often do not breed. Testis biopsies failed to identify any sperm abnormalities. The gri mutation does not cause a clotting disorder. (Davisson et al., 2000.) | ||
| 000847 | C3Sn.B6-KitW-39J/J | Cryopreserved - Ready for recovery |
| 001380 | C3Sn.Cg-KitlSl-con/J | Cryopreserved - Ready for recovery |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 005684 | C57BL/6-Ap3b2tm1Bur/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable with diminished fertility. A truncated transcript encoding of the first 120 amino acids followed by 63 extra residues is expressed in brain tissue. Antibodies against C terminal epitopes show no endogenous protein. Homozygous mice have complex neurological and behavioral impairments including tonic-clonic seizures and increased locomotor activity after handling. Compared to wildtype, mutant mice have significantly diminished adaptor complex 3 (AP-3) in dendritic processes and 62% less presynaptic zinc storage in the CA1 stratum oriens (total 25% decrease throughout the brain). The synaptic vesicle targeting of membrane proteins involved in zinc uptake (ZnT3 and ClC-3) is compromised. This mutant may be useful in studies of neuron biology, specifically membrane protein assembly and storage in synaptic vesicles. | ||
| 002197 | C57BL/6-Col1a1Mov13/J | Cryopreserved - Ready for recovery |
| The integration of the M-MuLV genome near the 5' end of the Col1a1 gene blocks transcription of the gene from this locus. Mice homozygous for this mutation suffer from arrested development at day 12 and die at about embryonic day 13-14. Heterozygotes in our colony rarely survived to 8 months of age. Many died at less than 3 months of age. | ||
| 004834 | C57BL/6-Tg(Fabp1-Ccnd1)4Rdb/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the mouse cyclin D1 under the direction of the rat fatty acid binding protein 1 promoter (–596 to +21 fragment). Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Hemizygous mutant mice exhibit reduced fertility after 3 months of age. Transgenic mice overexpress cyclin D1 in the liver and epithelial cells of the small intestine and colon. A lower level of expression occurs in the kidneys. Onset of progressive liver disease begins at one month of age with hepatomegaly. Male transgenic mice exhibit more severe hepatomegaly than transgenic females. By 6 months of age, all transgenic males and half of the transgenic females display hepatocellular dysplasia. 87% of transgenic males and 69% of transgenic females develop hepatocellular adenoma or hepatocellular carcinoma by 15 months of age. By 6 months of age, approximately half of mutant mice have lost hepatic expressio ..... For more information please see the full phenotype on the strain data sheet | ||
| 000569 | C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J | Cryopreserved - Ready for recovery |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby mutation (EdaTa) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 005095 | C57BL/6J-Clcn2nmf240/J | Cryopreserved - Ready for recovery |
| Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum ..... For more information please see the full phenotype on the strain data sheet | ||
| 002923 | C57BL/6J-Clockm1Jt/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this Clockdelta19 mutation (also called Clockmut or Clockm1Jt) show a lengthening of their circadian period by about 1 hour. Homozygous mice show a lengthening of 4 hours followed by a loss of circadian rhythm. Homozygous mice are viable. Male homozygotes are fertile, but female homozygotes appear to have reduced fertility. | ||
| 002009 | C57BL/6J-Hook1azh/J | Cryopreserved - Ready for recovery |
| The sperm of mice homozygous for the abnormal spermatozoon head shape mutation (azh) have a characteristic ladle shape and up to 40% lack a flagella. However, most male mice do breed and litter sizes are more than half as large as those of unaffected litter mates. There are defects in sperm-head packaging of the chromatin as well as acrosomal and flagellar development. Slight but significant reductions in measurements of sperm motility occur. In vitro, sperm from homozygous mutant mice fail to fertilize ova with intact zonae pellucidae, but are successful in fertilizing zona-free ova. Further analysis of these mice reveal defects in the microtubular manchette which surrounds the nucleus. | ||
| 000166 | C57BL/6J-KitW-17J/J | Cryopreserved - Ready for recovery |
| 000167 | C57BL/6J-KitW-18J/J | Cryopreserved - Ready for recovery |
| 000169 | C57BL/6J-KitW-20J/J | Cryopreserved - Ready for recovery |
| 000117 | C57BL/6J-KitW-34J/J | Cryopreserved - Ready for recovery |
| 000128 | C57BL/6J-KitW-35J/J | Cryopreserved - Ready for recovery |
| 000134 | C57BL/6J-KitW-37J/J | Cryopreserved - Ready for recovery |
| 000062 | C57BL/6J-KitW-39J/J | Cryopreserved - Ready for recovery |
| 000121 | C57BL/6J-KitW-40J/J | Cryopreserved - Ready for recovery |
| 000119 | C57BL/6J-KitW-41J/J | Cryopreserved - Ready for recovery |
| 000127 | C57BL/6J-KitW-42J/J | Cryopreserved - Ready for recovery |
| 000129 | C57BL/6J-KitW-43J/J | Cryopreserved - Ready for recovery |
| 000990 | C57BL/6J-KitW-55J/J | Cryopreserved - Ready for recovery |
| 001179 | C57BL/6J-KitW-62J/J | Cryopreserved - Ready for recovery |
| 003252 | C57BL/6J-KitlSl-20J/J | Cryopreserved - Ready for recovery |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. | ||
| 000529 | C57BL/6J-Lbric-J/J | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 001028 | C57BL/6J-Spnb4qv-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering 3 Jackson spontaneous mutation (Spnb4qv-3J) are very similar to mice homozygous for the quivering-Jackson mutation (Spnb4qv-J). Homozygous quivering mutant mice are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are st ..... For more information please see the full phenotype on the strain data sheet | ||
| 000708 | C57BL/6J-Utp14bjsd/J | Cryopreserved - Ready for recovery |
| 000707 | CBA.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Leprdb/Leprdb mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months (Leiter EH et al, 1981).
Because of the sterility of Leprdb homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Leprdb +/+ Dock7m) facilitates identification of heterozygotes for breeding, while the coupling ..... | ||
| 003398 | CBA/J-dal/GrsrJ | Cryopreserved - Ready for recovery |
| Dark-like dal is a recessive mutation causing a darkened coat color, smaller size, gonad abnormalities, and dark staining urine. dal maps to Chromosome 7 and a previously described mutation named dark da maps to the same chromosomal region. Dark-like may be a remutation to dark da.However a test for allelism is not possible because dark is thought to be extinct. Mice homozygous for the dal mutation are easily recognized by 14 days of age by their darkened coats and smaller size. Some homozygotes appear, both phenotypically and pathologically (dense bones), to have skeletal abnormalities however X-rays appear normal. At 7 months of age females had no follicles and many corpora lutea and males mild testicular degeneration with increased Leydig cells. Serum assays for Albumin, BUN, Creatine, Bilirubin, and iron showed no significant differences from controls. | ||
| 000965 | CBACa.C3-KitW-x/J | Cryopreserved - Ready for recovery |
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wild-type, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. These BALB/cByJ-apoB38.9 mice are also heterozygous for the BALB/cByJ-derived SCAD deletion (Acadsdel-J). While BALB/cByJ inbred mice have elevated liver TG f ..... For more information please see the full phenotype on the strain data sheet | ||
| 003219 | D2.129P2(B6)-Nr5a1tm1Klp/EiJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Nr5a1tm1Klp (formerly Ftzf1tm1Klp) targeted mutation exhibit adrenal and gonadal agenesis. There is also an absence of the ventromedial hypothalamic nucleus leading to impaired expression of gonadotrope specific markers. | ||
| 000643 | DW/J Mlphln Pou1f1dw/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 001595 | DW/J-Acdacd/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 000092 | FL/1Re-KitW/J | Cryopreserved - Ready for recovery |
| Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 005021 | FVB-Tg(ZP2)2Dean/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the human zona pellucida 2 (ZP2) protein. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes die shortly after birth. Transgene expression (mRNA and protein) is oocyte specific. This transgene rescues the homozygous null Zp2 infertility phenotype (see Stock No. 004129). This mutant mouse strain represents a model that may be useful in studies of reproduction and fertility. | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... For more information please see the full phenotype on the strain data sheet | ||
| 004064 | FVB/N-Morc1Tg(Tyr)1Az/J | Cryopreserved - Ready for recovery |
| Homozygous female mice and hemizygous male or female mice are viable, fertile and normal in size. Homozygous male mice are sterile as a result of arrested spermatogenesis at or prior to pachytene. Testes of homozygous mice are reduced in size, weighing less than one-third that observed for wild type mice. The transgenic insert imparts an effect on the appearance of the eyes. Wild type mice (FVB/N) will exhibit pink/albino eyes, mice hemizygous for the transgenic insert display brown eyes, while the eyes of homozygotes are black. | ||
| 002437 | FVB/N-Tg(MMTV-Notch4)3Rnc/J | Cryopreserved - Ready for recovery |
| Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands. | ||
| 003335 | FVB/N-Tg(ZP3)7812Dean/J | Cryopreserved - Ready for recovery |
| 000804 | HPG/BmJ | Cryopreserved - Ready for recovery |
| 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. | ||
| 000260 | JGBF/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al.> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000072 | JGBF/LeTyJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al. ..... For more information please see the full phenotype on the strain data sheet | ||
| 006775 | NOD.Cg-Foxp3sf/DoiJ | Cryopreserved - Ready for recovery |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development. | ||
| 001504 | NOR2/LtDn-Vsx2or-2J/J | Cryopreserved - Ready for recovery |
| 000993 | NZB/BlNJ-KitW-59J/J | Cryopreserved - Ready for recovery |
| 001427 | STOCK Aw us/J | Cryopreserved - Ready for recovery |
| 002130 | STOCK Agpsbs2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the blind-sterile 2 mutation display nuclear cataracts, microphthalmia, smaller than normal lens with improper differentiation of lens epithelial cells to fiber cells with vacuolation, morganian globules, bladder cells and detachment of the apical-apical junctions of epithelial and fiber cells, although the lens epithelial cells appear normal at the anterior of the lens. Males have abnormally small testes with disrupted seminiferous tubules lacking mature spermatozoa or elongating spermatids. Although male homozygotes are sterile, female homozygotes are not. | ||
| 002979 | STOCK Apaf1fog/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the forebrain overgrowth recessive spontaneous mutation (fog) display forebrain, lumbo-sacral, and facial defects most likely due to excessive growth or cellular proliferation ultimately causing abnormalities in neural tube closure. The phenotypes manifest as head bumps and sacral spina bifida and individual mice can have either or both. Three unique features of the mutant are (1) the growth of telencephalon cells into the surrounding mesenchyme, (2) presence of an encephalocele through the midline cleft in some mutants, and (3) dissociation of the tail defect from the caudal neural tube defect. The fog mutation maps to mouse Chromosome 10 near D10Mit262 and D10Mit230. | ||
| 000979 | STOCK KitlSl-16J/J | Cryopreserved - Ready for recovery |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. | ||
| 006846 | STOCK Leprdb-9J/Jgn | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutation exhibit moderate obesity and extreme diabetes. The primary investigator reports blood glucose levels reaching 600-850 mg/ml and low plasma insulin levels (1-4 ng/ml). Pancreatic beta cells are small, degranulated and atrophic. The liver is steatotic and strongly PAS-positive for glycogen. Adrenal glands are large with a hyperplastic zona reticularis and appear to be missing the medulla. Homozygous females have fewer primary oocytes and follicles, as well as a decreased amount of developing and ovulated follices. Fecundity is decreased resulting in smaller litter sizes and fewer litters. | ||
| 001253 | STOCK MitfMi-wh +/+ Wnt7apx/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7apx) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet | ||
| 002404 | STOCK Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 001584 | STOCK Oca2p-J/Oca2p-bs/J | Cryopreserved - Ready for recovery |
| Oca2p-J/Oca2p-J mice exhibit significant dilution of coat color with pink eyes, a phenotype similar to that produced by Oca2p/Oca2p. The Oca2p-J mutation is a partial deletion of the gene that completely ablates Oca2p function (Oakey et al. 1996). Oca2p-bs/Oca2p-bs mice show a less extreme coat color dilution and have black eyes from birth; the phenotype of Oca2p-bs homozygotes also includes stunted growth, jerky gait, male sterility, female semisterility, and impaired maternal behavior, and the smaller-than-expected proportion of Oca2p-bs homozygous intercross offspring implies reduced prenatal viability (Lyon et al. 1992). The Oca2p-bs mutation comprises a deletion that begins about 10 kb 5' of the Oca2p locus and extends for about 8 kb in the proximal direc ..... For more information please see the full phenotype on the strain data sheet | ||
| 001585 | STOCK Oca2p-d/Oca2p-25H/J | Cryopreserved - Ready for recovery |
| Oca2p-25H/Oca2p-25H mice exhibit significant dilution of coat color with pink eyes, similar in appearance to Oca2p/Oca2p mice. The Oca2p-25H phenotype also includes a slightly jerky gait with some tremor, small body size compared to control littermates, male sterility, female semisterility, and impaired maternal behavior, and the smaller-than-expected proportion of Oca2p-25H homozygous intercross offspring implies reduced prenatal viability (Lyon et al. 1992, Phillips et al. 1977). The Oca2p-25H mutation comprises an inversion of a segment of Chromsome 7 that alters the 5' end of the Oca2p gene so that no detectable ptranscript is produced, accounting for the pigment-dilution phenotype (Gardner et al. 1992). The deletion also disrupts the Herc2/rjs gene proximal to Oca2p so the transcript seq ..... For more information please see the full phenotype on the strain data sheet | ||
| 000823 | STOCK Oca2p-d/Oca2p-6H/J | Cryopreserved - Ready for recovery |
| 001747 | STOCK Oca2p-d/Oca2p-cp/J | Cryopreserved - Ready for recovery |
| Mice homozygous for Oca2p-d (dark pink-eye) are born with lightly pigmented eyes, darker than those of Oca2p/Oca2p mice, which darken by weaning and a coat color "considerably darker than that of Oca2p/Oca2p mice, somewhat resembling that of brown [Tyrp1b/Tyrp1b] mice"; both sexes are fertile (Gardner et al. 1977, Lyon et al. 1992). A normal-sized Oca2p transcript is present in eyes of Oca2p-d/Oca2p-d mice (Gardner et al. 1992), and Southern blot analysis revealed no gross alteration of the Oca2p gene (Gardner et al. 1992, Lyon et al. 1992); thus, the molecular nature of the defect is unknown. Most Oca2p-cp (p-cleft palate, formerly p11H) homozygotes die soon after birth with cleft palate; the few that survive to adulthood exhibit significant dilution of coat co ..... For more information please see the full phenotype on the strain data sheet | ||
| 010605 | STOCK Prkdcscid Gnrh1hpg/BmJ | Cryopreserved - Ready for recovery |
| 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 | ||
| 003119 | STOCK Sp4tm1Ssp/J | Cryopreserved - Ready for recovery |
| 004129 | STOCK Zp2tm1Dean/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Zp2 gene are viable, normal in size and do not display any gross physical abnormalities. No Zp2 gene protein product is immunodetectable in ovary tissue. Although the ovaries appear normal with follicles at all stages of development present, homozygous females are infertile. A thin zona matrix is present in early follicles but is not sustained in pre-ovulatory follicles. The abnormal zona matrix does not affect initial folliculogenesis, but there is a significant decrease in the number of antral stage follicles in ovaries isolated from mice lacking a zona pellucida. Few eggs are detected in the oviduct after stimulation with gonadotropins, and no two-cell embryos are recovered after mating Zp2-null females with normal male mice. Although zona-free oocytes mature and can be fertilized in vitro and successfully progress to the blastocyst stage, the developmental potential of blastocysts derived from homozygous Zp2-null egg ..... For more information please see the full phenotype on the strain data sheet | ||
| 000579 | STOCK a tp/J | Cryopreserved - Ready for recovery |
| Taupe is a recessive spontaneous mutation that causes a lightening of the coat color such that a/a tp/tp mice are slate grey. The coat color is similar to that of the ruby (Hps5ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. The homozygous females do not have normal nipple development, although the mammary ducts and alveoli develop normally. These females also have difficulty with pregnancy and birth. They can not rear their pups even if the pups are born alive so this strain is maintained by breeding heterozygous females to homozygous males. (Fielder, 1952; Fielder, 1950.) | ||
| 000319 | STOCK a us/J | Cryopreserved - Ready for recovery |
| 001432 | STOCK a/a Tyrp1b sks/Tyrp1b +/J | Cryopreserved - Ready for recovery |
| 001874 | STOCK tw82 tf/J | Cryopreserved - Ready for recovery |
| 006619 | STOCK Tg(Cga-LHB/CGB)94Jhn/J | Cryopreserved - Ready for recovery |
| Hemizygous females are not fertile and hemizygous males are sub-fertile. Hemizygotes hypersecrete luteinizing hormone (LH) from pituitary gonadotropes under hypothalamic control. Inclusion of a bovine luteinizing hormone beta (LHB) sequence in the transgene results in a longer hormone half-life. Transgenic females display a range of reproductive and endocrine anomalies, while males are largely phenotypically normal. Transgenic males do not have elevated serum LH or testosterone when compared to wildtype animals, although their testes are significantly smaller. Transgenic females display elevated serum LH, androgens, and estrogens, with subsequent phenotypes including infertility with chronic anovulation and ovarian pathologies ranging from ovarian cysts to strain-dependent granulosa and theca-interstitial cell tumors. Tumors have been noted in mice from age 4 to 9 months. Other major phenotypes include hyperandrogenemia and precocious puberty, defects in uterine receptivity and mid-ges ..... For more information please see the full phenotype on the strain data sheet | ||
| 009102 | STOCK Tg(Nefh-cre)12Kul/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this mNF-H-cre transgene are viable and fertile, with nuclear localized-Cre recombinase expression directed to neurons, coinciding with late stages of brain development, by the mouse neurofilament-H gene (Nefh) promoter. The cre expression in neurons (but not astrocytes) of the brain and spinal cord is mosaic with highest expression in the cortex and hippocampus. Cre recombinase activity begins around embryonic day (E)16.5-E18.5, with significantly robust activity observed after one week of age. The donating investigator reports that mNFHcre mouse line 12 homozygotes develop a neurological phenotype with seizures and become infertile and moribund. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the resulting offspring. | ||
| 006129 | STOCK Tg(Zp3-EGFP)1Dean/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile with no gross phenotypic abnormalities. These mice express the Zp3-EGFP fusion protein under the direction of the Zp3 promoter. As such, EGFP is readily detected throughout the width of the zona pellucida surrounding growing oocytes, with no expression in the surrounding somatic cells. Mutant mice have normal synthesis, intracellular trafficking, and secretion/incorporation into the zona pellucida matrix of the transgenic fusion protein. These mice may be useful in studies of reproductive biology, including intracellular trafficking of zona pellucida proteins to the cell surface, oocyte development, fertilization research, as well as developmental biology. | ||
| 007679 | SWR.129X1(B6)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38. ..... For more information please see the full phenotype on the strain data sheet | ||
| 000161 | WB.D2-KitlSl-d/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 016224 | B6.129S(Cg)-Id2tm2.1Blh/ZhuJ | Under Development - Now Accepting Orders |
| The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 016092 | B6.129S4-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Under Development - Now Accepting Orders |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression is restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent ..... For more information please see the full phenotype on the strain data sheet | ||
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