Search Criteria: Research Area is "Reproductive Biology Research: Fertility Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 000632 | B6.V-Lepob/J | Level 2 |
| Mice homozygous for the obese spontaneous mutation, (Lepob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase in body weight, and probably results from it. Homozygotes have an ab
..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol
..... For more information please see the full phenotype on the strain data sheet | ||
| 002468 | KK.Cg-Ay/J | Level 2 |
| 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 de
..... For more information please see the full phenotype on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 000697 | B6.Cg-m +/+ Leprdb/J | Level 3 |
| 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 diabet
..... 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. | ||
| 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. | ||
| 006102 | B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J | Repository- Live |
| 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. | ||
| 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. | ||
| 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. | ||
| 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. 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. | ||
| 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 studi
..... For more information please see the full phenotype on the strain data sheet | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Repository- Live |
| 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 | ||
| 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.
| ||
| 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 Foxp3sf/Y mice do not develop scurfy
..... | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Repository- Live |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 006098 | B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J | Repository- Live |
| 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. | ||
| 008278 | B6.Cg-Tg(tetO-Clock)1Jt/J | Repository- Live |
| Homozygous transgenic mice are viable and fertile. These animals express the wildtype Clock gene under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. Transgenic expression of the Clock gene in the suprachiasmatic nucleus and brain of mice regulates the period length of circadian locomotor rhythms. This wildtype transgene shortens the period of circadian locomotor rhythms in mice, whereas overexpression of the Clockdelta19 mutant transgene (Stock No. 008277) lengthens the period. These effects
..... For more information please see the full phenotype on the strain data sheet | ||
| 008277 | B6.Cg-Tg(tetO-Clockm1Jt)CL57Jt/J | Repository- Live |
| Homozygous transgenic mice are viable and fertile. These animals express the Clockdelta19 mutation under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline.
Transgenic expression of the Clock gene in the suprachiasmatic nucleus and brain of mice regulates the period length of circadian locomotor rhythms. This dominant negative mutant transgene lengthens the period of circadian locomotor rhythms in mice, whereas overexpression of the wild-type transgene (Stock No. 008278) shortens the period. These effect
..... | ||
| 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/Esr1)Nat/J | Repository- Live |
| These 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 abnormalities.
..... 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. | ||
| 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 | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Repository- Live |
| 25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 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. | ||
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/J | Repository- Live |
| Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminipherous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp. | ||
| 002169 | BALB/cByJ-mshi/J | Repository- Live |
| Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (mshi) are characterized by reduced testis size and sterility. The testes are highly disorganized and appear to have a block in the regulation of male germ cell proliferation. Reproduction is normal in homozygous mutant female mice. In addition to the male reproductive defects this mutation also affects histocompatibility in both sexes. Most homozygous mutant mice reject sex-matched skin grafts from BALB/cBy mice. | ||
| 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 | ||
| 004246 | C57BL/6J-sbse/J | Repository- Live |
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Repository- Live |
| 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 | ||
| 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. | ||
| 000643 | DW/J Mlphln Pou1f1dw/J | Repository- Live |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The phenotype of this congenic "FVB-db" strain varies from that previously published on other genetic backgrounds. Specifically, obese FVB-db mice show long-term hyperglycemia that is primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite escalating insulin secretion and a massive increase in pancreatic beta-cell mass. Obese FVB-db mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. Whereas the original C57BLKS/J-db mice are hyperglycemic due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of FVB-db appears to be due to severe insulin resistance with continual increases in insulin secretory capacity from beta-cell mass expansion. As the phenotype varies by genetic background, these mutant mice, along with db mutants on other genetic backgrounds (see Stock No. 000642, For more information please see the full phenotype on the strain data sheet | ||
| 000804 | HPG/BmJ | Repository- Live |
| Mice homozygous for the hypogonadal mutation (Gnrh1hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/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 (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are complet
..... 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. | ||
| 002979 | STOCK Apaf1fog/J | Repository- Live |
| 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. | ||
| 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 | ||
| 006619 | STOCK Tg(Cga-LHB/CGB)94Jhn/J | Repository- Live |
| 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 | ||
| 006129 | STOCK Tg(Zp3-EGFP)1Dean/J | Repository- Live |
| 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 | Repository- Live |
| 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 | ||
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 007659 | 129S-Atp8b3tm1Gar/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected 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 | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (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 | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 002722 | 129S6/SvEv-Mostm1Ev/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 000277 | ATEB/LeJ | Repository-Cryopreserved |
| 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). | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Repository-Cryopreserved |
| 002048 | B6 x C57BLKS-m Leprdb Myo15sh2-J/J | Repository-Cryopreserved |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wildtype 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 (m) and diabetes (Leprdb) spontaneous mutations. | ||
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease
..... For more information please see the full phenotype on the strain data sheet | ||
| 000552 | B6-Aw-J-EdaTa-6J.Cg-Sxr | Repository-Cryopreserved |
| 001730 | B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J | Repository-Cryopreserved |
| 003142 | B6.129P2-Prlrtm1Cnp/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 002442 | B6.129S4-Inhbbtm1Jae/J | Repository-Cryopreserved |
| 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. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Repository-Cryopreserved |
| 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. | ||
| 004038 | B6.129S4-Zp3tm1Dean/J | Repository-Cryopreserved |
| 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. | ||
| 004267 | B6.129S6-Dnmt3ltm1Bes/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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-Zfp179)1Jrl/J | Repository-Cryopreserved |
| 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 | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Repository-Cryopreserved |
| 000560 | B6.C-H7b/By KitW-50J/J | Repository-Cryopreserved |
| 000122 | B6.C3-KitW-44J/J | Repository-Cryopreserved |
| 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 | ||
| 000100 | B6.C3-Zbtb16Lu/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 000133 | B6.Cg-KitW-24J/J | Repository-Cryopreserved |
| 000139 | B6.Cg-KitW-25J/J | Repository-Cryopreserved |
| 000164 | B6.Cg-KitW/J | Repository-Cryopreserved |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva
..... For more information please see the full phenotype on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Repository-Cryopreserved |
| 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/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 000699 | B6.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| 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 | ||
| 000171 | B6.D2-KitW-45J/J | Repository-Cryopreserved |
| 001563 | B6.D2-KitW-73J/J | Repository-Cryopreserved |
| 000772 | B6.DW-Pou1f1dw/J | Repository-Cryopreserved |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 001177 | B6.LP-KitW-49J/J | Repository-Cryopreserved |
| 001271 | B6.RBF-Nek1kat/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full phenotype on the strain data sheet | ||
| 002784 | B6;129-Dhhtm1Amc/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. 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 | ||
| 006088 | B6;129-Mcl1tm3Sjk/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. 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
..... | ||
| 004362 | B6;129-Scarb1tm1Kri Apoetm1Unc/J | Repository-Cryopreserved |
| 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. | ||
| 002201 | B6;129S-Gja1tm1Kdr/J | Repository-Cryopreserved |
| 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. | ||
| 004153 | B6;129S-Mtap7Gt(ROSABetageo)1Sor/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Mice homozygous for the Cgatm1Sac targeted mutation are viable but both sexes are infertile. They lack TSH, LH, and FSH. Homozygous mutant mice are hypogonadal and exhibit severe hypothyroidism resulting in dwarfism. Development of the thyroid gland was arrested in late gestation. However, gonadotropin releasing hormone (GNRH) neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development are normal. Mice heterozygous for the Cgatm1Sac targeted mutation appear normal. | ||
| 002495 | B6;129S4-Col1a1tm1Jae/J | Repository-Cryopreserved |
| 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. | ||
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 003277 | B6;129S7-Acvr2atm1Zuk/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| Homozygous mice die within hours after birth due to a failure to breathe. They are smaller in size than normal wildtype siblings and show craniofacial, musculoskeletal, and skin defects. | ||
| 002793 | B6;129S7-Srd5a1tm1Mahe/J | Repository-Cryopreserved |
| 002404 | B6;CBA-Mostm1Ev/J | Repository-Cryopreserved |
| 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. | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Repository-Cryopreserved |
| 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 | ||
| 000221 | B6C3Fe a/a-Alx4lst-J/J | Repository-Cryopreserved |
| 002875 | B6C3Fe a/a-Hoxd13spdh/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 000506 | B6C3Fe a/a-Qkqk/J | Repository-Cryopreserved |
| 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. | ||
| 000248 | B6C3Fe a/a-Xpl/J | Repository-Cryopreserved |
| 006430 | B6Ei.129(Cg)-Figlatm1Dean/EiJ | Repository-Cryopreserved |
| 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. | ||
| 002088 | BALB/cByJ-Herc2J/J | Repository-Cryopreserved |
| Herc2J, Jackson; spontaneous; recessive: Arose spontaneously on a BALB/cJ background. Homozygous mutants are smaller than littermates and have a subtle tremor that is recognizable by 2.5 to 3 weeks of age. The visible tremor is not progressive with age. Males are functionally sterile and have reduced sperm numbers and sperm abnormalities similar to those seen in mice with the pink-eyed dilution deletion alleles, Herc2p-bs, Herc2p-6H, and Herc2p-25H. In vitro fertilization was not attempted. Females have poor fertility but ovaries are functional when transplanted into histocompatible hosts. Ovaries may exhibit fewer and smaller copora lutea based on limited sample. Herc2J was allele tested with Herc2p-6H/Herc2p-cp and with Herc2PJ/Herc2P-bs and found to be allelic with Herc2p-6H and Herc2p-bs
..... For more information please see the full phenotype on the strain data sheet | ||
| 000700 | BKS.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| 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. 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 efficiency and
..... For more information please see the full phenotype on the strain data sheet | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + m/J | Repository-Cryopreserved |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about 2 weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wiltype 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 +/+ m strain so it is also segregating for the diabetes (Leprdb) and misty (m) mutations. See strain description for BKS.Cg-Leprdb +/+ m (Stock No. 000642) for more information. | ||
| 000696 | BKS.V-Lepob/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 005143 | C3.B6-Tg(Fabp1-Ccnd1)4Rdb/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 | ||
| 004995 | C3H-Tg(Camk2a-Creb1/ESR1)3Sva/J | Repository-Cryopreserved |
| These transgenic mice have a tamoxifen inducible cAMP responsive element binding protein 1 (Creb1) repressor driven by the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. The transgene insert contains a fusion product involving a mutant Creb1 isoform (CREBS133A) and a mutant form of the human estrogen receptor ligand binding domain (LBDG521R). Expression of the transgene is detected in the hippocampus and cortex as analyzed by Northern and Western blot. In addition, transgene expression is detected in the amygdala by RT-PCR analysis. The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Tamoxifen administration activates the repressor, reducing cyclic AMP responsive element-mediated transcription. When the repressor system is activated, mutant mice exhibit impaired long term memory consolidation and retrieval in fear conditioning tra
..... For more information please see the full phenotype on the strain data sheet | ||
| 000627 | C3H/HeJ-KitW-x/J | Repository-Cryopreserved |
| 003401 | C3H/HeJ-Lpin1fld-2J/J | Repository-Cryopreserved |
| Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot | ||