Search Criteria: Research Area is "Reproductive Biology Research: Developmental Defects Affecting Gonads"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 007915 | 129S.FVB-Tg(Amh-cre)8815Reb/J | Repository- Live |
| Mice harboring the Amh-cre transgene are viable and fertile, with expression of Cre recombinase directed by the testis Sertoli cell-specific promoter elements of the anti-Mullerian hormone (Amh) gene. Cre-recombinase activity is reported in testis Sertoli cells during male sexual development as early as E14.5, with no evidence for cre expression detected in other tissues examined. When Amh-cre transgenic males are bred with female mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence specifically in testis Sertoli cells. These Amh-cre transgenic mice may be useful in generating conditional knockouts in testis Sertoli cells for studying male embryonic sexual differentiation and the regulation of spermatogenesis. | ||
| 000645 | A/HeJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm. | ||
| 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. | ||
| 016222 | B6.129S(Cg)-Id2tm1.1(cre/ERT2)Blh/ZhuJ | Repository- Live |
| The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreERT2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring.
No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 007899 | B6.129S4-Casp2tm1Yuan/J | Repository- Live |
| Mice homozygous for this caspase-2 targeted mutation are viable and fertile. As the mutation deletes the QACRG active site and the caspase-2S sequence of the endogenous enzyme, this deletion was shown to inactivate both the long and short form of caspase-2. As such, homozygous mice exhibit defects in regulation of apoptosis; including an enlarged oocyte reserve attributed to a germ cell-intrinsic death defect during prenatal ovarian development (resistance to oocyte cell death following complete cytokine starvation or exposure to an anticancer drug), as well as accelerated motor neuron cell death and defective B lymphoblast apoptosis. In addition, caspase-2-deficient mice exhibit characteristics of premature aging (including shortened maximum lifespan, impaired hair growth, increased bone loss, reduced body fat content, and higher hepatic levels of oxidized proteins). As caspase-2 acts as an upstream regulator of cell death in many cell types, caspase-2-deficient mice may b ..... For more information please see the full phenotype on the strain data sheet | ||
| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
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| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude (Foxn1nu/Foxn1nu) ..... | ||
| 013716 | B6.Cg-Lhfpl2vgim/GrsrJ | Repository- Live |
| 010905 | B6.Cg-Tg(Sry)2Ei Srydl1Rlb/ArnoJ | Repository- Live |
| The dl1Rlb allele (Y-) is an 11 kb deletion in the sex determining region of the Y chromosome, Sry , XY- mice (with ovaries) with this mutation are phenotypic gonadal females, although they lose germ cells and cease estrous cycling earlier in life. The donating investigator indicates that XY- mice generally infertile on the C57BL/6 background . XX mice carrying the Tg(Sry)2Ei transgene are phenotypic gonadal males (with testes), although they lack sperm and have smaller testes than normal males.
When the two mutations are combined, testis determination is transferred from the Y chromosome to an autosome. Mating the carrier male to a C57BL/6J female produces four "core" genotypes that can be used as a model to investigate relationships between sex chromosome complement (XX or XY) and gonadal type that influences phenotypic characteristics. The four genotypes produced are two types of gonadal females (XX, XY-), and two types ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 004847 | B6;129-Gt(ROSA)26Sortm1(cre/ERT)Nat/J | Repository- Live |
| These R26CreER mutant mice have a tamoxifen-inducible Cre-mediated recombination system driven by the endogenous mouse Gt(ROSA)26Sor promoter. The mutant allele consists of a fusion product involving Cre recombinase and an altered version of the mouse estrogen receptor ligand binding domain. The mutant ligand binding domain does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the CRE/ESR1 protein can only gain access to the nuclear compartment to mediate recombination after exposure to tamoxifen. Tamoxifen administration will also induce Cre recombination in the developing embryos of treated mothers. When crossed with a strain containing a loxP site-flanked sequence of interest, this mutant is useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnor ..... For more information please see the full phenotype on the strain data sheet | ||
| 010722 | B6;129S1-Snai2tm2Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, subfertile, and are smaller in size than wildtype controls. Homozygotes have diluted coat color and areas of depigmentation, sometimes exhibiting white forehead blaze and spots on tails and feet. From birth to weaning age (approximately 3 weeks), homozygotes exhibit slowed growth rate and by 3 weeks of age weigh approximately 70% of wildtype control. After weaning, mutant growth rates are similar to wildtype, but mutants remain small in size. Homozygous adults develop eye infections (suppurative conjunctivitis and blepharitis). Homozygous males have reduced testes size due to reduced seminiferous tubules and are slightly subfertile, producing smaller litters sizes. Approximately 15% of homozygous males are infertile. Spermatogenesis is normal, however, in fertile homozygotes. Homozygotes exhibit macrocytic anemia, decreased hematocrit and leukocyte numbers. T cell differentiation is impaired and thymus size is dimi ..... For more information please see the full phenotype on the strain data sheet | ||
| 008752 | B6;129S4-Nhlh2tm1Irk/J | Repository- Live |
| Male mice homozygous for this targeted mutation exhibit bilateral cryptochism, hypogonadism, azoospermia, low testosterone and follicle stimulating hormone levels and lack instinctual male sexual behavior. Homozygous females are hypogondal unless raised in the presence of male mice, have estrous cycle defects, and reduced fertility. No gene product (mRNA) is detected by Northern blot analysis of embryos. Initially, homozygous male mice, 4 to 7 weeks of age, have a reduced weight compared to wildtype controls. By 12 weeks of age, homozygous males are significantly heavier than wildtype, and mutants progressively increase weight with age. Female homozygotes 5 to 6 weeks of age have normal body weight, however by 7 weeks of age they are significantly heavier than wildtype controls. The increased body weight is due to increased adipose tissue, with the exception of female homozygotes more than 52 weeks of age that exhibit increased lean body mass. Male heterozygotes and homozygotes, ..... For more information please see the full phenotype on the strain data sheet | ||
| 001923 | B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J | Repository- Live |
| The Tim mutation (translocation induced circling mutation) was induced by ethylene oxide in a mutagenesis experiment. The mutation was induced simultaneously with a reciprocal translocation between Chrs 4 and 17. Because the mutation has so far been inseparable from the translocation, it may be that one of the translocation breakpoints has disrupted a gene on Chr 4 or 17. Heterozygotes exhibit circling, head tossing, poor limb coordination, and corneal clouding. The affected mice are usually smaller than wildtype littermates. Inner ear studies have not been done. The mutants swim poorly but can orient themselves in the water. One mutated copy of the gene is dominant over two normal alleles because segmentally trisomic mice with two normal Chrs 4 and 17 and the small 417 translocation product have the behavioral abnormalitites. Breeding is generally poor. | ||
| 002169 | BALB/cByJ-Mtap7mshi/J | Repository- Live |
| Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (Mtap7mshi) are characterized by reduced testis size and sterility. The testes are highly disorganized and appear to have a block in the regulation of male germ cell proliferation. Reproduction is normal in homozygous mutant female mice. In addition to the male reproductive defects this mutation also affects histocompatibility in both sexes. Most homozygous mutant mice reject sex-matched skin grafts from BALB/cBy mice. | ||
| 008172 | BKS(HRS)-Ddr2slie/JngJ | Repository- Live |
| Mice homozygous for this mutation appear normal at birth. By weaning, they exhibit a reduced body mass, gain weight slower and display minor craniofacial abnormalities such as protruding eyes and a shortened snout. Bone mineral content, but not density is reduced in homozygotes. Plasma glucose levels are significantly increased while blood urea nitrogen levels are decreased in homozygotes. By six weeks, it can be seen that homozygous females lack a corpora lutea. By four months, homozygous males exhibit atrophy of spermatogonia, Sertoli and Leydig cells. This mutant mouse strain has characteristics similar to human Levi type dwarfism and may be useful in studies related to dwarfism and infertility. | ||
| 010822 | CByJ(Cg)-dde/GrsrJ | Repository- Live |
| dde homozygotes have disproportionate dwarfing evident at birth by shortened limbs, although the axial skeleton appears normal. The back feet have fused toes. Retinal dysplasia presents as white lines in the retina and electroretinaograms show abnormal rod and cone function. Males are sterile and females are poor breeders and poor mothers, often requiring foster mothers to rear the pups. The lifespan of homozygotes varies with some dying shortly after wean and others surviving to approximately one year of age. Ailments identified in homozygotes include emphysema, stomach polyp, apoptitic cells of the tesis, thyroid cysts, holes in the thoracid chord white matter, and holes in the skeletal muscle fibers in the leg. While it has been proposed that dde may offer a model for Walker-Wardburg syndrome, this has not yet been proven. | ||
| 002718 | CByJ.Cg-hop/J | Repository- Live |
| Mice homozygous for the hop-sterile spontaneous mutation (hop) are viable, females are fertile but males are sterile. Homozygous mutant mice walk with a characteristic hopping gait using the hindlegs simultaneously. There is preaxial polydactyly of both fore- and hindfeet. Defects in spermatogenesis result in abnormal sperm tail development. Tailed sperm are completely absent from the lumen of the testicular tubules. The second meiotic division is frequently abnormal or incomplete, often leaving four centrioles per cell. These centrioles usually fail to form flagella, and tail development is arrested. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 010911 | STOCK Wt1tm1(EGFP/cre)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1GFPCre/+) mice are viable and fertile. The Wt1GFPCre "knock-in" allele both abolishes Wt1 gene function and expresses an enhanced green fluorescent protein-Cre recombinase fusion protein (EGFPCre) from the Wt1 promoter/enhancer elements. In heart from heterozygous mice, EGFPCre expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. When bred to mice containing loxP-flanked sequences, the resulting offspring will have Cre-mediated deletion of the floxed sequences in the Wt1-expressing cells (and their descendants). As Wt1 is expressed in the developing genitourinary system and in the mesothelia overlying most visceral organs, these mutant mice may be useful as fluorescent/Cre-lox tools for lineage-tracing/marking Wt1-expressin ..... For more information please see the full phenotype on the strain data sheet | ||
| 010912 | STOCK Wt1tm2(cre/ERT2)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1CreERT2/+) mice are viable and fertile. The Wt1CreERT2 "knock-in" allele both abolishes Wt1 gene function and has expression of the CreERT2 fusion protein (CreERT2) under control of the Wt1 promoter/enhancer elements. In heart from heterozygous mice, CreERT2 expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. CreERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Wt1CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Wt1-expressing cells of the offspring. The donating investigator reports that Cre activity may be observed prior to tamoxifen exposure only in ..... For more information please see the full phenotype on the strain data sheet | ||
| 008208 | STOCK Tg(Stra8-cre)1Reb/J | Repository- Live |
| Homozygous Stra8-cre transgenic mice are viable and fertile, with expression of an optimized variant of Cre recombinase (iCre) directed by the 1.4 kb mouse Stra8 (stimulated by retinoic acid gene 8) genomic promoter fragment. Postnatal Cre-recombinase expression is first observed in testes at postnatal day (P)3 (early-stage spermatogonia), increases out to P7 (pre-leptotene-stage spermatocytes), and is not detected in other tissues examined (including ovaries). In addition, no cre expression is reported in male or female embryos. When Stra8-cre transgenic males are bred with female mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence, specifically during these stages of spermatogenesis. These Stra8-cre transgenic mice may be useful in generating conditional knockouts in postnatal, premeiotic, male germ cells for studying spermatogenesis. | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J-KitlSl/KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet | ||
| 010750 | 129S.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts). Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002323 | 129S4/SvJae-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 002722 | 129S6/SvEv-Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 000385 | 129S;AKR-bs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spontaneous blind sterile mutation (bs) are characterized by bilateral nuclear cataracts, smaller than normal eyes, and glossy coats. Female mutant mice are fertile but males are sterile. Cataracts are visible in 16 day embryos and continue to adulthood. Adult male mice copulate normally but have smaller than normal testes. Defects in spermatogenesis lead to a reduced number of sperm and those that are formed completely lack acrosomes. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Cryopreserved - Ready for recovery |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet | ||
| 000552 | B6-Aw-J-EdaTa-6J.Cg-Sxr | Cryopreserved - Ready for recovery |
| 001730 | B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J | Cryopreserved - Ready for recovery |
| 010726 | B6.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts. Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 003808 | B6.129S2(Cg)-Prltm1Hmn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the null Prl allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null females have an irregular estrous cycle and are completely infertile. Homozygous null males and heterozygous females exhibit no fertility problems. The targeted insertion of a neomycin resistance gene into exon 4 results in a truncated Prl transcript that produces an 11 kDa prolactin protein that lacks any detectable bioactivity. Mammary gland development is marked by an absence of terminal or lateral lobulation. The disruption of the prolactin gene appears to have no effects on the hematopoietic system. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 002442 | B6.129S4-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 009603 | B6.129S4-Kcnn3tm1Jpad/J | Cryopreserved - Ready for recovery |
| The SK3T mutant allele has a tetracycline-based genetic switch inserted into the 5' UTR of the targeted gene, just upstream of the translation initiation site. This genetic switch harbors both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator); allowing transcription of the downstream Kcnn3 locus to be blocked by administration of tetracycline (or its analog doxycycline (dox)). SK3-tTA homozygotes (SK3T/T) exhibit approximately three-fold overexpression of SK3 before dox treatment, and SK3 expression is effectively eliminated by addition of dox. Heterozygous mice exhibit similar expression from both their wild-type and SK3T mutant allele before dox treatment, and no SK3 expression from the mutant allele during dox treatment. In the absence of dox, homozygous mice exhibit abnormal respiratory responses to hypoxia. Homozygous ..... For more information please see the full phenotype on the strain data sheet | ||
| 004267 | B6.129S6-Dnmt3ltm1Bes/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, normal in size, do not display any gross physical or behavioral abnormalities, but are sterile. Adult homozygous males display severe hypogonadism, Sertoli-cell-only phenotype and apoptotic death of spermatocytes prior to pachytene with loss of spermatogonia progressing to nonsyndromic azoospermia in later adulthood. Extreme abnormalities of meitotic pairing occur. There is a failure to methylate transposons in prospermatogonia with expression of very high levels of both LTR and non-LTR transposons in spermatogonia and spermatocytes. Homozygous females have normal oogenesis. Heterozygous progeny of homozygous females do not develop past 9.5 day post coitum, with pericardial edema with exencephaly and other neural tube defects. Maternally imprinted gene sequence that is usually heavily methylated in control oocytes is undermethylated in mutant mice oocytes. Paternally imprinted gene sequence is not effected and global genome ..... For more information please see the full phenotype on the strain data sheet | ||
| 002723 | B6.129S6-Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 002188 | B6.129S7-Amhtm1Bhr/J | Cryopreserved - Ready for recovery |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. Homozygous females are fertile. | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Cryopreserved - Ready for recovery |
| 000560 | B6.C-H7b/By KitW-50J/J | Cryopreserved - Ready for recovery |
| 000122 | B6.C3-KitW-44J/J | Cryopreserved - Ready for recovery |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full phenotype on the strain data sheet | ||
| 000100 | B6.C3-Zbtb16lu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the luxoid mutation exhibit preaxial polydactly or oligodactly of the hindfeet, preaxial polydactly of the forefeet, tail kinks, tibial hemimelia and occasionally radial hemimelia. Heterozygotes exhibit preaxial polydactly or hyperphalangy of the hindfeet. An increased number of vertebra, ribs and sternebrae are found in homozygotes and to a lesser extent in heterozygotes (Forsthoefel, 1958). Male mice are infertile with a complete lack of spermatogonia after six weeks (Johnson et al., 1971). By eight months, many seminiferous tubules are agametic, lacking one or more germ cell generations (Buaas et al., 2004). Histological and FACS analysis demonstrate that luxoid homozygotes have progressive germ-cell loss starting as early as eight days (Buaas et al., 2004). This mutant mouse strain may be useful in studies related to male infertility or contraception, limb or skeletal abnormalities, and stem cell research. | ||
| 000991 | B6.C58-KitW-57J/J | Cryopreserved - Ready for recovery |
| 008608 | B6.Cg-Dmc1tm1Jcs/JcsJ | Cryopreserved - Ready for recovery |
| While mice heterozygous for this meiosis-specific RecA homolog (Dmc1) mutation are viable and fertile, homozygotes are viable but sterile due to arrest of gametogenesis in the first meiotic prophase (prophase I). No RNA message from the targeted gene is observed in homozygous testis. Homozygous males have reduced testis size and no mature spermatozoa in the epididymis; spermatocytes undergo meiotic arrest from defective double strand break repair and extensive chromosome asynapsis. Homozygous females exhibit defective oogenesis due to similar aberrations occurring at the pachytene stage or earlier and thus have small, malformed ovaries with complete depletion of oocytes and follicles by adulthood. These Dmc1-mutant mice may be useful in studying gametogenesis and meiosis (including double strand breaks, chromosome asynapsis, DNA repair mechanisms, homologous recombination, and the pachytene checkpoint). | ||
| 002283 | B6.Cg-KitW-19H/EiJ | Cryopreserved - Ready for recovery |
| This deletion is a dominant mutation causing white spotting on the feet, tail, belly, and occasionally elsewhere. Homozygosity is embryonic lethal. On the C57BL/6 background approximately 60% of heterozygous females have a closed vagina. The ovaries from these heterozygotes are normal and fine for transplantation. On the C57BL/6 background in the presence of the YAKR/J Chromosome (available from Stock No. 007250), KitW-19H heterozygosity results in sex reversed XY females. | ||
| 000133 | B6.Cg-KitW-24J/J | Cryopreserved - Ready for recovery |
| 000139 | B6.Cg-KitW-25J/J | Cryopreserved - Ready for recovery |
| 000164 | B6.Cg-KitW/J | Cryopreserved - Ready for recovery |
| 008656 | B6.Cg-KitlSl-gb/MbeJ | Cryopreserved - Ready for recovery |
| The 120 Kb deletion in the spontaneous mutation, grizzle belly, represents the smallest complete deletion among the Kit ligand (Steel) alleles. Mice homozygous for the mutation die just before or after birth. Mice that survive to postnatal day 1 display a substantial decrease in peripheral red blood cells (RBC) and a severe anemia. Heterozygotes exhibit a mild anemia, and some decrease in peripheral RBC. In the homozygous embryo there is an absence of primordial germ cells (PGCs) by E11.5; an intermediate number of PGCs are found in the heterozygote. Like the other mutations at the Steel locus, this allele causes abnormal pigmentation. Heterozygotes can be identified by a head spot and light belly. This strain may be useful for research in hematopoiesis, pigmentation and gametogenesis. | ||
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/ | ||
| 000567 | B6.Cg-T2J +/+ Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation. | ||
| 000171 | B6.D2-KitW-45J/J | Cryopreserved - Ready for recovery |
| 001563 | B6.D2-KitW-73J/J | Cryopreserved - Ready for recovery |
| 001177 | B6.LP-KitW-49J/J | Cryopreserved - Ready for recovery |
| 004521 | B6.PL-Nppclbab/GrsrJ | Cryopreserved - Ready for recovery |
| 001271 | B6.RBF(C3Fe)-Nek1kat/J | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 002201 | B6;129-Gja1tm1Kdr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gja1tm1Kdr targeted mutation die at birth. The cause of death is a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. The cardiac abnormality involves a delay in the normal looping of the ascending limb of the heart tube, which includes the right ventricle and the outflow tract. This predisposes homozygous mutant mice to malformations of the subpulmonary outflow tract and tricuspid valve. The mutation also predisposes mice to lens cataracts and causes a severe reduction of germ cell numbers in homozygous mutant mice of both sexes. Both neonatal and adult mice heterozygous for the Gja1tm1Kdr targeted mutation have slower ventricular epicardial conduction of paced beats in the heart. | ||
| 007608 | B6;129-Smad1tm1Sor/J | Cryopreserved - Ready for recovery |
| Homozygotes for the Smad1tm1Sor (also called Smad1C) allele have an embryonic lethal phenotype and do not survive past ED9.5. These mice carry a mutation (the C-terminal SSVS motif was changed to AAVA) in exon 7, which effects transcriptional activity. Homozygous embryos display posterior truncation, abnormal turning, allantois malformations (failure of the allantois to connect to the chorionic plate), anterior truncation of the head with only one brachial arch, and enlarged pericardium. At ED7.5 homozygous embryos do not have any detectable primordial germ cells. Western blot analysis of ED9.5 homozygotes showed that protein levels were not affected. Heterozygotes for this mutant allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 007613 | B6;129-Smad1tm2Sor/J | Cryopreserved - Ready for recovery |
| Homozygotes for the Smad1tm2Sor (also called Smad1L) allele are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice carry a mutation in exon 3, which effects MAPK-mediated phosphorylation of the protein. Western blot analysis of MEFs from homozygotes showed that similar protein levels compared to wildtype. Homozygous embryos have fewer primordial germ cells than wildtype controls. Homozygous mice display abnormal gastric mucosa cell population ratios with fewer zymogenic cells and more parietal cells. The cytoskeleton of MEFs from homozygotes exhibit a loss of adhesion zippers, decreased stress fibers, and an accumulation of actin in the cortical regions with an increase in beta-catenin immunostaining localized to the cell membranes. This mutant mouse strain may be useful in studies of stomach development, gastic mucosal homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 008042 | B6;129P2-Adam2tm1Dgm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this fertilin β (Adam2) mutant allele are viable with no gross phenotypic abnormalities reported. Both precursor and processed fertilin β proteins were absent from spermatogenic cells and mature sperm isolated from homozygous males. While homozygous females are fertile with normal egg activation, homozygous males exhibit sperm deficiencies in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida, rendering them infertile. These fertilin β (Adam2) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the cyritestin (Adam3)-deficient strain (see Stock No. 00 ..... For more information please see the full phenotype on the strain data sheet | ||
| 008043 | B6;129P2-Adam3tm1Pmkf/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this cyritestin (Adam3) mutant allele are viable with no gross phenotypic abnormalities reported. No protein product is detected from the targeted gene in sperm isolated from homozygous males. While homozygous females are fertile, homozygous males exhibit sperm deficiencies in adhesion to the egg zona pellucida and to the egg plasma membrane rendering them infertile. These cyritestin (Adam3) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the fertilin β (Adam2)-deficient strain (see Stock No. 008042). | ||
| 010719 | B6;129P2-Prdm9tm1Ymat/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes are viable but sterile. No gene product (mRNA or protein) is detected by RT-PCR analysis of testes from homozygotes. Male homozygotes display decreased testis weight and incomplete spermatogenesis (arrest at the pachytene stage). Female homozygotes exhibit reduced germ cell number in neonatal ovaries and no forming follicles. Homozygotes have abnormal homologous chromosome pairing, impaired double strand break repair and defective sex body (XY body) formation. This mutant mouse strain may be useful in studies of meiotic arrest, infertility, and double-stranded break repair. | ||
| 004153 | B6;129S-Mtap7Gt(ROSABetageo)1Sor/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous for the gene-trapped Mtap7 allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although trace amounts of a presumably nonfunctional transcript can be detected in testis tissue, no protein product is immunodetectable. Male homozygotes are sterile. Expression of the reporter gene (B-galactosidase from the Bgeo fusion gene) employed by the gene trap vector indicates that the Mtap7 promoter directs expression in various tissues with highest levels seen in the seminiferous tubules. During the first wave of spermatogenesis at 5 weeks of age, deformed spermatids can be observed. Abnormalities are attributed to aberrant microtubule organization. Microtubule aberrations are also observed in Sertoli cells. Gradual loss of germ cells occurs. At three months of age, the testes of homozygous mutants are less than one-third the size of those of heterozygous littermates. | ||
| 007032 | B6;129S-Wnt4tm1.1Bhr/BhrEiJ | Cryopreserved - Ready for recovery |
| This strain contains loxP sites flanking exon 2 of Wnt4 resulting in a Cre-dependent conditional null allele. Homozygotes are normal. Studies by Kobayashi et al., determined that when this conditional allele is exposed to Cre expression by Amhr2tm3(cre)Bhr Mullerian duct regression proceeds normally. | ||
| 002494 | B6;129S2-Cgatm1Sac/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cgatm1Sac targeted mutation are viable but both sexes are infertile. They lack TSH, LH, and FSH. Homozygous mutant mice are hypogonadal and exhibit severe hypothyroidism resulting in dwarfism. Development of the thyroid gland was arrested in late gestation. However, gonadotropin releasing hormone (GNRH) neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development are normal. Mice heterozygous for the Cgatm1Sac targeted mutation appear normal. | ||
| 012715 | B6;129S6-Sun1tm1Mhan/J | Cryopreserved - Ready for recovery |
| Homozygous female and male Sun1 (Sad1 and UNC84 domain containing 1) targeted mutation mice are sterile due to massive apoptotic events that are induced in the gonads. The testes of homozygous males are much smaller than those of wildtype and heterozygous animals. Spermatids and spermatozoa are completely absent and only abnormal spermatocyte-like cells accumulate in some tubules. Ovaries of homozygous females are much smaller than those of their littermates and ovarian follicles are completely absent. No oocytes are detected in day 5 neonatal mice. Docking of chromosomal telomeres at the nuclear envelope is disrupted in both spermatocytes and oocytes of homozygous animals. Efficient chromosomal homolog pairing and synapsis formation in meiosis are disrupted. These mice otherwise develop normally into adults and live for more than a year with no overt differences in physical appearance compared to wildtype littermates. This strain may be useful in studies of meiosis, reproduct ..... For more information please see the full phenotype on the strain data sheet | ||
| 002187 | B6;129S7-Amhtm1Bhr/J | Cryopreserved - Ready for recovery |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. | ||
| 003283 | B6;129S7-Fshbtm1Zuk/J | Cryopreserved - Ready for recovery |
| Males carrying the targeted mutation are fertile, have small testes, reduced sperm number and sperm motility. Homozygous mutant females are infertile due to a preantral stage block in ovarian folliculogenesis. Heterozygotes are fertile. | ||
| 002793 | B6;129S7-Srd5a1tm1Mahe/J | Cryopreserved - Ready for recovery |
| 004966 | B6;CBA-Tg(Acrv1-EGFP)2727Redd/J | Cryopreserved - Ready for recovery |
| Mice carrying this "-408SP10-gfp" transgene express Enhanced Green Fluorescent Protein (EGFP) under the direction of the -408 to +28 bp mouse SP-10 (Acrv1) promoter region that contains the necessary transcription regulation signals responsible for both temporal and testis-specific gene expression in transgenic mice. In hemizygous mice, EGFP fluorescence is detected in postmeiotic round spermatid cells of testis beginning from post natal day 21 through adult life. Transgene expression is detected in testis by by northern hybridization as well as RT-PCR analysis. In situ hybridization examination of testis from transgenic mice reveals EGFP is expressed in a pattern mimicking endogenous Acrv1 spatial and temporal expression. This strain may be useful in studies related to spermatogenesis. | ||
| 004200 | B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice carrying the Npr2cn-2J display mutation short thick femurs, round heads, disorganized growth plates, and relatively normal vertebrae; A one month old female exhibited the same phenotype as above but also had splayed ribs. | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Cryopreserved - Ready for recovery |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut ..... For more information please see the full phenotype on the strain data sheet | ||
| 000506 | B6C3Fe a/a-Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 001430 | B6C3Fe a/a-Ptch1mes/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the mesenchymal dysplasia spontaneous mutation (mes) have a shortened face, wide set eyes, excessive skin, belly spot, kinked tail, preaxial polydactyly, and thickened foot pads. Homozygous mutant mice also display mineralization of tendons and multiple skeletal defects. Both sexes are infertile. Male mice have cryptorchid testes. | ||
| 000248 | B6C3Fe a/a-Xpl/J | Cryopreserved - Ready for recovery |
| 008044 | B6C3Fe a/a-bpck/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the bpck deletion develop bilateral polycystic kidneys and die by 3 weeks of age. There is an increased incidence of hydrocephalus. Homozygotes can be identified by their smaller size and swollen abdomens. At 2 weeks of age elevated blood urea nitrogen is found. Ovaries and testes are smaller than normal and progression of maturing cells from spermatocytes to spermatids is disorganized at 3 weeks of age. The primary cilia on the kidney proximal tubule epithelial cells are dysmorphic and vary in length at birth and by 14 days of age cilia are significantly longer than normal. Through overlapping BAC rescues the polycystic kidney disease and hydrocephalus has been traced to the absence of the Tmem67 gene. Although lacking some of the ancillary phenotypes associated with Meckel Syndrome Type 3 in humans, this deletion offers a model for that disease. | ||
| 006305 | B6Ei.Cg-Nr0b1tm1.1Lja Tg(Sry)2Ei Chr YAKR/EiJ | Cryopreserved - Ready for recovery |
| 002605 | B6Ei.MA-A Chr YMA/MyJ/EiJ | Cryopreserved - Ready for recovery |
| This consomic is valuable in the study of sex determination. The TOrl /+ XYMA/MyJ offspring, from the cross of B6.Cg-TOrl /+ females with C57BL/6JEi-Chr YMA/MyJ/EiJ males, are sex reversed, with ovarian tissue development. | ||
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminiferous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp. | ||
| 005898 | BKS(Cg)-trls/GrsrJ | Cryopreserved - Ready for recovery |
| Homozygotes can usually be identified at 14 days of age by a tremor and smaller than normal body size. Most homozygotes die around 3 weeks of age, although some have lived longer. | ||
| 006816 | BXA7/Pgn-Slc26a4pdsm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the pdsm mutation display head bobbing, circling, and occasional head tilt, evident by 3 weeks of age. The inner ear defects include diminished or absent otoconia, hair cells and spiral ganglion cells, malformed tectorial membrane, a reduction in the number of cochlear turns, degeneration of the organ of Corti, and displacement of Reissner's membrane resulting in enlarged scala media. Serum chemistry and histology failed to detect any signs of hypothyroidism. | ||
| 002368 | C.129S4(B6)-Inhbbtm1Jae/J | Cryopreserved - Ready for recovery |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full phenotype on the strain data sheet | ||
| 000627 | C3H/HeJ-KitW-x/J | Cryopreserved - Ready for recovery |
| 000847 | C3Sn.B6-KitW-39J/J | Cryopreserved - Ready for recovery |
| 001380 | C3Sn.Cg-KitlSl-con/J | Cryopreserved - Ready for recovery |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 000569 | C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J | Cryopreserved - Ready for recovery |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby mutation (EdaTa) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 005095 | C57BL/6J-Clcn2nmf240/J | Cryopreserved - Ready for recovery |
| Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum ..... For more information please see the full phenotype on the strain data sheet | ||
| 002009 | C57BL/6J-Hook1azh/J | Cryopreserved - Ready for recovery |
| The sperm of mice homozygous for the abnormal spermatozoon head shape mutation (azh) have a characteristic ladle shape and up to 40% lack a flagella. However, most male mice do breed and litter sizes are more than half as large as those of unaffected litter mates. There are defects in sperm-head packaging of the chromatin as well as acrosomal and flagellar development. Slight but significant reductions in measurements of sperm motility occur. In vitro, sperm from homozygous mutant mice fail to fertilize ova with intact zonae pellucidae, but are successful in fertilizing zona-free ova. Further analysis of these mice reveal defects in the microtubular manchette which surrounds the nucleus. | ||
| 000166 | C57BL/6J-KitW-17J/J | Cryopreserved - Ready for recovery |
| 000167 | C57BL/6J-KitW-18J/J | Cryopreserved - Ready for recovery |
| 000169 | C57BL/6J-KitW-20J/J | Cryopreserved - Ready for recovery |
| 000117 | C57BL/6J-KitW-34J/J | Cryopreserved - Ready for recovery |
| 000128 | C57BL/6J-KitW-35J/J | Cryopreserved - Ready for recovery |
| 000134 | C57BL/6J-KitW-37J/J | Cryopreserved - Ready for recovery |
| 000062 | C57BL/6J-KitW-39J/J | Cryopreserved - Ready for recovery |
| 000121 | C57BL/6J-KitW-40J/J | Cryopreserved - Ready for recovery |
| 000119 | C57BL/6J-KitW-41J/J | Cryopreserved - Ready for recovery |
| 000127 | C57BL/6J-KitW-42J/J | Cryopreserved - Ready for recovery |
| 000129 | C57BL/6J-KitW-43J/J | Cryopreserved - Ready for recovery |
| 000990 | C57BL/6J-KitW-55J/J | Cryopreserved - Ready for recovery |
| 001179 | C57BL/6J-KitW-62J/J | Cryopreserved - Ready for recovery |
| 003252 | C57BL/6J-KitlSl-20J/J | Cryopreserved - Ready for recovery |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. | ||
| 002854 | C57BL/6J-Nek1kat-2J/J | Cryopreserved - Ready for recovery |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J ..... For more information please see the full phenotype on the strain data sheet | ||
| 000708 | C57BL/6J-Utp14bjsd/J | Cryopreserved - Ready for recovery |
| 002602 | C57BL/6JEi-Chr YA/HeJ/EiJ | Cryopreserved - Ready for recovery |
| 007250 | C57BL/6JEi-Chr YAKR/J/Ei | Cryopreserved - Ready for recovery |
| This consomic is valuable in the study of sex determination. The TOrl /+ XYAKR/J offspring, from the cross of B6.Cg-TOrl /+ females with C57BL/6JEi-Chr YAKR/J/EiJ males, are sex reversed, with ovarian tissue development. | ||
| 002890 | C57BL/6JEi-Chr YAPP/EiJ | Cryopreserved - Ready for recovery |
| 001543 | C57BL/6JEi-Chr YCB/EiJ | Cryopreserved - Ready for recovery |
| This YCB Chromosome on the C57BL/6J background results in Y-linked sex reversal wherein XYCB are frequently hermaphrodites. These hermaphrodites often do breed. | ||
| 002604 | C57BL/6JEi-Chr YRF/J/EiJ | Cryopreserved - Ready for recovery |
| This consomic is valuable in the study of sex determination. The TOrl /+ XYRF offspring, from the cross of B6.Cg-TOrl /+ females with C57BL/6JEi-Chr YRF/J males, are sex reversed, having ovarian tissue development. | ||
| 001574 | C57BL/6JEi-Chr YWSB/Ei/EiJ | Cryopreserved - Ready for recovery |
| This consomic is valuable in the study of sex determination. The TOrl /+ XYWSB offspring, from the cross of B6.Cg-TOrl /+ females with C57BL/6JEi-Chr YWSB/EiJ males, are sex reversed, with ovarian tissue development. | ||
| 002063 | C57BL/6JEi-Tg(Sry)1Ei Chr YAKR/J/EiJ | Cryopreserved - Ready for recovery |
| In this strain, XX mice that carry the Tg(Sry)1Ei transgene are sex-reversed males. XYAKR/J mice heterozygous for TOrl on a C57BL/6J background develop as sex reversed females, but in the presence of the Tg(Sry)1Ei transgene these XY mice develop as normal males with testes. | ||
| 002708 | C57BL/6JEi-Tg(Sry)2Ei Chr YAKR/J/EiJ | Cryopreserved - Ready for recovery |
| In this strain, XX mice that carry the Tg(Sry)2Ei transgene are sex-reversed males. | ||
| 003398 | CBA/J-dal/GrsrJ | Cryopreserved - Ready for recovery |
| Dark-like dal is a recessive mutation causing a darkened coat color, smaller size, gonad abnormalities, and dark staining urine. dal maps to Chromosome 7 and a previously described mutation named dark da maps to the same chromosomal region. Dark-like may be a remutation to dark da.However a test for allelism is not possible because dark is thought to be extinct. Mice homozygous for the dal mutation are easily recognized by 14 days of age by their darkened coats and smaller size. Some homozygotes appear, both phenotypically and pathologically (dense bones), to have skeletal abnormalities however X-rays appear normal. At 7 months of age females had no follicles and many corpora lutea and males mild testicular degeneration with increased Leydig cells. Serum assays for Albumin, BUN, Creatine, Bilirubin, and iron showed no significant differences from controls. | ||
| 000965 | CBACa.C3-KitW-x/J | Cryopreserved - Ready for recovery |
| 003219 | D2.129P2(B6)-Nr5a1tm1Klp/EiJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Nr5a1tm1Klp (formerly Ftzf1tm1Klp) targeted mutation exhibit adrenal and gonadal agenesis. There is also an absence of the ventromedial hypothalamic nucleus leading to impaired expression of gonadotrope specific markers. | ||
| 000092 | FL/1Re-KitW/J | Cryopreserved - Ready for recovery |
| Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... For more information please see the full phenotype on the strain data sheet | ||
| 004064 | FVB/N-Morc1Tg(Tyr)1Az/J | Cryopreserved - Ready for recovery |
| Homozygous female mice and hemizygous male or female mice are viable, fertile and normal in size. Homozygous male mice are sterile as a result of arrested spermatogenesis at or prior to pachytene. Testes of homozygous mice are reduced in size, weighing less than one-third that observed for wild type mice. The transgenic insert imparts an effect on the appearance of the eyes. Wild type mice (FVB/N) will exhibit pink/albino eyes, mice hemizygous for the transgenic insert display brown eyes, while the eyes of homozygotes are black. | ||
| 003335 | FVB/N-Tg(ZP3)7812Dean/J | Cryopreserved - Ready for recovery |
| 000804 | HPG/BmJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the hypogonadal mutation (Gnrh1hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement. | ||
| 000260 | JGBF/LeJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al.> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000072 | JGBF/LeTyJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al. ..... For more information please see the full phenotype on the strain data sheet | ||
| 006775 | NOD.Cg-Foxp3sf/DoiJ | Cryopreserved - Ready for recovery |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development. | ||
| 000993 | NZB/BlNJ-KitW-59J/J | Cryopreserved - Ready for recovery |
| 001427 | STOCK Aw us/J | Cryopreserved - Ready for recovery |
| 002130 | STOCK Agpsbs2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the blind-sterile 2 mutation display nuclear cataracts, microphthalmia, smaller than normal lens with improper differentiation of lens epithelial cells to fiber cells with vacuolation, morganian globules, bladder cells and detachment of the apical-apical junctions of epithelial and fiber cells, although the lens epithelial cells appear normal at the anterior of the lens. Males have abnormally small testes with disrupted seminiferous tubules lacking mature spermatozoa or elongating spermatids. Although male homozygotes are sterile, female homozygotes are not. | ||
| 000979 | STOCK KitlSl-16J/J | Cryopreserved - Ready for recovery |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. | ||
| 001253 | STOCK MitfMi-wh +/+ Wnt7apx/J | Cryopreserved - Ready for recovery |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7apx) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet | ||
| 002404 | STOCK Mostm1Ev/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 010605 | STOCK Prkdcscid Gnrh1hpg/BmJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet | ||
| 000319 | STOCK a us/J | Cryopreserved - Ready for recovery |
| 006129 | STOCK Tg(Zp3-EGFP)1Dean/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile with no gross phenotypic abnormalities. These mice express the Zp3-EGFP fusion protein under the direction of the Zp3 promoter. As such, EGFP is readily detected throughout the width of the zona pellucida surrounding growing oocytes, with no expression in the surrounding somatic cells. Mutant mice have normal synthesis, intracellular trafficking, and secretion/incorporation into the zona pellucida matrix of the transgenic fusion protein. These mice may be useful in studies of reproductive biology, including intracellular trafficking of zona pellucida proteins to the cell surface, oocyte development, fertilization research, as well as developmental biology. | ||
| 000161 | WB.D2-KitlSl-d/J | Cryopreserved - Ready for recovery |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet | ||
| 016224 | B6.129S(Cg)-Id2tm2.1Blh/ZhuJ | Under Development - Now Accepting Orders |
| The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 017337 | B6;129S4-Mirc5tm1Jae/J | Under Development - Now Accepting Orders |
| Approximately 75% of homozygotes die before birth of unknown causes. The surviving homozygous females are sterile. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot or real-time RT-PCR analysis of homozygous knockout ES cells lines produced from mutant mice. Homozygous embryos exhibit development delays as early as embryonic day 8.5, and loss of homozygous embryos occurs E11.5 to E18.5. Approximately 16% of homozygous embryos, at E10.5 or younger, are partially or completely outside the yolk sac. Embryonic primordial germ cell migration is mislocalized. A reduced number of gonocytes/germ cells in homozygotes is detectable as early as E11.5. Homozygous adult females have smaller size ovaries when compared to wildtype littermates. Ovaries from 5 to 8 week old homozygotes have few follicles, and in ovaries from homozygous fem ..... For more information please see the full phenotype on the strain data sheet | ||
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