Search Criteria: Research Area is "Reproductive Biology Research: Fertility Defects: males only"
New Strains Awaiting Transfer from the Donor
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 014607 | B6.129-Mkkstm1Vcs/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exon 3 of the McKusick-Kaufman syndrome protein (Mkks or Bbs6) gene, abolishing gene function. Homozygous females are viable and fertile, while homozygous males are infertile due to lack of flagellated sperm. These mice are also smaller at birth than littermates. Mutations in Mkks have been known to cause McKusick-Kaufman syndrome (MKS) and Bardet-Biedl syndrome (BBS). MKS is a disorder characterized by post-axial polydactyly, congenital heart defects and hydrometrocolpos, while BBS is a pleiotropic disorder characterized by retinal and photoreceptor degeneration, obesity, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. Mkks-/- mice lack MKKS expression in brain, lung, heart, kidney, eye, liver, spleen, testes, and muscle. They develop age-related blindness due to retinal degeneration, are obese, and have elevated blood pressure. These mice may be useful for ..... For more information please see the full phenotype on the strain data sheet | ||
| 013584 | B6.129P2-Hspa2tm1Dix/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are infertile, homozygous female mice are fertile. No gene product (mRNA) is detected by Northern blot analysis of testis tissue from homozygous male animals. Immunohistochemical examination of seminiferous tubules does not detect protein gene product. Homozygous males have testes that weigh significantly less than testes from controls. Spermatogenesis in homozygotes is arrested in prophase of meiosis I with a reduced number of postmeitotic spermatids in seminiferous tubules, many with abnormal morphology, and no spermatozoa in the epididymis. Apoptosis of germ cells (late pachytene spermatocytes) in the testes is greatly increased in mutants. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background. | ||
| 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, ..... | ||
| 010823 | B6.Cg-Cntnap1shm-5J/GrsrJ | Repository- Live |
| By three weeks of age homozygotes have a wobbly gait and splay their rear legs when they walk. They have a reduced body size compared with littermate controls and when picked up by the tail they have an overall body tremor. Although they survive to adulthood and females are fertile and will rear their young, male homozygotes are usually sterile. | ||
| 008596 | B6.Cg-Tg(Prnp-Abca1)EHol/J | Repository- Live |
| These transgenic mice express the mouse Abca1 (ATP-binding cassette, sub-family A (ABC1), member 1) gene under the control of the mouse Prnp (prion protein) promoter. These founder line E mice have a 6-fold increase in expression of ABCA1 in the cortex over wild-type levels. Trangene expression is high in total brain tissue, kidney, testis and muscle as detected by Western blot analysis. Transgenic mice exhibit reduced apoE levels: 40% of wild-type levels in the hippocampus, approximately half of wild-type levels in cerebrospinal fluid (CSF). The apoE protein that is overexpressed has altered biochemical properties and is not as soluble as that found in controls. Lipoprotein particles from the CSF that contain apoE protein are larger in size than wild-type, indicating that the transgenic apoE particles are more lipidated.
Male transgenic mice have atropied testes, defective spermatogenesis and are infertile. The strain can be maintained by mating hemizygous femal ..... | ||
| 008219 | B6;129S7-Zpbptm1Zuk/J | Repository- Live |
| Female mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous males are infertile due to severe abnormal spermatozoa morphology and diminished sperm motility. Heterozygous males exhibit terato-asthenozoospermia (increase in the percentage of abnormal sperm) and globozoospermia, but are fertile with normal fecundity. Electron microscopic examination of sperm reveals ultrastructural abnormalties. No gene product (mRNA or protein) is detected by Northern or Western blot analysis or testicular tissue and sperm. This mutant mouse strain may be useful in studies of acrosomal biogenesis and spermiogenesis. | ||
| 012711 | B6;129X1-Dkkl1tm1.1Mldp/J | Repository- Live |
| In this strain, exons 2-4 of the endogenous mouse Dickkopf-Like 1 (Dkkl1) gene are removed, abolishing gene function. Homozygous mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. While homozygous females have no fertility problems, homozygous males have reduced fertilization efficiency. In these mice, DKKL1 expression was absent in developing trophectoderm and spermatocytes, and in the acrosome of mature sperm. This absence of expression did not result in infertility as it is not required for development of sperm or fertility in vivo. These mice may be useful for studying spermatogenesis and fertility. | ||
| 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. | ||
| 016093 | C.129S4(B6)-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Repository- Live |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent dur ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 014179 | STOCK Mov10l1tm1.1Eno/J | Repository- Live |
| These mice possess loxP sites on either side of exon 20, which encodes a helicase domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 20 deleted in the cre-expressing tissue(s).
When bred to a strain with widespread expression of Cre recombinase, this mutant mouse strain may be useful in studies of retrotransposon activiation in male germ cells. Global homozygous deletion results in male infertility due to apoptosis of pachytene spermatocytes. | ||
| 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. | ||
| 016224 | B6.129S(Cg)-Id2tm2.1Blh/ZhuJ | Under Development - Now Accepting Orders |
| The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 016092 | B6.129S4-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Under Development - Now Accepting Orders |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression is restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent ..... For more information please see the full phenotype on the strain data sheet | ||
| 017616 | B6;129X1-Slc19a2tm1Gelb/SaidJ | Under Development - Now Accepting Orders |
| In this strain, a neo cassette is inserted into exon 2 of the solute carrier family 19 (thiamine transporter), member 2 (Slc19a2) gene, abolishing gene function. Slc19a2 encodes the high-affinity thiamin carrier expressed on epithelial cells of kidney, small intestine and liver. Thiamin, also known as Vitamin B1, is involved in carbohydrate metabolism, and nervous system and muscle function. Homozygous females are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities, when maintained on a standard chow diet. Homozygous males mice are infertile when fed a normal chow diet, with fertility being restored after 20 days on a high thiamin diet. After 17 days on a thiamine deficient diet these mice are glucose intolerant and they exhibit impaired insulin secretion. After 6 weeks on a normal diet (including thiamin) glucose tolerance is restored. On a thiamin deficient diet these mice also exhibit hearing loss, which is reversib ..... For more information please see the full phenotype on the strain data sheet | ||
| 007659 | 129S-Atp8b3tm1Gar/J | Cryopreserved - Ready for recovery |
| Both male and female homozygotes are fertile, but the average litter sizes from homozygous males are slightly smaller than observed with wildtype males. Sperm morphology and motility are unaffected, but tests show that phosphatidylserine (PS) already exists in the outer membrane leaflet before sperm capacitation. When the zona pellucida (ZP) is removed from eggs, fertilization rates are normal; although when the extracellular matrix is intact, fewer spermatozoa bind tightly or penetrate the ZP, and fewer undergo acrosome reactions. Homozygous mice do not express protein as determined by Western blot analysis of testis tissues and immunostaining of mature spermatozoa. This published information is based on studies of mixed background C57BL/6 and 129S6 background animals; the line offered here is on a pure 129S6 background. This strain may be useful in studies of male fertility. | ||
| 006820 | 129S-Catsper3tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 006821 | 129S-Catsper4tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 004511 | 129S-Tnp1tm1Mlm/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected in testicular homogenates. Levels of transition nuclear protein 2 and protamine 2 precursor are elevated. Homozygous female mice are fertile. Homozygous male mice are subfertile, approximately 60% are infertile, and display diminished sperm motility, sperm tail abnormalities and sperm chromatin abnormalities. Electron microscopy analysis of spermatids reveals both abnormal large rod-like chromatin condensation units as well as normal fine fibrillar chromatin morphology. This mutant mouse strain may be useful in studies of male infertility and/or subfertility. | ||
| 004514 | 129S-Tnp2tm1Mzh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis. Homozygous female mice are fertile. Homozygous male mice are subfertile, producing small litters. Sperm retention in seminiferous tubules of mutant mice is due to increased sperm tail abnormalities. Transition protein 1 and precursor and partially processed protamine 2 levels are elevated in testis tissue. Electron microscopy analysis of mutant testis tissue reveals abnormal cylindrical focal chromatin condensation morphology in spermatids and incomplete chromatin condensation with lacunae and granularity in late stage spermatids and epididymal sperm. Increased uptake of DNA intercalating dyes by mutant sperm nuclei and susceptibility of mutant sperm DNA to acid denaturation is indicative of DNA strand breakage. This mutant mouse strain may be useful in studies ..... For more information please see the full phenotype on the strain data sheet | ||
| 010750 | 129S.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts). Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010751 | 129S.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. | ||
| 010752 | 129S.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. | ||
| 010726 | B6.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts. Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010727 | B6.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. This strain may be useful as a model for Bardet-Biedl syndrome. | ||
| 010728 | B6.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. This strain may be useful as a model for some features of Bardet-Biedl syndrome. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 010945 | B6.129S2-Pms2tm1Lisk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, but show an increased incidence of sarcomas and lymphomas. Sperm, tail and tumor cells from homozygous mice exhibit microsatellite instability. Male mice on the mixed C57BL/6 and 129S2 background are infertile with reduced numbers of spermatozoa. Spermatozoa exhibit misshapen heads, truncated, irregular flagella. This strain may be useful in the studies of spermatogenesis, cancer and DNA mismatch repair. | ||
| 009680 | B6.B-Vps54wr/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this spontaneous mutation on the C57BL/6 background are viable, but infertile and die prematurely. The average lifespan is 3 months, although this can be increased if littermates are present in the cage, the Donating Investigator reports. Homozygotes exhibit progressive locomotor impairment with corresponding motor neuron and muscular degeneration. Homozygous males have defective spermiogenesis and are sterile. Homozygotes of both sexes have reduced serum estrogen. Mitochondria in motor neurons are abnormal. This mutant mouse strain may be useful in studies of Spinal Muscular Atrophy, Distal Hereditary Motor Neuronopathy and Amyotrophic Lateral Sclerosis 1. | ||
| 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. | ||
| 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. | ||
| 007733 | B6;129-4930579C15Riktm1Gar/J | Cryopreserved - Ready for recovery |
| Female mice that are homozygous for the targeted mutation are healthy and fully fertile. Male homozygous mice do not display any gross physical or behavioral abnormalities, however they are subfertile. No RNA message is detected by Northern blot analysis of testis tissue from homozygotes. The mechanism for sub-fertility is unknown. This mutant strain may be useful in the study of sperm biology. | ||
| 002784 | B6;129-Dhhtm1Amc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are sterile due to arrested spermatogenesis at the late meiosis, primary spermatocyte stage. Female homozygotes are fertile. No gene product (mRNA) was detectable by semiquantitative RT-PCR analysis of peripheral nerve. Embryonic testis development is impaired. By six weeks of age, the mass of testes from homozygous males is 90% smaller than testes from heterozygous males. Histological examination reveals a diminished number of germ cells and no mature sperm in the testis or epididymis. Peripheral nerves from mutant mice appear flattened with structurally disorganized protective sheaths. The perineural cells, glia and mesenchymal cells, develop defective tight junctions, causing the perineurium to be permeable. This mutant mouse strain may be useful in studies related to male sterility and regulation of peripheral nerve de ..... For more information please see the full phenotype on the strain data sheet | ||
| 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). | ||
| 008370 | B6;129S-Cstf2ttm1Ccma/J | Cryopreserved - Ready for recovery |
| Male mice that are homozygous for this targeted mutation are infertile due to defective spermatogenesis, similar to oligoasthenoteratozoospermia. Homozygous females are fertile. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of testes tissue. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Lesions in developing sperm appear in stage-XII secondary spermatocytes and progressively worsen with spermatogenesis. Epididymal spermatozoa exhibit variable morphology. This mutant mouse strain may be useful in studies of polyadenylation and translational regulation of protein synthesis during gametogenesis. | ||
| 004153 | B6;129S-Mtap7Gt(ROSABetageo)1Sor/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous for the gene-trapped Mtap7 allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although trace amounts of a presumably nonfunctional transcript can be detected in testis tissue, no protein product is immunodetectable. Male homozygotes are sterile. Expression of the reporter gene (B-galactosidase from the Bgeo fusion gene) employed by the gene trap vector indicates that the Mtap7 promoter directs expression in various tissues with highest levels seen in the seminiferous tubules. During the first wave of spermatogenesis at 5 weeks of age, deformed spermatids can be observed. Abnormalities are attributed to aberrant microtubule organization. Microtubule aberrations are also observed in Sertoli cells. Gradual loss of germ cells occurs. At three months of age, the testes of homozygous mutants are less than one-third the size of those of heterozygous littermates. | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Cryopreserved - Ready for recovery |
| 25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007656 | B6;129S6-Catsper2tm1Gar/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable. Males, but not females, are completely infertile. The targeted mutation fails to significantly alter sperm production, protein tyrosine phosphorylation associated with capacitation, induction of the acrosome reaction, forward velocity or percentage of motility. Sperm cells fail to acquire hyperactivated motility associated with penetration of the extracellular matrix of the egg. SDS/PAGE and immunoblotting of total sperm protein were used to confirm the absence of gene product. This strain may be useful in studies of male fertility. | ||
| 007661 | B6;129S6-Slc9a10tm1Gar/J | Cryopreserved - Ready for recovery |
| Homozygous females are fully fertile, but males are completely infertile and have severely diminished sperm motility. Body weight, testis size, and caudal epididymal sperm counts of null male mice are no different from those of wildtype or heterozygous littermates. No apparent defects in spermatogenesis were found. The addition of ammonium chloride, which elevates intracellular pH, partially rescues the motility and fertility defects. Cyclic AMP analogues almost completely rescue the motility and infertility phenotypes. Northern blot analysis confirmed the absence of full-length mRNA in homozygous mutants, but a truncated product was found. No stable protein was detected in null mice by immunohistochemistry or western blot analysis. This strain may be useful in studies of male fertility and the molecular basis of fertilization. | ||
| 008220 | B6;129S7-Zpbp2tm1Zuk/J | Cryopreserved - Ready for recovery |
| Female mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous males are subfertile with approximately 20% reduction in average litter size. Heterozygous males have normal fertility and fecundity. Homozygous males have slightly abnormal sperm morphology. Although sperm from homozygotes bind to oocyte zona pellucida normally, the slower in vitro fertilization rate indicates reduced zona pellucida penetration. No gene product (mRNA or protein) is detected by Northern or Western blot analysis or testicular tissue and sperm. This mutant mouse strain may be useful in studies of spermiogenesis and sperm-egg interaction. | ||
| 000506 | B6C3Fe a/a-Qkqk-v/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. | ||
| 000221 | B6C3Fe a/a-Alx4lst-J/J | Cryopreserved - Ready for recovery |
| 002875 | B6C3Fe a/a-Hoxd13spdh/J | Cryopreserved - Ready for recovery |
| The spdh/spdh mutants have a normal body size but exhibit shortened, fused, and duplicated digits in both front and rear feet. Ossification is severely delayed and ossification centers are mis-patterned in developing metacarpal, metatarsal and phalangeal bones. Joint formation is severely disrupted in the phalanges, with forelimbs more affected compared to the hindlimbs. Reduced rates of proliferation and differentiation of mutant chondrocytes contribute to altered cartiledge/bone morphology. Although expression patterns of Hoxd13/11/12 and Hoxa13 do not seem to be disrupted, their function does seem to be disrupted, indicating HOX protein interactions are altered as a result of the spdh mutation. Additionally, the spdh mutant phenotype is much more severe than mutants carrying a targeted disruption of the spdh gene, supporting a dominant-negative effect. The preputial glands of the genital tract are absent in both male and female spdh ..... For more information please see the full phenotype on the strain data sheet | ||
| 000248 | B6C3Fe a/a-Xpl/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 000638 | C3FeB6 A/Aw-J-Spnb4qv-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering-Jackson spontaneous mutation (Spnb4qv-J) are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their young. | ||
| 002333 | C3H/HeSnJ-gri/J | Cryopreserved - Ready for recovery |
| On an agouti background gri homozygotes resemble Tyrc-ch homozygotes. There is a graying of the coat due to a lighter than normal phaeomelanin band. There is no change in eye color. gri homozygotes are slightly smaller than their unaffected littermates. Homozygous females breed well, but homozygous males often do not breed. Testis biopsies failed to identify any sperm abnormalities. The gri mutation does not cause a clotting disorder. (Davisson et al., 2000.) | ||
| 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 | ||
| 001028 | C57BL/6J-Spnb4qv-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the quivering 3 Jackson spontaneous mutation (Spnb4qv-3J) are very similar to mice homozygous for the quivering-Jackson mutation (Spnb4qv-J). Homozygous quivering mutant mice are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are st ..... For more information please see the full phenotype on the strain data sheet | ||
| 000708 | C57BL/6J-Utp14bjsd/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 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. | ||
| 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. | ||
| 010605 | STOCK Prkdcscid Gnrh1hpg/BmJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet | ||
| 003119 | STOCK Sp4tm1Ssp/J | Cryopreserved - Ready for recovery |
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