Search Criteria: Research Area is "Reproductive Biology Research: Endocrine Deficiencies Affecting Gonads"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002468 | KK.Cg-Ay/J | Level 3 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and ..... For more information please see the full phenotype on the strain data sheet | ||
| 004745 | B6.129P2-Esr2tm1Unc/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical abnormalities. Stop codons inserted into exon 3 result in the production of truncated transcripts that are unlikely to be translated into a functional protein. Immunostaining of ovary tissue derived from homozygous females fails to detect protein product. Homozygous females are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation (6 compared to 33.7 in wildtype controls). Male homozygotes are fertile and present no marked abnormalities other than epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system. | ||
| 008519 | B6.129S4-Nos1tm2Plh/J | Repository- Live |
| In this targeted mutation exon 6, which encodes the heme-binding domain, is deleted. Mice that are homozygous for the targeted mutation are viable only when maintained on a liquid diet and are not fertile. Some truncated gene product (mRNA) containing exon 2 but completely lacking exon 6 is detected by RR-PCR of brain. Nitric oxide synthase activity is only 0.3% of wildtype levels in the brain. Homozygotes have smaller total body and gonad weight and develop pyloric stenosis. Female homozygotes have fewer ovarian corpora lutea and increased hypothalmic gonadotropin-releasing hormone and circulating luteinizing hormone. Homozygous males have decreased follicle stimulating hormone levels and do not display mating behavior. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of hypothalamo-pituitary axis and neuroendocrine regulation of ..... For more information please see the full phenotype on the strain data sheet | ||
| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of ..... For more information please see the full phenotype on the strain data sheet | ||
| 009358 | B6;129S2-Lats1tm1Tx/J | Repository- Live |
| Homozygous animals exhibit a lack of mammary gland development, infertility and growth retardation. Accompanying these defects are hyperplastic changes in the pituitary and decreased serum hormone levels. The reproductive hormone defects of homozygotes are reminiscent of isolated luteinizing hormone (LH)-hypogonadotropic hypogonadism and corpus luteum insufficiency in humans. Furthermore, Homozygous mice develop soft tissue sarcomas (some by 4-10 months of age) and ovarian stromal cell tumors (by 3 months of age) and are highly sensitive to carcinogenic treatments. Data demonstrates a role for this gene in mammalian tumorigenesis and specific endocrine dysfunction. | ||
| 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 | ||
| 000355 | CXB5/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 008104 | B6.129(FVB)-Ptgs2tm2.1(Ptgs1)Fun/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. Female homozygotes have a longer period between successive pregnancies and reduced litter sizes. Ptgs1 gene product (protein), COX1, is increased approximately 5 fold in LPS-stimulated macrophages from homozygotes. Prostacyclin metabolite level in urine is reduced by 55% when compared to wildtype controls. No increase in prostaglandin-glycerol in mutant macrophages after LPS challenge is observed. Homozygotes exhibit reduced bradykinin-induced vasculature permeability and at 6 months of age have enlarged glomeruli due to increased inflammatory infiltrate. By 5 months of age, mutant mice develop chronic peritonitis and progressive renal cortex deterioration. This mutant mouse strain may be useful in studies of prostaglandin synthesis and inflammation. | ||
| 003142 | B6.129P2-Prlrtm1Cnp/J | Cryopreserved - Ready for recovery |
| There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants. | ||
| 009640 | B6.129S4-Viptm1Clw/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by immunohistochemical analysis of homozygotes. Homozygous females are subfertile, 15-20% of homozygous females can have litters. Homozygotes exhibit impaired circadian rhythm generation, muscle weakness, increased motor activity and increased induced airway hyperresponsiveness and inflammation. In constant darkness, homozygotes initially display shortened circadian period. Some homozygotes develop arrhythmic circadian periods after extended darkness. Heterozygotes also display abnormal circadian rhythm. Homozygotes have both gross and microscopic anatomical abnormalities of the gastrointestinal tract. 10-15% of homozygotes die of stenosis of the gut before one year of age. Male homozygotes exhibit moderate right ventricular (RV) hypertension, RV hypertrophy, thickened and remodeled pulmonary arteries, perivascular inflammation of smaller pulmonary vessels and airways, red ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 006941 | B6.129S7-B4galt1tm1Shur/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. Ninety percent of homozygotes die soon after birth or within two to three weeks of birth. Surviving homozygotes are initially smaller than wild-type or heterozygotes and exhibit abnormal skin and coat, but assume a normal growth rate and appearance at three to four weeks of age. No gene product (mRNA) is detected by RT-PCR analysis of homozygous tissues. Neither the long or short isoform is expressed. Beta 1,4-galactosyltransferase enzyme activity is undetectable except for residual activity in brain and testis. Galactose residues are absent from testis. Heterozygotes have an intermediate enzyme activity level. Surviving homozygotes exhibit puffy faces (hypothyroid myxedema), thin skin, decreased density of hair follicles, reduction in subdermal adipose tissue, delayed spermatogenesis and incomplete lung development. Histological an ..... For more information please see the full phenotype on the strain data sheet | ||
| 006943 | B6.129S7-B4galt1tm2Shur/J | Cryopreserved - Ready for recovery |
| These mice carry a mutant allele that has a point mutation in the first translation initiation codon in exon 1, which initiates translation of the long isoform of beta 1,4-galactosyltransferase. The second translation initiation codon in exon 1 is not affected. These mice express only the shorter isoform of beta 1,4-galactosyltransferase. No long isoform protein is detected in mammary tissue by Western blot analysis. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Total Beta 1,4-galactosyltransferase activity is reduced to 72% of wildtype levels in mammary gland epithelial cells while activity on mammary epithelial cell surfaces is diminished by over 60%. Sperm and testis exhibit near wildtype levels of enzyme activity and glycoprotein galactosylation. The short isoform is expressed ectopically in sperm. Although able to undergo normal acrosomal exocytosis induced by calcium ionoph ..... For more information please see the full phenotype on the strain data sheet | ||
| 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). | ||
| 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 | ||
| 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. | ||
| 003277 | B6;129S7-Acvr2atm1Zuk/J | Cryopreserved - Ready for recovery |
| Activin receptor IIA deficient mice are viable. Homozygous males are fertile, while homozygous females are infertile. Follicle-stimulating hormone levels are reduced in mutant mice. Some skeletal and facial abnormalities, including micrognathia, cleft palate and defects in Meckel's cartilage are observed. These defects are reminiscent of Pierre-Robin syndrome in humans. Severe defects occasionally result in the perinatal or in utero death of a small number of homozygous mutant embryos. | ||
| 002187 | B6;129S7-Amhtm1Bhr/J | Cryopreserved - Ready for recovery |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. | ||
| 003283 | B6;129S7-Fshbtm1Zuk/J | Cryopreserved - Ready for recovery |
| Males carrying the targeted mutation are fertile, have small testes, reduced sperm number and sperm motility. Homozygous mutant females are infertile due to a preantral stage block in ovarian folliculogenesis. Heterozygotes are fertile. | ||
| 002788 | B6;129S7-Fsttm1Zuk/J | Cryopreserved - Ready for recovery |
| Homozygous mice die within hours after birth due to a failure to breathe. They are smaller in size than normal wildtype siblings and show craniofacial, musculoskeletal, and skin defects. | ||
| 010816 | B6;C-Ghrhrlit Prkdcscid/BmJ | Cryopreserved - Ready for recovery |
| B6;C-GhrhrlitPrkdcscid/BmJ mice are deficient in growth hormone and IGF1 and are useful for determining endocrine dependence of grafted cells and tissues (Beamer et al., 1993, Cancer Research, v53:3741; Friend et al., 2001 Growth Hormone & IGF Research, v11:84). | ||
| 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. | ||
| 001595 | DW/J-Acdacd/J | Cryopreserved - Ready for recovery |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic ..... For more information please see the full phenotype on the strain data sheet | ||
| 002437 | FVB/N-Tg(MMTV-Notch4)3Rnc/J | Cryopreserved - Ready for recovery |
| Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands. | ||
| 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. | ||
| 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 | ||
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