Search Criteria: Research Area is "Reproductive Biology Research: Fertility Defects (males only)"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name   Strain Description	Standard Supply
008042	B6;129P2-Adam2tm1Dgm/J	Repository- Live
	Mice homozygous for this fertilin b (Adam2) mutant allele are viable with no gross phenotypic abnormalities reported. Both precursor and processed fertilin b 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 b (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 ( ..... For more information please see the full descriiption on the strain data sheet
008043	B6;129P2-Adam3tm1Pmkf/J	Repository- Live
	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 b (Adam2)-deficient strain (see Stock No. 008042).
007201	B6;129S4-Plekha1Gt(ROSA)82Sor/J	Repository- Live
	25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation.
002169	BALB/cByJ-mshi/J	Repository- Live
	Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (mshi) are characterized by reduced testis size and sterility. The testes are highly disorganized and appear to have a block in the regulation of male germ cell proliferation. Reproduction is normal in homozygous mutant female mice. In addition to the male reproductive defects this mutation also affects histocompatibility in both sexes. Most homozygous mutant mice reject sex-matched skin grafts from BALB/cBy mice.
008425	C3FeLe.B6-a Trl/J	Repository- Live
	Mice heterozygous for the trembler-like mutation have an abnormal gait and tremors by approximately three weeks of age. Males are poor breeders.
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.
000804	HPG/BmJ	Repository- Live
	Mice homozygous for the hypogonadal mutation (Gnrh1hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement.
007659	129S-Atp8b3tm1Gar/J	Repository-Cryopreserved
	Both male and female homozygotes are fertile, but the average litter sizes from homozygous males are slightly smaller than observed with wildtype males. Sperm morphology and motility are unaffected, but tests show that phosphatidylserine (PS) already exists in the outer membrane leaflet before sperm capacitation. When the zona pellucida (ZP) is removed from eggs, fertilization rates are normal; although when the extracellular matrix is intact, fewer spermatozoa bind tightly or penetrate the ZP, and fewer undergo acrosome reactions. Homozygous mice do not express protein as determined by Western blot analysis of testis tissues and immunostaining of mature spermatozoa. This published information is based on studies of mixed background C57BL/6 and 129S6 background animals; the line offered here is on a pure 129S6 background. This strain may be useful in studies of male fertility.
006820	129S-Catsper3tm1Clph/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility.
006821	129S-Catsper4tm1Clph/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility.
004511	129S-Tnp1tm1Mlm/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected in testicular homogenates. Levels of transition nuclear protein 2 and protamine 2 precursor are elevated. Homozygous female mice are fertile. Homozygous male mice are subfertile, approximately 60% are infertile, and display diminished sperm motility, sperm tail abnormalities and sperm chromatin abnormalities. Electron microscopy analysis of spermatids reveals both abnormal large rod-like chromatin condensation units as well as normal fine fibrillar chromatin morphology. This mutant mouse strain may be useful in studies of male infertility and/or subfertility.
004514	129S-Tnp2tm1Mzh/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis. Homozygous female mice are fertile. Homozygous male mice are subfertile, producing small litters. Sperm retention in seminiferous tubules of mutant mice is due to increased sperm tail abnormalities. Transition protein 1 and precursor and partially processed protamine 2 levels are elevated in testis tissue. Electron microscopy analysis of mutant testis tissue reveals abnormal cylindrical focal chromatin condensation morphology in spermatids and incomplete chromatin condensation with lacunae and granularity in late stage spermatids and epididymal sperm. Increased uptake of DNA intercalating dyes by mutant sperm nuclei and susceptibility of mutant sperm DNA to acid denaturation is indicative of DNA strand breakage. This mutant mouse strain may be useful in studies ..... For more information please see the full descriiption on the strain data sheet
000100	B6.C3-Zbtb16Lu/J	Repository-Cryopreserved
	Mice homozygous for the luxoid mutation exhibit preaxial polydactly or oligodactly of the hindfeet, preaxial polydactly of the forefeet, tail kinks, tibial hemimelia and occasionally radial hemimelia. Heterozygotes exhibit preaxial polydactly or hyperphalangy of the hindfeet. An increased number of vertebra, ribs and sternebrae are found in homozygotes and to a lesser extent in heterozygotes (Forsthoefel, 1958). Male mice are infertile with a complete lack of spermatogonia after six weeks (Johnson et al., 1971). By eight months, many seminiferous tubules are agametic, lacking one or more germ cell generations (Buaas et al., 2004). Histological and FACS analysis demonstrate that luxoid homozygotes have progressive germ-cell loss starting as early as eight days (Buaas et al., 2004). This mutant mouse strain may be useful in studies related to male infertility or contraception, limb or skeletal abnormalities, and stem cell research.
000567	B6.Cg-T2J +/+ Qkqk/J	Repository-Cryopreserved
	Mice homozygous for the quaking spontaneous mutation (Qkqk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T2J) is maintained in repulsion with the quaking mutation.
002784	B6;129-Dhhtm1Amc/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are sterile due to arrested spermatogenesis at the late meiosis, primary spermatocyte stage. Female homozygotes are fertile. No gene product (mRNA) was detectable by semiquantitative RT-PCR analysis of peripheral nerve. Embryonic testis development is impaired. By six weeks of age, the mass of testes from homozygous males is 90% smaller than testes from heterozygous males. Histological examination reveals a diminished number of germ cells and no mature sperm in the testis or epididymis. Peripheral nerves from mutant mice appear flattened with structurally disorganized protective sheaths. The perineural cells, glia and mesenchymal cells, develop defective tight junctions, causing the perineurium to be permeable. This mutant mouse strain may be useful in studies related to male sterility and regulation of peripheral nerve de ..... For more information please see the full descriiption on the strain data sheet
004153	B6;129S-Mtap7Gt(ROSABetageo)1Sor/J	Repository-Cryopreserved
	At birth, mice homozygous for the gene-trapped Mtap7 allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although trace amounts of a presumably nonfunctional transcript can be detected in testis tissue, no protein product is immunodetectable. Male homozygotes are sterile. Expression of the reporter gene (B-galactosidase from the Bgeo fusion gene) employed by the gene trap vector indicates that the Mtap7 promoter directs expression in various tissues with highest levels seen in the seminiferous tubules. During the first wave of spermatogenesis at 5 weeks of age, deformed spermatids can be observed. Abnormalities are attributed to aberrant microtubule organization. Microtubule aberrations are also observed in Sertoli cells. Gradual loss of germ cells occurs. At three months of age, the testes of homozygous mutants are less than one-third the size of those of heterozygous littermates.
007656	B6;129S6-Catsper2tm1Gar/J	Repository-Cryopreserved
	Homozygotes are viable. Males, but not females, are completely infertile. The targeted mutation fails to significantly alter sperm production, protein tyrosine phosphorylation associated with capacitation, induction of the acrosome reaction, forward velocity or percentage of motility. Sperm cells fail to acquire hyperactivated motility associated with penetration of the extracellular matrix of the egg. SDS/PAGE and immunoblotting of total sperm protein were used to confirm the absence of gene product. This strain may be useful in studies of male fertility.
000221	B6C3Fe a/a-Alx4lst-J/J	Repository-Cryopreserved
002875	B6C3Fe a/a-Hoxd13spdh/J	Repository-Cryopreserved
	The spdh/spdh mutants have a normal body size but exhibit shortened, fused, and duplicated digits in both front and rear feet. Ossification is severely delayed and ossification centers are mis-patterned in developing metacarpal, metatarsal and phalangeal bones. Joint formation is severely disrupted in the phalanges, with forelimbs more affected compared to the hindlimbs. Reduced rates of proliferation and differentiation of mutant chondrocytes contribute to altered cartiledge/bone morphology. Although expression patterns of Hoxd13/11/12 and Hoxa13 do not seem to be disrupted, their function does seem to be disrupted, indicating HOX protein interactions are altered as a result of the spdh mutation. Additionally, the spdh mutant phenotype is much more severe than mutants carrying a targeted disruption of the spdh gene, supporting a dominant-negative effect. The preputial glands of the genital tract are absent in both male and female spdh ..... For more information please see the full descriiption on the strain data sheet
000506	B6C3Fe a/a-Qkqk/J	Repository-Cryopreserved
	Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS.
000248	B6C3Fe a/a-Xpl/J	Repository-Cryopreserved
005898	BKS(Cg)-trls/J	Repository-Cryopreserved
000638	C3FeB6 A/Aw-J-Spnb4qv-J/J	Repository-Cryopreserved
	Mice homozygous for the quivering-Jackson spontaneous mutation (Spnb4qv-J) are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males. Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal. The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that the deafness, unlike that of any other deaf mutants in the mouse, is of central origin. Viability of homozygous mutant mice at weaning is normal, but the life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their young.
002333	C3H/HeSnJ-gri/J	Repository-Cryopreserved
	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.)
001028	C57BL/6J-Spnb4qv-3J/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
000708	C57BL/6J-Utp14bjsd/J	Repository-Cryopreserved
004064	FVB/N-Morc1Tg(Tyr)1Az/J	Repository-Cryopreserved
	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.
003119	STOCK Sp4tm1Ssp/J	Repository-Cryopreserved

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Strains from the Research Colonies of Jackson Laboratory Scientists

IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.

Stock Number	Strain Name   Strain Description	Standard Supply
002038	CB17;HPG-Prkdcscid Gnrh1hpg/Bm	Research Strain
	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 description on the strain data sheet

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New Strains Under Development

(See informational text following listing of strains)

How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.

	Stock Number	Strain Name   Strain Description	Standard Supply
	007915	129S.FVB-Tg(Amh-cre)8815Reb/J	Under Development for Production
	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.
	008370	B6.129S-Cstf2ttm1Ccma/J	Under Development for Production
	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.
	008596	B6.Cg-Tg(Prnp-Abca1)EHol/J	Under Development for Production
	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 ..... For more information please see the full description on the strain data sheet
	008220	B6;129S7-Zpbp2tm1Zuk/J	Under Development for Production
	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.
	008219	B6;129S7-Zpbptm1Zuk/J	Under Development for Production
	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.
	008208	FVB/N-Tg(Stra8-cre)1Reb/J	Under Development for Production
	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.

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New Strains Under Development

• Receive periodic updates on the status of the colony UNDER DEVELOPMENT
• Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
• Provide input affecting speed and quantity of availability

The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.

1. Strains that will be made available from a live distribution colony at The Jackson Laboratory.
   These strains are designated as: "Under Development for Distribution Colony"
2. Strains that will be made available through the Cryopreservation Repository.
   These strains are designated as: "Under Development for Cryopreservation Repository"

It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

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