JAX Mice Database - (germ cell deficient)

Search Criteria: Research Area is "Reproductive Biology Research: Developmental Defects Affecting Gonads (germ cell deficient)"

New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
100410	WBB6F1/J-Kit^W/Kit^W-v/J	Level 2
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
000049	C57BL/6J-Kit^W-v/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
000692	WB/ReJ Kit^W/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
004744	B6.129P2-Esr1^tm1Ksk/J	Repository- Live
	At birth, mice homozygous for the targeted allele are viable and normal in size and appearence. Female mice exhibit ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. In males, below normal testis weight is associated with a diminished sperm count (10% of normal). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished.
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet
004847	B6;129-Gt(ROSA)26Sor^{tm1(cre/Esr1)Nat}/J	Repository- Live
	These R26CreER mutant mice have a tamoxifen-inducible Cre-mediated recombination system driven by the endogenous mouse Gt(ROSA)26Sor promoter. The mutant allele consists of a fusion product involving Cre recombinase and an altered version of the mouse estrogen receptor ligand binding domain. The mutant ligand binding domain does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the CRE/ESR1 protein can only gain access to the nuclear compartment to mediate recombination after exposure to tamoxifen. Tamoxifen administration will also induce Cre recombination in the developing embryos of treated mothers. When crossed with a strain containing a loxP site-flanked sequence of interest, this mutant is useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnor ..... For more information please see the full descriiption on the strain data sheet
007608	B6;129-Smad1^tm1Sor/J	Repository- Live
	Homozygotes for the Smad1^tm1Sor (also called Smad1C) allele have an embryonic lethal phenotype and do not survive past ED9.5. These mice carry a mutation (the C-terminal SSVS motif was changed to AAVA) in exon 7, which effects transcriptional activity. Homozygous embryos display posterior truncation, abnormal turning, allantois malformations (failure of the allantois to connect to the chorionic plate), anterior truncation of the head with only one brachial arch, and enlarged pericardium. At ED7.5 homozygous embryos do not have any detectable primordial germ cells. Western blot analysis of ED9.5 homozygotes showed that protein levels were not affected. Heterozygotes for this mutant allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of homeostasis and BMP and MAPK signaling pathways during development and in the adult.
007613	B6;129-Smad1^tm2Sor/J	Repository- Live
	Homozygotes for the Smad1^tm2Sor (also called Smad1L) allele are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice carry a mutation in exon 3, which effects MAPK-mediated phosphorylation of the protein. Western blot analysis of MEFs from homozygotes showed that similar protein levels compared to wildtype. Homozygous embryos have fewer primordial germ cells than wildtype controls. Homozygous mice display abnormal gastric mucosa cell population ratios with fewer zymogenic cells and more parietal cells. The cytoskeleton of MEFs from homozygotes exhibit a loss of adhesion zippers, decreased stress fibers, and an accumulation of actin in the cortical regions with an increase in beta-catenin immunostaining localized to the cell membranes. This mutant mouse strain may be useful in studies of stomach development, gastic mucosal homeostasis and BMP and MAPK signaling pathways during development and in the adult.
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full descriiption on the strain data sheet
100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full descriiption on the strain data sheet
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full descriiption on the strain data sheet
000599	B6 x B6CBCa A^w-J/A-T(5;13)264Ca Kit^W-v/J	Repository-Cryopreserved

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Repository-Cryopreserved
	Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous Kit^W-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease ..... For more information please see the full descriiption on the strain data sheet
000495	B6.C-H38^c/By-Kit^W-56J/J	Repository-Cryopreserved

000560	B6.C-H7^b/By Kit^W-50J/J	Repository-Cryopreserved

000122	B6.C3-Kit^W-44J/J	Repository-Cryopreserved
	Kit^W-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in Kit^W* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many Kit^W-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The Kit^W-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t ..... For more information please see the full descriiption on the strain data sheet
000991	B6.C58-Kit^W-57J/J	Repository-Cryopreserved

000133	B6.Cg-Kit^W-24J/J	Repository-Cryopreserved

000139	B6.Cg-Kit^W-25J/J	Repository-Cryopreserved

000164	B6.Cg-Kit^W/J	Repository-Cryopreserved

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
000194	B6.Cg-Lx Kit^W-v/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter. Although homozygous Kit^W-v/ ..... For more information please see the full descriiption on the strain data sheet
000171	B6.D2-Kit^W-45J/J	Repository-Cryopreserved

001563	B6.D2-Kit^W-73J/J	Repository-Cryopreserved

001177	B6.LP-Kit^W-49J/J	Repository-Cryopreserved

004153	B6;129S-Mtap7^{Gt(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.
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (Mitf^Mi-wh/+) have a dilut ..... For more information please see the full descriiption on the strain data sheet
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
004995	C3H-Tg(Camk2a-Creb1/ESR1)3Sva/J	Repository-Cryopreserved
	These transgenic mice have a tamoxifen inducible cAMP responsive element binding protein 1 (Creb1) repressor driven by the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. The transgene insert contains a fusion product involving a mutant Creb1 isoform (CREB^S133A) and a mutant form of the human estrogen receptor ligand binding domain (LBD^G521R). Expression of the transgene is detected in the hippocampus and cortex as analyzed by Northern and Western blot. In addition, transgene expression is detected in the amygdala by RT-PCR analysis. The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Tamoxifen administration activates the repressor, reducing cyclic AMP responsive element-mediated transcription. When the repressor system is activated, mutant mice exhibit impaired long term memory consolidation and retrieval in fear conditioning tra ..... For more information please see the full descriiption on the strain data sheet
000627	C3H/HeJ-Kit^W-x/J	Repository-Cryopreserved

000847	C3Sn.B6-Kit^W-39J/J	Repository-Cryopreserved

001380	C3Sn.Cg-Kitl^Sl-con/J	Repository-Cryopreserved
	Both homozygous and heterozygous mice with the contrasted induced mutation (Kitl^Sl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia.
000166	C57BL/6J-Kit^W-17J/J	Repository-Cryopreserved

000167	C57BL/6J-Kit^W-18J/J	Repository-Cryopreserved

000169	C57BL/6J-Kit^W-20J/J	Repository-Cryopreserved

000117	C57BL/6J-Kit^W-34J/J	Repository-Cryopreserved

000128	C57BL/6J-Kit^W-35J/J	Repository-Cryopreserved

000134	C57BL/6J-Kit^W-37J/J	Repository-Cryopreserved

000062	C57BL/6J-Kit^W-39J/J	Repository-Cryopreserved

000121	C57BL/6J-Kit^W-40J/J	Repository-Cryopreserved

000119	C57BL/6J-Kit^W-41J/J	Repository-Cryopreserved

000127	C57BL/6J-Kit^W-42J/J	Repository-Cryopreserved

000129	C57BL/6J-Kit^W-43J/J	Repository-Cryopreserved

000990	C57BL/6J-Kit^W-55J/J	Repository-Cryopreserved

001179	C57BL/6J-Kit^W-62J/J	Repository-Cryopreserved

003252	C57BL/6J-Kitl^Sl-20J/J	Repository-Cryopreserved
	Kitl^Sl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile.
000965	CBACa.C3-Kit^W-x/J	Repository-Cryopreserved

000092	FL/1Re-Kit^W/J	Repository-Cryopreserved

004064	FVB/N-Morc1^Tg(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.
000993	NZB/BlNJ-Kit^W-59J/J	Repository-Cryopreserved

000979	STOCK Kitl^Sl-16J/J	Repository-Cryopreserved
	The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two Mgf^Sl mutants (e.g. Mgf^Sl/Mgf^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable Mgf^Sl/ Mgf^Sl homozygotes and deficient in the Mgf^Sl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.
000161	WB.D2-Kitl^Sl-d/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet

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New Strains Under Development

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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.
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Stock Number	Strain Name Strain Description	Standard Supply
008608	B6.Cg-Dmc1^tm1Jcs/JcsJ	Under Development for Production
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).
008656	B6.Cg-Kitl^Sl-gb/MbeJ	Under Development for Production
The 120 Kb deletion in the spontaneous mutation, grizzle belly, represents the smallest complete deletion among the Kit ligand (Steel) alleles. Mice homozygous for the mutation die just before or after birth. Mice that survive to postnatal day 1 display a substantial decrease in peripheral red blood cells (RBC) and a severe anemia. Heterozygotes exhibit a mild anemia, and some decrease in peripheral RBC. In the homozygous embryo there is an absence of primordial germ cells (PGCs) by E11.5; an intermediate number of PGCs are found in the heterozygote. Like the other mutations at the Steel locus, this allele causes abnormal pigmentation. Heterozygotes can be identified by a head spot and light belly. This strain may be useful for research in hematopoiesis, pigmentation and gametogenesis.

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New Strains Under Development
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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.
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JAX® Mice Strains

New Strains Under Development

JAX^® Mice Strains