JAX Mice Database - Dermatology Research

Search Criteria: Research Area is "Dermatology Research"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000058	B6(Cg)-Tyr^c-2J/J	Level 2
	Mice homozygous for Tyr^c-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyr^c-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004).
000642	BKS.Cg-Dock7^m +/+ Lepr^db/J	Level 2
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Lepr^db homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol ..... For more information please see the full phenotype on the strain data sheet
000670	DBA/1J	Level 2
	DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). There is high incidence of calcified lesions of the tongue with age. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975).
000671	DBA/2J	Level 2
	DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between three to four weeks of age) and becoming severe by two to three months of age. The age related hearing loss 8 mutation arose spontaneously in DBA/2J between 1951 and 1975. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroven ..... For more information please see the full phenotype on the strain data sheet
002468	KK.Cg-A^y/J	Level 3
	A^y 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 A^y 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 (A^y) die before implantation, or shortly thereafter. The time of death and ..... For more information please see the full phenotype on the strain data sheet
002019	NU/J	Level 3
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d ..... For more information please see the full phenotype on the strain data sheet
000819	B6.Cg-Foxn1^nu/J	Level 4
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when ..... For more information please see the full phenotype on the strain data sheet
002282	BTBR T⁺ tf/J	Level 4
	BTBR mice exhibit a 100% absence of the corpus callosum and a severly reduced hippocampal commissure (Wahlsten D, 2003 Brain Res). This strain exhibits several symptoms of autism including: reduced social interactions, impaired play, low exploratory behavior, unusual vocalizations and high anxiety as compared to other inbred strains (McFarlane HG, 2008, Gen, Brain Behav; Moy SS, 2007, Behav Br Res, Scattoni ML, 2008, PLos).
000051	C57BL/6J-A^w-J/J	Level 4
	Mice are agouti (hairs are black with a subapical yellow band) with a cream or white belly. Females may be used as foster mothers for ovary transplantation of mutations maintained in a/a strains because A^w-J is dominant to the nonagouti a. Since a to A^w is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin.
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.
000668	C57L/J	Level 4
	C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE) and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um² atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences.
007850	J:NU	Level 4
	Outbred homozygous nude (Foxn1^nu/Foxn1^nu) mice are the standard in vivo model for drug efficacy testing in oncology. Nude mice are athymic and hairless as a result of the recessive nu mutation. T cell precursors exist but development is blocked in the absence of a thymus, resulting in an immunodeficiency that permits transplantation of tumor cell xenografts. Homozygous females are poor breeders and fail to lactate. Heterozygous males and females breed well and have normal immune function. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers.
000676	LP/J	Level 4
	LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrb^s). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced.
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.
100410	WBB6F1/J-Kit^W/Kit^W-v	Level 4
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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.
014103	129;FVB-Tmem79^m1J/GrsrJ	Repository- Live
	Homozygotes can be identified by 7 to 8 days of age. They have a slightly shiny, off-white coat color with sparse hair, and some adults develop an irritation around the eyes. The zigzag hairs are abnormal, having extra kinks.
006859	129X1/SvJ-Lamc2^jeb/DcrJ	Repository- Live
	Mice that are heterozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis of skin from homozygotes detects the wildtype and a dominant larger sized mutant gene product (mRNA). Homozygotes express a reduced level of gene product (protein), as detected by Western blot analysis of keratinocytes. Mean onset of progressive skin blistering disease in homozygotes on the 129X1 background is age 154 days. Homozygotes exhibit ulcerated lesions and tissue granulation in ear skin, which develops into deformed pinna; ulcerated lesions in the footpads and tail. Thickened epidermis (hyperplasia) and subepidermal separation, with little to no inflammation, occurs in the skin of the footpads and tail. Ultrastructural analysis of skin with electron microscopy reveals that the dermal-epidermal separation occurs at the lamina lucida.
002655	Mus pahari/EiJ	Repository- Live

001934	B6(D2)-Lmna^Dhe/TyGrsrJ	Repository- Live
	Heterozygotes are slightly smaller than normal and develop a sparse, graying, scruffy coat. They have short ear pinnae, an underdeveloped lower jaw, malocclusion, protruding eyes, and low bone mineral density. The skulls are small and disproportionate, and the cranial sutures fail to close. Females can have decreased fertility, but males do not. Males have diminished total body fat. Homozygotes die by approximately 10 days of age, have dysplastic, ulcerated skin and oral mucosae, and a more severe deficiency in skull growth and mineralization.
001809	B6-A^w-J.Cg-Eda^Ta-6J +/+ Ar^Tfm/J	Repository- Live
	Testicular feminization (Ar^Tfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (Eda^Ta-6J) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
013787	B6.129S1-Abcc6^tm1Jfk/J	Repository- Live
	Mice that are homozygous for this targeted mutation develop patchy, progressive mineralization of the dermis, kidneys, eyes, arteries, heart and subcutaneous tissues, mimicking the human disease symptoms of pseudoxanthoma elasticum. Mineralization of connective tissue capsule surrounding vibrissae is detectable at 5 weeks of age. Mineralization is associated with collagen fibrils and elastic fibers. Oxidative stress, as indicated by lipid peroxidation and protein oxidation, is higher in liver tissue and serum of mutant mice when compared to wildtype controls. Antioxidant diet reduces the oxidative stress levels in knock out mice, but does not prevent ectopic mineralization. The severity of mineralization can be altered by mineral intake as a diet with elevated magnesium levels prevents pathological connective tissue mineralization in mutants. Serum matrix gla protein (MGP) levels are reduced in homozygotes and the protein is under-carboxylated with diminished activity. Fetuin-A ..... For more information please see the full phenotype on the strain data sheet
006133	B6.129S4-Vdr^tm1Mbd/J	Repository- Live
	Heterozygous mice are phenotypically indistinguishable from wildtype siblings. As originally characterized on a mixed B6;129 genetic background, homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire bod ..... For more information please see the full phenotype on the strain data sheet
012564	B6.129S5-Dhcr24^tm1Fein/SbpaJ	Repository- Live
	Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized. <> ..... For more information please see the full phenotype on the strain data sheet
002128	B6.129S7-Itgb2^tm1Bay/J	Repository- Live
	Mice homozygous for the Itgb2^tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2^tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency.
015813	B6.129S7-Kit^tm1Rosay/J	Repository- Live
	Mice that are heterozygous for this alelle are viable, normal in size and do not display any gross behavioral abnormalities. Heterozygotes exhibit white patches at the end of the tail, the belly and paws. Homozygotes exhibit an embryonic lethal phenotype. Mutant allele expression levels (mRNA) are similar to endogenous Kit expression in multiple tissues as detected by qPCR analysis (brain, heart, liver, lung, kidney, stomach, small intestine, colon). High expression levels are detected in lung. copGFP fluorescence is detected in KIT immuno-positive gastrointestinal interstitial cells of Cajal (ICC) by immunohistochemical and flow cytometric analysis. When crossed with mice homozygous for the Lep^ob allele (see Stock No. 000632), loss in the intramuscular and myenteric populations of ICC in the intestine and colon can be visualized with confocal microscopy.
003568	B6.129S7-Trp63^tm2Brd/J	Repository- Live
	Mills 1999 Nature 398:708 describes the homozygous phenotype on a mixed B6-Tyr^c-Brd;129S7(129S5) background. Further, they not distinguish between the two targeted alleles (pTV6H(90)-generated p63^Brdm1 [Trp63^tm1Brd] or pTV12E(60)-generated p63^Brdm2 [Trp63^tm2Brd]) as both "produced an identical phenotype." Homozygous mice are born alive, but die several hours after birth. No transcripts have been detected in homozygotes. They have striking developmental defects, exhibiting truncated forelimbs, absent hindlimbs, and transparent skin with a complete lack of hair follicles. Both the gross and histological appearance of internal organs is normal. Functional permeability of the skin is dramatically increased; homozygous mice lose thirty times more water than normal littermates. It is presumed that death occurs from dehydration. Heterozygous mice are viable, fertile, and do not exhibit any overt developm ..... For more information please see the full phenotype on the strain data sheet
008712	B6.129X1-Twist2^{tm1.1(cre)Dor}/J	Repository- Live
	Dermo1-cre (Twist2-cre) mutant mice harbor a Cre recombinase "knock-in" allele that also abolishes endogenous Twist2 gene function. Heterozygotes are viable and fertile, while homozygotes (twist-2^-/-) die a few days after birth. Under control of the upstream promoter/enhancer elements, cre expression is observed in a pattern consistent with the wildtype gene; Cre recombinase activity is reported in mesoderm as early as embryonic day 9.5, in mesodermal tissues such as branchial arches and somites, and in condensed mesenchyme-derived chondrocytes and osteoblasts. When heterozygotes are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequences in Dermo1-expressing tissues of the offspring. Homozygous mice exhibit elevated expression of proinflammatory cytokines resulting in perinatal death from cachexia (wasting), as well as progressive growth retardation, impaired movement, th ..... For more information please see the full phenotype on the strain data sheet
004684	B6.Cg Nos2^tm1Lau-chtl/GrsrJ	Repository- Live
	This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock.
000021	B6.Cg-A^y/J	Repository- Live
	Mice homozygous for the yellow spontaneous mutation (A^y) 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
000305	B6.Cg-Fbn1^Tsk +/+ Pldn^pa/J	Repository- Live
	Mice homozygous for the pallid spontaneous mutation Pldn^pa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldn^pa/Pldn^pa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2^p/Oca2^p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi ..... For more information please see the full phenotype on the strain data sheet
014632	B6.Cg-Fbn1^Tsk/J	Repository- Live
	The Fbn1^Tsk allele contains a 30 to 40kb genomic tandem duplication resulting in a larger than normal in-frame transcript. Homozygotes are embryonic lethal, failing to survive past somite formation (7-8 days of gestation). Heterozygotes are viable and fertile, exhibiting excessive growth and hyperplasia of connective tissue, cartilage, tendon sheaths and bone. Skin tightness, due to hyperplasic thickening of subcutaneous loose connective tissue and abnormal organization and distribution of skin microfibrillar arrays, develops by the first week after birth. Although the size of the skeleton is increased, body weight remains normal. Mutant mice exhibit polyuria during the light cycle. Collagens and glycosaminoglycans accumulate in the skin, heart, lungs and bladder. Hypertrophy is also observed in the enlarged heart (aortic adventitia). Mutant mice have enlarged thoracic size and lungs with abnormal alveolar walls, irregular shaped alveoli, and increased lung cap ..... For more information please see the full phenotype on the strain data sheet
004088	B6.Cg-Foxp3^sf/J	Repository- Live
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude (Foxn1^nu/Foxn1^nu) ..... For more information please see the full phenotype on the strain data sheet
003819	B6.Cg-Per2^tm1Brd Tyr^c-Brd/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. By 9-12 months of age, homozygous females exhibit low reproductive success and produce small litters when compared to wildtype. These mice also carry the recessive Tyr^c-Brd mutation that, when homozygous, results in albino coat color. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle.
007484	B6.Cg-Tyr^c-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ	Repository- Live
	On an albino background the X-linked transgene Tg(Tyr)3412ARpw permits visual identification of XX versus XY as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyr^c-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother. This strain is also homozygous for Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not ..... For more information please see the full phenotype on the strain data sheet
008548	B6.Cg-oda/GrsrJ	Repository- Live
	Homozygotes can be identified by two weeks of age on this nonagouti background by their diluted steel grey coat color, which includes dilited pigment in the ears, feet, and tail. Homozygotes are viable and fertile.
005244	B6.Cg-Tg(Krt1-15-EGFP)2Cot/J	Repository- Live
	Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse keratin complex 1, acidic, gene 15 promoter. The high levels of specific transgene expression observed in 'bulge cells' (hair follicle stem cells) allow these cells to be isolated with FACS techniques. This mutant mouse strain may be useful in studies of epithelial stem cells.
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 phenotype on the strain data sheet
004293	B6;129-Shh^tm2Amc/J	Repository- Live
	Mice that are homozygous for the Shh^tm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways. When bred to a strain expressing Cre recombinase under the control of a tet ..... For more information please see the full phenotype on the strain data sheet
013193	B6;129S-Barhl1^tm1Xia/J	Repository- Live
	In this strain, the entire coding region of the endogenous BarH-like 1 (Barhl1) gene is replaced with a lacZ (β-galactosidase) reporter gene and a loxP-flanked neomycin resistance (neo) cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size, with β-gal staining in Barhl1 expressing tissues. LacZ expression in embryos and neonates is evident in all hair cells, but is more abundantly observed in the cochlear outer hair cells. LacZ expression in adults is strong in the outer hair cells, and weak in the inner and vestibular hair cells, with persistent expression in hair cells of the organ of Corti. These mice exhibit age-related progressive degeneration of both cochlear outer and cochlear inner hair cells in the organ of Corti, resulting in hearing loss. The progression is apical-to-basal for outer hair cell and basal-to-apical for inner hair cells. Barhl1^-/- mice have elevated audit ..... For more information please see the full phenotype on the strain data sheet
005956	B6;D1Lac-Scd1^ab-2J/J	Repository- Live
	The overall appearance of mice homozygous for either the Scd1^ab-J allele or the Scd1^ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1^ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1^ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in ..... For more information please see the full phenotype on the strain data sheet
000314	B6CBACa A^w-J/A-Eda^Ta/J-XO	Repository- Live
	XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles.
000501	B6CBACa A^w-J/A-Aifm1^Hq/J	Repository- Live
	Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 ..... For more information please see the full phenotype on the strain data sheet
006449	B6Ei.P-Ass1^fold/GrsrJ	Repository- Live
	At 1 week of age fold homozygotes lack hair such that they can be distinguished from their control littermates, and at 2 weeks of age fold homozygotes have wrinkled skin. A sparse coat does grow in. Homozygotes are smaller than littermate controls throughout their lives and most die at 3 weeks of age.
003544	B6Ei;AKR-rhg/J	Repository- Live
	Homozygotes are much smaller than their wildtype littermates at birth and hair development is retarded at 3 weeks of age, but similar to normal by 10 weeks of age.
002167	BALB/cJ-Cst6^ichq/J	Repository- Live

012624	BALB/cJ-Pld4^thss/GrsrJ	Repository- Live
	Homozygotes are smaller than normal and the coat comes in sparse and fails to fill in even in the adult.
000036	BXD1/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000013	BXD16/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. A mutation has been identified in the BXD16 strain in the amylase 1 gene from the parental Amy1^a allele to an allele that has an electrophoretic mobility closer to that of Amy1^b. This allele is distinct from all others identified and no evidence of genetic contamination was found. Thus, this is believed to have resulted from a spontaneous mutation. (Hjorth, 1982.)
000015	BXD18/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000010	BXD19/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000077	BXD21/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000043	BXD22/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000029	BXD29-Tlr4^lps-2J/J	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. This subline of BXD29/Ty is homozygous for the mutation defective lipopolysaccharide response 2 Jackson, which arose spontaneously in the parental strain. The non-mutant parental strain is available as stock number 010981.
010981	BXD29/Ty	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. This strain has the wild-type allele of Tlr4. For the subline homozygous for the mutation defective lipopolysaccharide response 2 Jackson, please see stock number 000029.
000037	BXD5/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000007	BXD6/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000084	BXD8/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
000105	BXD9/TyJ	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
005440	C.129S4-Ccr3^tm1Cge/J	Repository- Live
	Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (M ..... For more information please see the full phenotype on the strain data sheet
000899	C.B6-Tyr⁺ Hbb^s/J	Repository- Live

000198	C3FeLe.B6-a/J	Repository- Live

009157	C57BL/6J-Ank1^pale/GrsrJ	Repository- Live
	Pale lethal homozygotes are smaller than normal littermates, have a pale light grey skin color, evident at birth, and most die by one week of age, although some have survived to 3 or 4 weeks of age. Some prenatal lethality is implied by the fact that heterozygous crosses yield fewer than 25% homozygotes.
006926	C57BL/6J-Egfr^Vel/J	Repository- Live
	Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series.
017307	C57BL/6J-Krt71^Ca-17J/GrsrJ	Repository- Live
	As with other caracul mutants, heterozygotes have a very wavy coat and curved vibrissae. The mutation can be detected when the coat first comes in at about 7 to 8 days of age, is easily recognized at 3 weeks of age, and remains ruffled throughout life but is less wavy with age.
000629	C57BL/6J-Lyst^bg-J/J	Repository- Live
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet
002469	C57BL/6J-Pax3^Sp/J	Repository- Live
	Mice homozygous for the splotch spontaneous mutation (Pax3^Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. Splotch is a point mutation within intron 3 of the paired homeobox 3 (Pax3) gene on mouse Chromosome 1. The mutation interferes with normal splicing of intron 3 and leads to at least 4 aberrantly spliced mRNAs with exon 4 deleted. The Pax3^Sp mutation also impairs homodimerization of the protein, a function associated with the octapeptide-encoding central segment of the gene. There are multiple alleles at this locus including splotch-delayed (Pax3^Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only.
000811	C57BL/6J-Ptpn6^me-v/J	Repository- Live
	Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6^me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo ..... For more information please see the full phenotype on the strain data sheet
004624	FVB.129P2-Pde6b⁺ Tyr^c-ch Fmr1^tm1Cgr/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable and fertile. Quantitative morphological analysis of dendritic spines of visual cortex pyramidal cells reveals mutant mice have more long dendritic spines, fewer short dendritic spines and more spines with an immature morphology than wildtype littermates. These mice were backcrossed for 11 generations onto the FVB background, are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. This mutant mouse strain may be useful in studies related to Fragile X Syndrome.
004828	FVB.129P2-Pde6b⁺ Tyr^c-ch/AntJ	Repository- Live
	These mice are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. Mice from the colony of FVB.129P2-Fmr1^tm1Cgr/J, Stock No. 004624, that no longer carried the mutant allele for Fmr1 were used to establish this line. Mice are pigmented as a result of the homozygosity of the Tyr^c-ch allele. This mutant mouse strain may be useful in studies where a sighted mouse on the FVB background is an appropriate control, such as behavioral studies. This strain serves as the control for the FVB.129P2-Fmr1^tm1Cgr/J strain, Stock No. 004624 .
000674	I/LnJ	Repository- Live
	I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet
000679	P/J	Repository- Live
	P/J mice exhibit a high incidence of lymphatic leukaemia. They also show a high susceptibility to audiogenic and electroconvulsive seizures. P/J mice are also homozygous for a number of other mutations including nonagouti (a), brown (Tyrp1^b), pink-eyed dilution (Oca2^p), short ear (Bmp5^se), dilute Myo5a^d), and retinal degeneration 1 (Pdeb1^rd1).
005354	RB156Bnr/Ei rul-Gulo^sfx-2J/GrsrJ	Repository- Live
	The phenotype of the sfx^2J remutation is identifiable at 4-5 weeks of age when the mutants appear smaller than their control littermates and begin to hobble about their cage. Between 5 and 8 weeks of age the mutants develop rear limb paralysis and many die by 8 weeks of age. The phenotypic characteristics of this mutation are similar to the original mutation spontaneous fracture (Gulo^sfx) except for the eye phenotype described below that is inherent in the background strain on which the sfx^2J mutation arose. Mice homozygous for the sfx^2J remutation also had cataracts and rosettes and wavy outer nuclear layer of retinas. The eyes of a female mutant were checked using an opthalmascope and it was found to have cataracts on both eyes (as the strain background has characteristically). It has not yet been determined if the rosettes and wavy outer nuclear layer of the retinas is also characteristic of the background s ..... For more information please see the full phenotype on the strain data sheet
005362	RB156Bnr/Ei-rul/GrsrJ	Repository- Live
	The phenotype of this mutation can be identified at about 10 days of age by a ruffled looking coat, which is different than the smooth coat of control littermates. The hair of mutant mice is sparse and has some curling. The ruffled looking coat is maintained throughout the animal's lifespan, unlike the caracul and caracul-like mutants who lose some of their curly coat with age. Mice homozygous for the ruffled mutation have a normal lifespan and both sexes breed normally.
000644	SEA/GnJ	Repository- Live

005051	STOCK Kit^W-sh/HNihrJaeBsmJ	Repository- Live
	Kit mutations affect melanogenesis, hematopoiesis and gametogenesis. The sash mutation affects melanoblast survival. Melanoblast density is severely reduced in homozygotes by E12 (Cable et al., 1995). Homozygote are white with black eyes and some pigment around the ears. Heterozygotes are black with a white sash at the midline. The Kit^W-sh mutation affects Kit expression in a tissue specific manner. Kit expression is abolished in mast cells and mutant mice have a mast cell deficit (Tono et al., 1992, Berrozpe et al., 1999). However, young animals (<4 weeks) have been reported to have mast cells in skin (Yamakazi et al., 1994). Kit^W-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the Kit^W and Kit^W-v mutations, Kit^W-sh germ cells and erythrocytes are not affected. Homozygtes have some ..... For more information please see the full phenotype on the strain data sheet
012874	STOCK Map3k11^m1J/GrsrJ	Repository- Live
	Mice homozygous for the Map3k11^m1J mutation can be identified easily as early as 3 to 4 days of age by the dorsal lines of dark red skin that run from head to tail along the spine and from left to right across the crown of the head, base of the neck in front of the shoulders, and between the base of the ribs and the pelvis. These lines fade away and by 3 weeks of age are no longer evident even when the homozygote is shaved to expose the skin. Homozygotes have necrotic dental pulp, which also improves with age.
001618	STOCK Oca2^p Prop1^df/J	Repository- Live
	Mice homozygous for the Ames dwarf spontaneous mutation (Prop1^df) resemble mice homozygous for the Snell's dwarf mutation (Pit1^dw). Homozygous Ames dwarf mutant mice show growth retardation after the first postnatal week, and weight at 2 months is only about one-half normal. Females and most males are sterile. There is no detectable growth hormone or prolactin. Ames dwarf mice have a secondary immune deficiency presumably resulting from the lack of growth hormone.
004623	STOCK Tg(Fos-lacZ)34Efu/J	Repository- Live
	These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and ..... For more information please see the full phenotype on the strain data sheet
005107	STOCK Tg(KRT14-cre/ERT)20Efu/J	Repository- Live
	These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the human keratin 14 (KRT14) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen (tamoxifen). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted keratinocyte-specific deletions. Oral tamoxifen administration induces Cre recombination in toe, back skin and tongue. Topically administered tamoxifen induces Cre-mediated recombination in a specific localized area of the skin, occuring in 50 to 60% of the ..... For more information please see the full phenotype on the strain data sheet
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 phenotype 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 phenotype on the strain data sheet
001145	WSB/EiJ	Repository- Live

001392	ZALENDE/EiJ	Repository- Live
	This wild-derived inbred strain is homozygous for 7 Robertsonian translocations: Rb(1.3)1Bnr, Rb(4.6)2Bnr, Rb(5.15)3Bnr, Rb(11.13)4Bnr, Rb(8.12)5Bnr, Rb(9.14)6Bnr, and Rb(16.17)7Bnr (abbreviated Rb1Bnr - Rb7Bnr, respectively)(LL Washburn, pers. comm.).
000002	B6.C3-Pde6b^rd1 Hps4^le/J	Research Strain

003215	B6Pin.C3-Ap3b1^pe/J	Research Strain
	The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness.
002134	C57BL/6J-Mitf^mi-vit/J	Research Strain
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitf^mi-vit are only mildly affected compared to other Mitf alleles. Homozygous mutant mice have a lighter initial coat color than normal with extensive white spotting. After eight weeks of age, the mice producing increasing numbers of white hairs with each hair cycles resembling human vitiligo. Homozygotes exhibit uneven pigmentation of the retina and slow, progressive photoreceptor cell loss, eventually leading to blindness.
000516	C57BLKS-Rpl24^Bst/J	Research Strain
	Belly spot and tail (Rpl24^Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24^Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1 ..... For more information please see the full phenotype on the strain data sheet
002516	129-Edn3^tm1Ywa/J	Cryopreserved - Ready for recovery
	This mutation is alleleic with the lethal spotting spontaneous mutation. Homozygous mice are viable at birth, but most die within about a month. They show a disruption in neural crest lineage development. They die from peritonitis subsequent to aganglionic megacolon. They may serve as a model for human Hirschsprung's disease.
006403	129S.B6-Tg(KRT14-Esr1/HRAS)1Pkha/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this "K14-ER:Ras" transgene are viable and fertile, with expression of the ER:Ras fusion protein (constitutively active G12V mutant form of the catalytic domain of human H-ras (H-rasV12) fused at its amino terminal with the G525R mutant murine estrogen receptor ligand binding domain (ER^TM)) directed to epidermis by the human keratin 14 promoter. Because of the ER^TM region of the fusion protein, ER:Ras is restricted to the cytoplasm and the biochemical activity of the ER:Ras fusion gene can be induced following tamoxifen administration. For example, prolonged (4 weeks) induction of human H-Ras^G12V activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. H-Ras^G12V-induced skin abnormalities were entirely reversed ..... For more information please see the full phenotype on the strain data sheet
006661	129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile, with expression of the Raf:ER fusion protein (a constitutively active Y340D/Y341D mutant form of the catalytic domain of human Raf-1 (Raf-1[DD]) fused at its carboxy terminal with the G525R mutant human estrogen receptor ligand binding domain (ER^TM)) directed to epidermis by the human keratin 14 promoter. Because of the ER^TM region of the fusion protein, Raf:ER is restricted to the cytoplasm and the biochemical activity of the Raf:ER fusion gene can be induced following tamoxifen administration. For example, prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one m ..... For more information please see the full phenotype on the strain data sheet
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
005730	129S6.CB(B6)-Del(1)1Brk Gpi1^b/Gpi1^c/BrkMdfJ	Cryopreserved - Ready for recovery
	Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood.
000091	129T1/Sv-Oca2⁺ Tyr^c-ch Dnd1^Ter/J	Cryopreserved - Ready for recovery

005445	A.B6 Tyr⁺-Cyba^nmf333/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry.
005012	A.B6 Tyr⁺-Myo5a^d-l31J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page.
002565	A.B6-Tyr⁺/J	Cryopreserved - Ready for recovery

000004	ABP/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Mice homozygous for the recessive Adamts20^bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported findin ..... For more information please see the full phenotype on the strain data sheet
000251	AEJ.Cg-a^e +/a Gdf5^bp-H/J	Cryopreserved - Ready for recovery

000202	AEJ/Gn-bd/J	Cryopreserved - Ready for recovery

000199	AEJ/GnLeJ	Cryopreserved - Ready for recovery

000820	AKR/J-Foxn1^nu-str/J	Cryopreserved - Ready for recovery
	Mice homozygous for the streaker spontaneous have a phenotype that is very similar to nude mice. Homozygosity prevents the development of T cell lymphomas seen in AKR mice.
003656	AKR/J-we^4J/J	Cryopreserved - Ready for recovery

001005	AKXD1/TyJ	Cryopreserved - Ready for recovery

001017	AKXD10/TyJ	Cryopreserved - Ready for recovery

001003	AKXD11/TyJ	Cryopreserved - Ready for recovery

000765	AKXD13/TyJ	Cryopreserved - Ready for recovery

000779	AKXD14/TyJ	Cryopreserved - Ready for recovery

000954	AKXD15/TyJ	Cryopreserved - Ready for recovery

000958	AKXD16/TyJ	Cryopreserved - Ready for recovery

001093	AKXD18/TyJ	Cryopreserved - Ready for recovery

000776	AKXD2/TyJ	Cryopreserved - Ready for recovery

001062	AKXD21/TyJ	Cryopreserved - Ready for recovery

000947	AKXD22/TyJ	Cryopreserved - Ready for recovery

000969	AKXD24/TyJ	Cryopreserved - Ready for recovery

000949	AKXD25/TyJ	Cryopreserved - Ready for recovery

000764	AKXD27/TyJ	Cryopreserved - Ready for recovery

000959	AKXD3/TyJ	Cryopreserved - Ready for recovery

000777	AKXD6/TyJ	Cryopreserved - Ready for recovery

000763	AKXD9/TyJ	Cryopreserved - Ready for recovery

000277	ATEB/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the atrichosis spontaneous mutation (at) are characterized by sparsely distributed hair, especially on the trunk. The amount of hair varies, but affected mice can be easily recognized at 8 to 10 days old. Both sexes are sterile and have very small gonads with few germ cells. There is a great deficiency of primary spermatogonia in the testes. A quantitative study of maturation of ovarian oocytes showed that the proportion of resident oocytes recruited into the first wave of growth was much higher than in phenotypically normal heterozygous controls (J.J. Eppig, personal communication). This strain is also segregating for the eye blebs spontaneous mutation (Grip1^eb).
000475	B10.129-we^Bkr/CyJ	Cryopreserved - Ready for recovery

000409	B10.129P-H1^b Hbb^d Tyr^c Ea7^a/(5M)oSnJ	Cryopreserved - Ready for recovery

000418	B10.129P-H1^b Tyr^c Hbb^d/(5M)nSnJ	Cryopreserved - Ready for recovery

002472	B10.A/SgSnJ-Hps3^coa-5J/J	Cryopreserved - Ready for recovery

000432	B10.C-H1^b Hbb^d Tyr^c/(41N)SnJ	Cryopreserved - Ready for recovery

000427	B10.CE-H13^b A^w/(30NX)SnJ	Cryopreserved - Ready for recovery

000580	B10.D2/nSn-Tyr^c-4J/J	Cryopreserved - Ready for recovery

001013	B10.D2/nSnJ-Myo5a^d-n/J	Cryopreserved - Ready for recovery
	Mice homozygous for the dilute-neurological spontaneous mutation (Myo5a^d-n) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal mutant mice (Myo5a^d-l, Stock No. 000253).
000420	B10.LP-H13^b A^w/Sn	Cryopreserved - Ready for recovery

000422	B10.LP-H3^b H13^b/(36NS)Sn	Cryopreserved - Ready for recovery

000477	B10.PA-Pldn^pa H3^e a^t/SnJ	Cryopreserved - Ready for recovery
	This minor histocompatibility 3 (H3^e) congenic strain is also carrying the closely linked pallid mutation (Pldn^pa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga ..... For more information please see the full phenotype on the strain data sheet
000456	B10.SM H2^v H2-T18^b/(70NS)Sn-cw/J	Cryopreserved - Ready for recovery

000419	B10.UW-H3^b we Pax1^un a^t/SnJ	Cryopreserved - Ready for recovery

003879	B10;TFLe-a/a T tf/+ tf/J	Cryopreserved - Ready for recovery

000234	B10Gn.Cg-Rn/J	Cryopreserved - Ready for recovery

000822	B6 x 129S1/SvEi Oca2⁺ Tyr⁺-Vsx2^or-J/J	Cryopreserved - Ready for recovery

000593	B6 x B6CBCa A^w-J/A-Grid2^Lc T(2;6)7Ca Mitf^Mi-wh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Mitf^Mi spontaneous mutation are characterized by decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity.
000599	B6 x B6CBCa A^w-J/A-T(5;13)264Ca Kit^W-v/J	Cryopreserved - Ready for recovery

000507	B6 x B6EiC3 a/A-Otc^spf/J	Cryopreserved - Ready for recovery

002048	B6 x C57BLKS-Dock7^m Lepr^db Myo15^sh2-J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15^sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15^sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7a^sh1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7^m) and diabetes (Lepr^db) spontaneous mutations.
002542	B6 x CByJ.Cg-Crm/J	Cryopreserved - Ready for recovery

000618	B6 x FSB/GnEi a/a Ctsl^fs/J	Cryopreserved - Ready for recovery

003602	B6 x STOCK Cln6^nclf-Edar^dl-3J/J	Cryopreserved - Ready for recovery

001518	B6 x STOCK T tf/t^h45 tf/J	Cryopreserved - Ready for recovery

000578	B6 x STOCK Tyr^c-ch Bmp5^se +/+ Myo6^sv/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6^sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females. Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6^sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil ..... For more information please see the full phenotype on the strain data sheet
000577	B6 x STOCK a Oca2^p Hps5^ru2 Ednrb^s/J	Cryopreserved - Ready for recovery

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Cryopreserved - Ready for recovery
	Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous Kit^W-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet
002016	B6(Cg)-A^w-J Eda^Ta-6J Chr Y^B6-Sxr/EiJ	Cryopreserved - Ready for recovery

005071	B6(Cg)-Dct^Slt-lt3J/J	Cryopreserved - Ready for recovery
	Dct^Slt-lt3J heterozygous mice are diluted to a dark brown and homozygous mice are diluted to a light brown.
003046	B6(FVB)-Mitf^Mi-Mee/J	Cryopreserved - Ready for recovery
	On the C57BL/6 background, homozygotes have a white coat color while heterozygotes have a black coat. Clinically, heterozygotes have variable amounts of pigment in the retina with a normal optic cup and retinal vessels. Homozygotes have an iris coloboma, a large optic cup and poor or no retinal vessels. Homozygotes show some pigment in the iris, which does not dilate.
008129	B6(V)-Bhrd/GrsrJ	Cryopreserved - Ready for recovery
	Females heterozygous for the bad hair day mutation have patches of fur missing from the coat, male hemizygotes are almost bald, and female homozygotes are nearly as bald as hemizygous males. Hairs from heterozygous females are morphologically normal, while those from hemizygous males are short and thin. There is increased pigment in the hairs of both hemizygotes and heterozygotes.
005565	B6(V)-chtl^2J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for this spontaneous recessive mutation are recognized by a diluted coat color that appears chocolate brown. This color dilution also lightens the eyes, feet, ears, and tail of affected animals.
000552	B6-A^w-J-Eda^Ta-6J.Cg-Sxr	Cryopreserved - Ready for recovery

001730	B6-A^w-J-Eda^Ta-6J.Cg-Sxr^b Hya^-/J	Cryopreserved - Ready for recovery

000841	B6-A^w-J.CBy-Eda^Ta-By/J	Cryopreserved - Ready for recovery

000311	B6-Pax3^Sp.Cg-N/J	Cryopreserved - Ready for recovery
	Mice homozygous for the splotch spontaneous mutation (Pax3^Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. There are multiple alleles at this locus including splotch-delayed (Pax3^Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. This C57BL/6 congenic strain is also carrying the semidominant naked spontaneous mutation (N).
003509	B6.129-Blmh^tm1Geh/J	Cryopreserved - Ready for recovery
	Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment.
005951	B6.129-Dgat2^tm1Far/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation have a perinatal lethal phenotype, most fail to survive past 6 hours after birth due to dehydration, skin barrier abnormalities, hypothermia and energy deficiencies. Reduced levels of gene product (mRNA) are detected by RT-PCR analysis of brown adipose tissue and livers of neonate homozygous mutants. Growth retardation is observed in homozygous embryos after embryonic day 12.5. Newborn homozygotes are hypoglycemic and lipopenic, exhibiting reduced plasma triglyceride, free fatty acid and glucose levels and have almost no white fat tissue. Within a few hours of birth, the skin of homozygotes becomes dry and cracked. Homozygous mutants rapidly lose weight due to dehydration caused by impaired permeability barrier function. Histological analysis of skin tissue from homozygotes reveals abnormally thin epidermis and compact orthohyperkeratosis of the stratum corneum. Homozygotes surviving between 8 and 24 hours develop tail necrosis. Hetero ..... For more information please see the full phenotype on the strain data sheet
003360	B6.129-Jup^tm1Kem/J	Cryopreserved - Ready for recovery
	Plakoglobin Jup null-mutant embryos die from embryonic day 10.5 onward due to severe heart defects. Some mutant embryos develop further, especially on a C57BL/6 background. These mice die around birth, presumably due to cardiac dysfunction, and with skin blistering and subcorneal acantholysis. The skin phenotype in plakoglobin-deficient mice is reminiscent of the human blistering disease, epidermolytic hyperkeratosis.
006201	B6.129-Scd1^tm1Ntam/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background differ ..... For more information please see the full phenotype on the strain data sheet
006879	B6.129-Scd2^tm1Myz/J	Cryopreserved - Ready for recovery
	While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes.
006156	B6.129-Scel^tm1Hba/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and have no overt morphological or developmental abnormalities. The donating investigator reports that fertility may be impaired in homozygous mice (limited number of litters possible). No endogenous gene expression is observed in skin or stratified squamous epithelia. These mutant mice may be useful in dermatological studies, such as cornified envelope formation, organization of the intima, as well as structural distinctions between arteries and veins, and respiratory structure and function.
003533	B6.129P-B2m^tm1Unc-rs^2J/J	Cryopreserved - Ready for recovery

002037	B6.129P-cpy/J	Cryopreserved - Ready for recovery

008647	B6.129P2(Cg)-Trpa1^tm1Kykw Tyr^c-2J/J	Cryopreserved - Ready for recovery
	Exons encoding the pore domain of the transient receptor potential cation channel, subfamily A, member 1 gene were deleted in this targeted mutation strain. Animals show reduced sensitivity to pain. RT-PCR of dorsal root ganglia confirmed the absence of mRNA in homozygous mutant mice. Homozygotes are viable and fertile.
002219	B6.129P2-Tgfa^tm1Ard/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tgfa^tm1Ard mutation develop normally, are of normal size, weight, and health, and are fertile. They display a pronounced waviness in the coat and whiskers, and dramatic derangement of the hair follicles. Older homozygous mice occasionally show some corneal inflammation that may be the result of a defect in wound healing.
007015	B6.129S1-Gadd45g^tm1Flv/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile, but are poor breeders. TH1 helper T cells from homozygotes are severely compromised in their abilities to activate p38 (MAPK14)and JNK (MAPK8) in response to T cell receptor (TCR) signaling, produce much less interferon gamma (IFNG) upon restimulation, and are deficient in activation-induced cell death (AICD). Deficiencies in this gene also cause reduced contact hypersensitivity in the animals.
004042	B6.129S2-Alox12^tm1Fun/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals.
002612	B6.129S2-Bmp4^tm1Blh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Bmp4^tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities.
003321	B6.129S6-Gba^tm1Nsb/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutation die neonatally due to a defect in the skin vapor barrier. Homozygous mice are small at birth and display an abnormal respiration that progresses to cyanosis and death. This phenotype is similar to a severe infantile form of Gaucher's disease in humans.
007621	B6.129S6-Hr^tm1Cct/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile, but optimal breeding is done with heterozygotes. The mice appear normal at birth and for about two weeks postnatally. Once the animals begin to shed, the hair is lost and does not grow back. They remain bald and over time, the skin becomes thicker and progressively more wrinkled. The degree of wrinkling is variable but can be severe; frequently the skin protrudes over the eyes and off the sides of the animals. Wrinkling is more severe than in the hairless rhino allele. Northern analysis of mRNA from back skin confirmed the absence of expression. This strain maybe be useful in studies of skin and hair.
003329	B6.129S7-Itgb2^tm2Bay/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Itgb2^tm2Bay targeted mutation are viable and fertile, though not good breeders. This mutation differs from the Itgb2^tm1Bay mutation (Stock No. 2128) in that it is a null mutation for the Itgb2 subunit of leukocyte integrins. Mutant mice develop chronic dermatitis with extensive facial and submandibular erosions. They also exhibit elevated neutrophil counts, increased immunoglobulin levels, lymphadenopathy, splenomegaly, and abundant plasma cells in skin, lymph nodes, gut and kidney. A severe defect in T cell proliferation can be found in mutant mice when T cell receptors are stimulated either by staphylococcal enterotoxin A or by major histocompatibility complex alloantigens. The phenotype of the mutant mice resembles the phenotype for the human disorder Leukocyte Adhesion Deficiency Type I (LADI).
008115	B6.129X1-Pomc^tm2Ute/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. 60 to 75% of homozygotes die perinatally. Surviving homozygotes have decreased fertility and homozygous females produce milk that does not allow pups to survive past 14 days of age. No serum adrenocorticotropic hormone (ACTH) or corticosterone was detected by radioimmunoassay (RIA) of homozygotes. Serum epinephrine and aldosterone levels are reduced. Although homozygotes are born with adrenal glands or normal size, adrenal glands fail to grow postnatally and become almost undetectable with age. By 3 months of age, mice homozygous for the mutation are twice the weight of wildtype controls and increased serum leptin levels. Heterozygotes exhibit elevated serum leptin levels, but not increased weight and reduced levels of serum adrenocorticotropic hormone (ACTH), corticosterone, and aldosterone levels. Both heterozygotes and homozygote ..... For more information please see the full phenotype on the strain data sheet
000521	B6.AK-Foxn1^nu-str/J	Cryopreserved - Ready for recovery
	Mice homozygous for the streaker spontaneous have a phenotype that is very similar to nude mice. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
000977	B6.B10(PL)-Slc45a2^Uw-dbr/J	Cryopreserved - Ready for recovery

000526	B6.C-Fgf5^go/J	Cryopreserved - Ready for recovery
	Mice homozygous for Fgf5^go, the angora allele, have a prolonged anagen VI phase of the hair follicle cycle resulting in hair lengths that are longer than normal for all coat hair types. These mice begin to appear shaggy by 15-21 days of age and remain so throughout their lives. Fgf5^go/Fgf5^go skin grafts continue to yield long fur but do not alter the fur growth in surrounding host tissue indicating that FGF5 does not function in a systemic manner but rather must be produced in the follicle in which it has an effect. A subtle follicular dystrophy has been described in mice on the B6.C congenic background (See Sundberg et al., 1997). (Dickie MM, 1966; Pennycuik and Raphael, 1984.)
003625	B6.C-H2-Ab1^bm12/KhEg-Mc1r^e-J/J	Cryopreserved - Ready for recovery

000495	B6.C-H38^c/By-Kit^W-56J/J	Cryopreserved - Ready for recovery

000560	B6.C-H7^b/By Kit^W-50J/J	Cryopreserved - Ready for recovery

000383	B6.C-Tyr^c H1^b Hbb^d/ByJ	Cryopreserved - Ready for recovery

000769	B6.C/(HZ18)By-a^t-44J/J	Cryopreserved - Ready for recovery

000001	B6.C3 A/a Mgrn1^md/J	Cryopreserved - Ready for recovery

004202	B6.C3 Pde6b^rd1 Hps4^le/+ +-Lmx1a^dr-8J/J	Cryopreserved - Ready for recovery

000203	B6.C3-A^iy/a/J	Cryopreserved - Ready for recovery

000017	B6.C3-A^vy/J	Cryopreserved - Ready for recovery
	Homozygous (A^vy/A^vy) and heterozygotes (A^vy/A and A^vy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. A^vy resembles A^y in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in A^vy/a mice of mottled phenotype but not in those of agouti phenotype.
000102	B6.C3-Ap3b1^pe/J	Cryopreserved - Ready for recovery

007623	B6.C3-Cno^cno/LlpJ	Cryopreserved - Ready for recovery
	Mice homozygous for the cappuccino mutation have a severe dilution in coat color and diminished eye pigmentation. The BLOC-1 complex is disrupted and melanosome development appears arrested at an early stage. These homozygotes have significantly increased bleed times due to defective platelet aggregation. This mutation provides a model for Hermansky-Pudlak Syndrome.
000122	B6.C3-Kit^W-44J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
002624	B6.C3-Lmx1a^dr-6J/J	Cryopreserved - Ready for recovery

000309	B6.C3-Mgrn1^md/J	Cryopreserved - Ready for recovery

001572	B6.C3-a^m-J/J	Cryopreserved - Ready for recovery

000449	B6.C3-rs/J	Cryopreserved - Ready for recovery

000050	B6.C3Fe-H51 Hps1^ep /ByJ	Cryopreserved - Ready for recovery

000525	B6.C3Fe-Hps1^ep/J	Cryopreserved - Ready for recovery

000204	B6.C3Rl-Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
000991	B6.C58-Kit^W-57J/J	Cryopreserved - Ready for recovery

000022	B6.CBAGr-ma/J	Cryopreserved - Ready for recovery

003628	B6.Cg cub-Mcub/J	Cryopreserved - Ready for recovery
	Mice homozygous for both curly bare (cub) and the recessive, C57BL/6 allele at the modifier of curly bare locus (mcub) appear hairless or "fuzzy." cub homozygotes that are either heterozygous or homozygous for the dominant, V/Le-derived Mcub allele have wavy fur. cub/+ mice of any Mcub genotype have normal fur. The "breathing" colony of Stock no. 003628 is homozygous for both cub and Mcub, so all the mice exhibit wavy coats. (Stock no. 003826 is maintained segregating for cub and is homozygous for mcub, so the cub/cub mice of that strain are hairless.) Embryos (also designated 003628) have been cryopreserved from a cross of C57BL/6J female mice and males of 003628; pups recovered from these embryos will be heterozygous at both loci and so will have normal fur. Interbreeding of these animals will produce mice of genotypes cub/cub mcub/mcub (hairless); cub/cub ..... For more information please see the full phenotype on the strain data sheet
002560	B6.Cg-Aars^sti/J	Cryopreserved - Ready for recovery
	Mice homozygous for this spontaneous mutation exhibit a rough, sticky coat, progressive ataxia and Purkinje cell degeneration. Cerebellar Purkinje cell loss is first observed by three weeks of age becomes extensive by six weeks of age and continues to progress slowly over the course of a year. This mutant mouse strain may be useful in studies related to neurodegeneration, protein misfolding and aberrant transfer RNAs.
006253	B6.Cg-Ap3b1^tm1.1Sms/J	Cryopreserved - Ready for recovery
	Ap3b1 encodes the beta-3A subunit of the adaptor protein complex 3 (AP-3). Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Ap3b1 mRNA is detected by Northern blot analysis of spleen and kidney tissue, and beta-3A immunoreactivity is absent in monocytes from homozygous mice. In brain tissue from homozygous mutants, expression levels of the AP-3 beta-3B (beta-NAP), mu-3 and sigma-3 subunit proteins are normal, but expression of the delta-3 subunit protein is reduced. In kidney, no sigma-3 protein is detected, and mu-3 and delta-3 subunit proteins levels are greatly reduced. Homozygotes have a diluted coat color (light gray), which is lighter than the coats of homozygotes carrying the allelic pearl (Ap3b1^pe) spontaneous mutation. Cultured melanocytes from homozygous mutant mice have very few pigment granules. Lysosomal-associated membrane ..... For more information please see the full phenotype on the strain data sheet
000535	B6.Cg-Atp7a^Mo-blo/J	Cryopreserved - Ready for recovery
	Female mice heterozygous for the blotchy alleles (Atp7a^Mo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to 6 ..... For more information please see the full phenotype on the strain data sheet
001381	B6.Cg-Atp7a^Mo-pew2J/J	Cryopreserved - Ready for recovery

000053	B6.Cg-Atp7a^Mo-to/J	Cryopreserved - Ready for recovery

000131	B6.Cg-Dct^slt/J	Cryopreserved - Ready for recovery

000699	B6.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed, and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Lepr^db/+) also have increased metabolic efficiency, and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Lepr^db may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabe ..... For more information please see the full phenotype on the strain data sheet
006429	B6.Cg-Dwh/GrsrJ	Cryopreserved - Ready for recovery
	Mice carrying the dominant mutation dispersed white hair on this predominantly C57BL/6J background have white hairs dispersed throughout the normally black coat along with patches of white hairs on the back or belly.
001368	B6.Cg-Gsdma3^Bsk/J	Cryopreserved - Ready for recovery

000103	B6.Cg-Hps6^ru/J	Cryopreserved - Ready for recovery

001737	B6.Cg-Hr^hr H2-T18^a/J	Cryopreserved - Ready for recovery
	Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles ..... For more information please see the full phenotype on the strain data sheet
002283	B6.Cg-Kit^W-19H/EiJ	Cryopreserved - Ready for recovery
	This deletion is a dominant mutation causing white spotting on the feet, tail, belly, and occasionally elsewhere. Homozygosity is embryonic lethal. On the C57BL/6 background approximately 60% of heterozygous females have a closed vagina. The ovaries from these heterozygotes are normal and fine for transplantation. On the C57BL/6 background in the presence of the Y^AKR/J Chromosome (available from Stock No. 007250), Kit^W-19H heterozygosity results in sex reversed XY females.
000133	B6.Cg-Kit^W-24J/J	Cryopreserved - Ready for recovery

000139	B6.Cg-Kit^W-25J/J	Cryopreserved - Ready for recovery

000164	B6.Cg-Kit^W/J	Cryopreserved - Ready for recovery

002993	B6.Cg-Kitl^Sl-18H/EiJ	Cryopreserved - Ready for recovery

008656	B6.Cg-Kitl^Sl-gb/MbeJ	Cryopreserved - Ready for recovery
	The 120 Kb deletion in the spontaneous mutation, grizzle belly, represents the smallest complete deletion among the Kit ligand (Steel) alleles. Mice homozygous for the mutation die just before or after birth. Mice that survive to postnatal day 1 display a substantial decrease in peripheral red blood cells (RBC) and a severe anemia. Heterozygotes exhibit a mild anemia, and some decrease in peripheral RBC. In the homozygous embryo there is an absence of primordial germ cells (PGCs) by E11.5; an intermediate number of PGCs are found in the heterozygote. Like the other mutations at the Steel locus, this allele causes abnormal pigmentation. Heterozygotes can be identified by a head spot and light belly. This strain may be useful for research in hematopoiesis, pigmentation and gametogenesis.
000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000194	B6.Cg-Lx Kit^W-v/J	Cryopreserved - Ready for recovery
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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 phenotype on the strain data sheet
000071	B6.Cg-Mcoln3^Va/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3^Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3^Va-J> ..... For more information please see the full phenotype on the strain data sheet
000158	B6.Cg-Mitf^Mi-wh/Mitf^Mi/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (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 white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (Mitf^Mi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac ..... For more information please see the full phenotype on the strain data sheet
000184	B6.Cg-Mitf^Mi-wh/Mitf^mi-rw/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitf^mi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (Mitf^Mi-wh/Mitf^mi-rw) are mostly white with tan spots and red eyes.
000157	B6.Cg-Mitf^Mi-wh/Mitf^mi-sp/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (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 white mutant mice show slight microphthalmic but normal skeleton. Both homozygous and heterozygous mice for the microphthalmia-spotted spontaneous mutation (Mitf^mi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (Mitf^Mi-wh/Mitf^mi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes.
000057	B6.Cg-Mitf^Mi-wh/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (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 diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear.
000024	B6.Cg-Pldn^pa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the pallid spontaneous mutation pa and nonagouti (a) are pink-eyed and have a light, yellow-brown coat. The coat is a little lighter than that of pink-eyed dilution homozygotes (p/p). Viability of homozygote mutant mice is slightly reduced. Some homoygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosidase, and a-mannosidase, accompanied by lowered enzyme excretion in the urine. Pallid mice have a deficiency in serum a1-antitrypsi ..... For more information please see the full phenotype on the strain data sheet
000568	B6.Cg-Pmp22^Tr-J Krt25^Re/+ +/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the trembler-Jackson spontaneous mutation (Pmp22^Tr-J) are similar to heterozygotes carrying the original trembler mutation (Pmp22^Tr). However, the behavior and neuropathology of trembler-Jackson heterozygotes is less severe. The tremor phenotype cannot be reliably recognized before 20 to 25 days. There are no obvious seizures and only a mild gait abnormality. In the PNS, the myelin deficiency is considerably less severe than that of trembler mice. Homozygous trembler-Jackson mice are recognizable by 8 days of age after which they become progressively disabled. Homozygous mutant mice are unable to walk normally and can right themselves only with great difficulty; most are dead by 18 days. It should be noted that although trembler homozygotes are more severely demyelinated than trembler-Jackson homozygotes, the trembler mice live a normal lifespan while trembler-Jackson mice die prior to weaning. Survival of trembler homozygotes ..... For more information please see the full phenotype on the strain data sheet
000285	B6.Cg-Rora^sg + +/+ Myo5a^d Bmp5^se/J	Cryopreserved - Ready for recovery
	Mice homozygous for the staggerer spontaneous mutation (Rora^sg) show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex of homozygous mutant mice is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The remaining granule cells migrate inward from the external layer prematurely and then degenerate. Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur. Staggerer mutant mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells. Kopmels et al. have reported a hyperproduction of IL1 biological activity and mRNA from LPS stimulated spleen cells of Rora^sg/Rora^sg mice on the C57BL/6J background relative to wild type siblings. In this congenic strain the staggerer mutation is maintain ..... For more information please see the full phenotype on the strain data sheet
001176	B6.Cg-Rw/J	Cryopreserved - Ready for recovery
	Rump-white is a dominant lethal mutation from which homozygotes die in utero around embryonic day 9.5. From the earliest developmental stage assessed, E7.5, smaller size is detectable in Rw/Rw embryos. Developmental arrest is found at E7.5-E8.0 likely during or near the end of gastrulation. E7.5 embryos do not have the expanded cylindrical shape normally seen at this stage. All three germ layers form, but the mesoderm is sparse and loosely organized. A rudimentary notochordal plate can be detected in some of the larger mutant embryos by E9.5. Resorption of necrotic mutant embryos appears to be underway at this point. (Searle and Truslove, 1970; Bucan et al., 1995.) Rump-white heterozygotes have hypopigmentation in the front digits and hindquarters including white hindlegs, white tail with the tip often pigmented, and a variable degree of white in the sacral and lumbar regions with the ventral area more consistently affected than the dorsal area. At E10.5 a norma ..... For more information please see the full phenotype on the strain data sheet
000112	B6.Cg-Sgk3^fz H54 Mlph^ln/+ H54 +/J	Cryopreserved - Ready for recovery

000018	B6.Cg-Sox18^Ra/J	Cryopreserved - Ready for recovery
	The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18^Ra/+ coats have longer g ..... For more information please see the full phenotype on the strain data sheet
002863	B6.Cg-Tgfa^wa1/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Ventricular enlargement and striatal reduction is observed in adult homozygous wa1 mice. The phenotype is more severe in males. In addition, adult males exhibit reduced hippocampal volume and impaired auditory and contextural fear learning. Both sexes demonstrate an abnormal fear response. Peripubertal mice do not exhibit behavioral deficits despite slight forebrain structural abnormalities. (Koshibu K, et al., 2005)
000035	B6.Cg-Tyr^c-J/J	Cryopreserved - Ready for recovery

000104	B6.Cg-Tyr^c-h/J	Cryopreserved - Ready for recovery

000981	B6.Cg-Ve/J	Cryopreserved - Ready for recovery
	Velvet heterozygotes have a ruffled, silky coat, which is especially easy to classify on the ventral surface. Their vibrissae are straggly and can be classified by 10 days of age. Homozygotes die in utero and show ectodermal and endodermal defects as early as embryonic day 6.5.
000571	B6.Cg-Whrn^wi Tyrp1^b/+ +/J	Cryopreserved - Ready for recovery
	At 9 to 10 days of age Whrn^wi homozygotes display increased activity, decreased ability to right their selves, and are generally smaller than unaffected siblings. By 14 to 16 days of age homozygotes display head bobbing, circling, and an unsteady gate. Adults display head tossing and circling behavior and deafness is indicated by 20 days of age. Sackler and Weltman reported the average number of circles by a prodded 12-week old female homozygote to be 407 in 10 minutes. They found female homozygotes to have an increased metabolic rate and adrenocorticosteroid activity and decreased body weights. Homozygous males were reported to have decreased blood glucose and liver glycogen levels, decreased white blood cell and eosinophil counts, increased plasma albumin levels, and decreased globulin levels, in addition to decreased weight and increased food intake. (Lane 1963; Sackler and Weltman 1967, 1970, 1971.) While the organ of Corti in whirler homozygotes shows normal ..... For more information please see the full phenotype on the strain data sheet
003826	B6.Cg-cub/J	Cryopreserved - Ready for recovery
	Mice homozygous for both curly bare (cub) and the recessive, C57BL/6 allele at the modifier of curly bare locus (mcub) appear hairless or "fuzzy." cub homozygotes that are either heterozygous or homozygous for the dominant, V/Le-derived Mcub allele have wavy fur. cub/+ mice of any Mcub genotype have normal fur. Stock no. 003826 is maintained segregating for cub and is homozygous for mcub, so the cub/cub mice of this strain are hairless.
001959	B6.Cg-jb/J	Cryopreserved - Ready for recovery

006086	B6.Cg-Tg(HBB-GH1)420King/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly.
009687	B6.Cg-Tg(KRT14-Kitl*)4XTG2Bjl/J	Cryopreserved - Ready for recovery
	These transgenic mice express a mutant mouse Kitl (kit ligand) cDNA, TG2 or membrane SCF, under the control of the human keratin 14 (epidermolysis bullosa simplex, Dowling-Meara, Koebner), KRT14, promoter. The mutant kit ligand carries a site directed mutation that deletes the cleavage site which produces mostly membrane bound protein. These transgenic mice have epidermal melanocytes that persist into adulthood and cause grey-black pigmented skin and increased coat pigment. Shortly after birth, transgenic pups develop visibly pigmented footpads. Transgenic mice exhibit increased sensitivity to irritants. Mice that are homozygous for the targeted mutation are viable, and do not display any gross behavioral abnormalities. Homozygotes are sometimes smaller in size than wildtype controls (as reported by the Donating Investigator). This mutant mouse strain may be useful in studies of hyperpigmentation and allergic contact dermatitis.
000027	B6.D-Tyrp1^b Dock7^m/J	Cryopreserved - Ready for recovery
	The recessive misty mutation causes a mild dilution of coat color and on certain backgrounds a white tail tip often accompanied by a belly spot. Melanocytes from Dock7^m/Dock7^m mice have a highly dendritic shape, show deficient proliferation in culture and have much more melanin content. Fewer melanoblasts are found in primary cultures from Dock7^m/Dock7^m mice than from wildtype controls. Between two and five weeks of age, Dock7^m/Dock7^m mice are smaller than controls. At 35 days of age they are shorter, weigh 15% less on average, and have less inguinal adipose mass than controls. Misty homozygotes completely lack brown fat. Although platelet count, seratonin content and ATP content are normal, there is increased bleed time and reduced platelet AD levels in Dock7^m/Dock7^m homozygotes. (Woolley, 1941 and 1945; Truett et al., 1998; Sviderskaya ..... For more information please see the full phenotype on the strain data sheet
009659	B6.D2(BKS)-Dock7^m/J	Cryopreserved - Ready for recovery
	The recessive misty mutation causes a mild dilution of coat color and on certain backgrounds a white tail tip often accompanied by a belly spot. Melanocytes from m/m mice have a highly dendritic shape, show deficient proliferation in culture and have much more melanin content. Fewer melanoblasts are found in primary cultures from m/m mice than from wildtype controls. Between two and five weeks of age, m/m mice are smaller than controls. At 35 days of age they are shorter, weigh 15% less on average, and have less inguinal adipose mass than controls. Misty homozygotes completely lack brown fat. Although platelet count, seratonin content and ATP content are normal, there is increased bleed time and reduced platelet AD levels in m/m homozygotes. (Woolley, 1941 and 1945; Truett et al., 1998; Sviderskaya et al., 1998.)
000541	B6.D2-Hps5^ru2-hz/J	Cryopreserved - Ready for recovery

000171	B6.D2-Kit^W-45J/J	Cryopreserved - Ready for recovery

001563	B6.D2-Kit^W-73J/J	Cryopreserved - Ready for recovery

000054	B6.D2-Tyr^c-p/J	Cryopreserved - Ready for recovery
	The coat color of mice homozygous for the platinum mutation is nearly albino, cream colored, and these mice have pink eyes and a sheen to their coat. These homozygotes are lighter in color than chinchilla homozygotes despite having more tyrosinase activity in their cells. This is due to the altered subcellular localization of platinum tyrosinase. (Dickie M., 1966.)
000342	B6.D2-lt/J	Cryopreserved - Ready for recovery

000539	B6.D2-pk/J	Cryopreserved - Ready for recovery

001177	B6.LP-Kit^W-49J/J	Cryopreserved - Ready for recovery

002550	B6.TF-Slc45a2^uw-d/J	Cryopreserved - Ready for recovery

004338	B6;129-E2f2^tm1Zubi/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full phenotype on the strain data sheet
003295	B6;129-Ednrb^tm1Ywa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Ednrb^tm1Ywa targeted mutation are viable at birth, but usually die within the first month. They show a disruption of neural crest lineage development, which is characterized by a lack of hair or skin pigmentation in 90% of their body. They die due to peritonitis from distention caused by an aganglionic megacolon. This strain may be used as a model for human Hirschsprung's disease. This mutation is allelic with the piebald lethal spontaneous mutation.
004161	B6;129-Fgf7^tm1Efu/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease.
002495	B6;129S4-Col1a1^tm1Jae/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and develop to young adulthood without obvious differences from wildtype mice. As the mice age they develop fibrosis in the dermis characterized by a thickening and roughening of the skin, which is similar to that seen in human scleroderma. Homozygous females develop postpartum abnormalities of the uterus caused by a failure of collagen resorption. They have slightly reduced litter sizes and significantly fewer litters than normal wildtype mice. A secondary collagenase cleavage site was found in the mutant protein that could be cleaved by rat collagenase but not by human collagenase.
003366	B6;129S4-Cux1^tm1Ejn/J	Cryopreserved - Ready for recovery
	CDP, a ubiquitous homeoprotein homologous to Drosophila cut, is implicated as a transcriptional repressor in several developmental systems. It contains four independent DNA binding domains: three "cut repeats" plus the homeodomain. The mouse Cux/CDP gene spans more than 200 kb and is composed of at least 21 exons. B6;129-Cutl1^tm1Ejn mice express a mutant form of the Cutl1 protein. Homozygotes display curly vibrissae and wavy hair. There is a high degree of pup loss in litters born to mutant females. The mutant protein is present at levels slightly greater than wild-type, but exhibits the same tissue distribution as wild-type protein, and has approximately normal affinity for known target sequences.
002850	B6;129S4-Nfkbia^tm1Bal/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Nfkbia^tm1Bal mutation are runted, and have granulocytosis as well as abnormalities in epithelial keratinization. Neonates die at around 8 days of age.
006238	B6;129S4-Thbs2^tm1Bst/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre ..... For more information please see the full phenotype on the strain data sheet
002594	B6;129S6-Gba^tm1Nsb/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutation die neonatally due to a defect in the skin vapor barrier. Homozygous mice are small at birth and display an abnormal respiration that progresses to cyanosis and death. This phenotype is similar to a severe infantile form of Gaucher's disease in humans.
002788	B6;129S7-Fst^tm1Zuk/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.
002911	B6;129X1-Dsg3^tm1Stan/J	Cryopreserved - Ready for recovery
	Mice homozygous for Dsg3^tm1Stan targeted mutation show loss of cell adhesion, resulting in a phenotype that resembles pemphigus vulgaris. By 15-20 days of age, homozygotes are smaller than unaffected littermates, perhaps due to erosions in the mouth (resulting in decreased food intake). Older mice show crusting lesions in areas of trauma. Histology shows suprabasilar acantholysis (i.e. loss of cell-cell adhesion in the basal and immediate suprabasal area). This is most prominent on oral and vaginal mucous membranes, but is also seen on on the skin and eyelids. The mice start to lose hair at 3-4 weeks. The runting and hair loss phenotype are identical to that of a mouse mutant, balding bal. Allele testing indicated that bal is co-allelic with the targeted mutation.
001025	B6;B10-Hps3^coa/J	Cryopreserved - Ready for recovery

006157	B6;B10SnJ-baw/J	Cryopreserved - Ready for recovery
	The mutation black and white (baw) causes a light coat color on the ventrum of affected mice. The pattern is like that seen on mice carrying the black and tan mutation (a^t), but the hair is white on baw homozygotes rather than tan. In addition, the remaining coat is flecked with white hairs, particularly obvious as the mice age.
007622	B6;SJL-Tg(KRT14-Hr)551Cct/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable and fertile. When young, these mice look similar to wildtype mice, but as they age, their coats become shorter and more sparse. Molecular analysis shows delayed development of sebaceous glands, accelerated hair cycle and less-differentiated epidermis. RNA and protein expressed from the transgene are detected in skin as determined by Western and Northern analysis. This strain may be useful as a model for skin and hair development studies.
007678	B6;SJL-Tg(KRT14-rtTA)208Jek/J	Cryopreserved - Ready for recovery
	Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTA_X) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells.
000522	B6By.B10-Gsdma3^Re-den/J	Cryopreserved - Ready for recovery

000795	B6By.C-H52 Fgf5^go/J	Cryopreserved - Ready for recovery

000523	B6By.Cg-Eh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the hairy ears mutation die within a day of birth. The palatal shelves fail to fuse resulting in complete clefting of the secondary palate, and the tympanic rings are shortened and deformed. Heterozygotes can be identified by tufts of hair on the inner ear and smaller than normal ear pinnae.
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Cryopreserved - Ready for recovery
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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 phenotype on the strain data sheet
001059	B6By.Cg-Oca2^p/J	Cryopreserved - Ready for recovery
	A normal-size Oca2^p mRNA is present in the skin of mice homozygous for the Oca2^p mutation, but in greatly reduced amounts; thus, this appears to be a hypomorphic rather than a null allele. B6By.Cg-Oca2^p/Oca2^p/J mice are grey with pink eyes. The Oca2^p mutation affects the amount of eumelanin (brown/black pigment) and the size and morphology of eumelanosomes (black pigment granules), but has little or no effect on pheomelanin (red/yellow pigment).
000126	B6By.Cg-Sd Mcoln3^Va-J Krt25^Re/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3^Va-J) are more pigmented than the original varitint waddler mice (Mcoln3 ^Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes for the two alleles (Mcoln3^Va-J/Mcoln3^Va) are similar to Mcoln3^Va-J/Mcoln3^Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3^Va-J/Mcoln3^Va mice are considerably reduced. This strain is also carrying two other mutations, rex (Krt25^Re) and Danforth's short tail (Sd).
000125	B6By.Cg-Sox18^Ra Pt Os/J	Cryopreserved - Ready for recovery
	The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18^Ra/+ coats have longer g ..... For more information please see the full phenotype on the strain data sheet
000505	B6C3 A^w-J/A-Muted^mu/J	Cryopreserved - Ready for recovery
	Mice homozygous for the muted spontaneous mutation (Muted^mu) have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldn^pa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths from the sacculus and utriculus of one or both ears. The bony labyrinth is normal; the mice are not deaf and do not circle. Mutant mice have prolonged bleeding times and a platelet storage pool deficiency (SPD) associated with abnormalities of the dense granules of the blood platelets. The combination of pigment, otolith, and SPD abnormalities also occurs in two other mouse mutants, pallid and mocha (Ap3d1^mh), and is also seen in human Hermansky-Pudlak syndrome.
000604	B6C3 a/A-T(10;13)199H +/+ Lyst^bg-J/J or Lyst^bg-2J/J	Cryopreserved - Ready for recovery

001750	B6C3Fe a/a-Eif3c^Xs-J/J	Cryopreserved - Ready for recovery

000210	B6C3Fe a/a-Edar^dl-J/J	Cryopreserved - Ready for recovery

000207	B6C3Fe a/a-Edaradd^cr/J	Cryopreserved - Ready for recovery

000304	B6C3Fe a/a-Krt71^Ca Scn8a^med-J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the motor end plate disease-Jackson spontaneous mutation (Scn8a^med-J) have a phenotype that resembles the original mutation (Scn8a^med). Homozygous motor end plate disease mutant mice show progressive skeletal muscle weakness beginning 8 to 10 days postnatally and usually die within 2 weeks of onset. Other disease characteristics include progressive atrophy of skeletal muscle, marked terminal sprouting of motor nerves along with slower conduction velocity and prolonged refraction, and eventually failure of muscle fibers to show end-plate potentials or action potentials in response to nerve stimulation. Heterozygotes may show mild manifestations of the disease during the first 2 weeks of life but symptoms disappear with age. Both homozygotes and heterozygotes exhibit immunological aberrations.
001573	B6C3Fe a/a-Mitf^Mi/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the Mitf^Mi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity.
000278	B6C3Fe a/a-Papss2^bm Hps1^ep Hps6^ru/J	Cryopreserved - Ready for recovery

001430	B6C3Fe a/a-Ptch1^mes/J	Cryopreserved - Ready for recovery
	Mice homozygous for the mesenchymal dysplasia spontaneous mutation (mes) have a shortened face, wide set eyes, excessive skin, belly spot, kinked tail, preaxial polydactyly, and thickened foot pads. Homozygous mutant mice also display mineralization of tendons and multiple skeletal defects. Both sexes are infertile. Male mice have cryptorchid testes.
000290	B6C3Fe a/a-Sox10^Dom/J	Cryopreserved - Ready for recovery

000005	B6C3Fe a/a-Wc/J	Cryopreserved - Ready for recovery
	Homozygotes die in utero and some of the more severely affected heterozgyotes will die before wean age. Heterozygotes can be identified by 5 days of age by the sparce, wavy coat, diluted coat color, fuzzy hair on the head and upper back, and wavy vibrissae. Some have dry, scaly skin and fail to develop hair.
002018	B6C3Fe a/a-din/J	Cryopreserved - Ready for recovery

000240	B6C3Fe a/a-soc/J	Cryopreserved - Ready for recovery

000065	B6C3Fe a/a-we Pax1^un a^t/J	Cryopreserved - Ready for recovery
	The affected mutant (we Pax1^un a^t/we Pax1^un a^?) has a wavy coat, wavy tail, and is black and tan.
000296	B6C3Fe-a/a Hoxa13^Hd Mcoln3^Va-J/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3^Va-J) are more pigmented than the original varitint waddler mice (Mcoln3^Va) and behave normally although they are deaf. They have slightly diluted coat color, a large irregular belly spot, and white feet and tail tip. Homozygous mutant mice have extensive white spotting interspersed with patches of diluted color. They are deaf but behave normally and are fertile. Compound heterozygotes of the two alleles (Mcoln3^Va-J/Mcoln3^Va) are similar to Mcoln3^Va-J/Mcoln3^Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3^Va-J/Mcoln3^Va mice are considerably reduced. This strain is also carrying the semidominant hypodactyly spontaneous mutation (Hoxa13^Hd). Heterozygous hyp ..... For more information please see the full phenotype on the strain data sheet
000956	B6CB-Mitf^mi-rw/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitf^mi-rw have some pigmentation around the neck and have small red eyes.
000500	B6CBACa A^w-J/A-Gs/J	Cryopreserved - Ready for recovery

000287	B6CBACa A^w-J/A-Plp1^jp Eda^Ta/J	Cryopreserved - Ready for recovery
	Hemizygous males carrying the X-linked jimpy spontaneous mutation (Plp1^jp) appear normal when sitting quietly, but beginning at about 3 weeks of age they show a marked tremor of the hindquarters when attempting movement. After 3 weeks of age convulsions may occur. These males die between 20 and 40 days of age. In males, the CNS is very deficient in myelin, but the PNS is normally myelinated. Heterozygous jimpy females have normal lifespans with no overt phenotype. However, jimpy heterozygous females are reported to have reduced numbers of oligodendrocytes compared to wildtype females. While the mutation is recessive, only partial phenotypic rescue was attained by the transgenic expression of the two major isoforms, PLP and DM20, suggesting a dominant negative action from this allele (Nandon et al., 1994). This stock is also carrying the X-linked tabby mutation (Eda^Ta).
000515	B6CBACa A^w-J/A-Sfn^Er/J	Cryopreserved - Ready for recovery
	This mutation shows complete penetrance in heterozygotes. These mice grow a normal appearing but probably somewhat dry first coat until the age of about 13 days; then hair loss begins and continues until the fur becomes sparse. Repeated growth and re-epilation follow without a definite pattern. Heterozygotes are slightly reduced in size and some may die before weaning, but adults are fully viable and fertile. Homozygotes die at birth from inability to breathe because of a closed oral cavity. At embryonic day 17 the skin of homozygotes is extremely thin and smooth with few vibrissae and hair follicles. The snout is truncated and the mouth closed. The limbs and tail are greatly shortened and held close to the trunk and the anal and urogenital orifices are closed. There are marked skeletal abnormalities and cleft palate. Homozygotes can be recognized at 13 days of gestation by their blunt limbs and stumpy tail. Between 13 and 15 days the nares and oral opening close, resulting in marked c ..... For more information please see the full phenotype on the strain data sheet
000242	B6CBACa A^w-J/A-spc/J	Cryopreserved - Ready for recovery

000288	B6CBACa A^w-J/A-we a Mafb^kr/J	Cryopreserved - Ready for recovery

000508	B6D2-Sox18^Ra-Op/J	Cryopreserved - Ready for recovery
	The Sox18^Ra-Op allele causes a more severe phenotype than either the Sox18^Ra or Sox18^Ra-J allele. Green and Mann determined that only approximately 17% of the Sox18^Ra-Op/+ heterozygotes are born and survive to wean age. Heterozygotes have a deficiency of vibrissae, a distinguishing feature in utero and usually evident at birth, and can be distinguished at three days of age by their pink skin which, with its delayed coat development, fails to darken like that of wildtype siblings. A paucity of fur is apparent by 9 days of age and persists throughout life. Heterozygotes are smaller in overall size and many of those that die shortly after birth are cyanotic and edematous. Dead pups have glossy skin with red patches that may result from superficial hemorrhages. Homozygotes die by embryonic day 11.5. (Green and Mann, 1961; Mann, 1963.)
002044	B6Ei.Cg-Atp7a^Mo-blo/J	Cryopreserved - Ready for recovery
	Female mice heterozygous for the blotchy alleles (Atp7a^Mo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs.. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to ..... For more information please see the full phenotype on the strain data sheet
002622	B6Ei.Cg-pwk/J	Cryopreserved - Ready for recovery
	Homozygous patchwork mice have hairs that are either totally white or totally pigmented, but no diluted coloration of the hair. On a nonagouti background this produces a salt-and-pepper appearance from white hairs juxtaposed with black hairs. This occurs throughout the coat and does not vary by anatomic region. The absence of pigment in the white hairs is due to an absence of melanocytes in the hair follicles of the white hairs; functioning melanocytes are present in the hair follicles of the black hairs. The absence of melanotyes in the follicles of the white hairs results from premature death of melanoblasts during development. TUNEL staining indicates that this melanoblast death is apoptotic and begins around embryonic day 18.5. This suggests that patchwork melanoblasts can survive and function if enough survive, but fail to survive when adequately reduced in number. Analysis of aggregation chimeras between patchwork and albino donors revealed gray hairs at the boundaries bet ..... For more information please see the full phenotype on the strain data sheet
000971	B6EiC3 a/A-Och/J	Cryopreserved - Ready for recovery

000553	B6EiC3Sn a/A-Egfr^wa2 Wnt3a^vt/J	Cryopreserved - Ready for recovery
	Mice homozygous for the spontaneous waved 2 mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3a^vt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae.
001811	B6EiC3Sn a/A-Otc^spf-ash/J	Cryopreserved - Ready for recovery

002343	B6EiC3Sn a/A-Otc^spf/J	Cryopreserved - Ready for recovery

012889	B6N;TKDU-Myo5a^d Cacna2d2^du/J	Cryopreserved - Ready for recovery
	Mice homozygous for the ducky spontaneous mutation (Cacna2d2^du) show a waddling or reeling gait and a tendency to fall to one side. Homozygous mutant mice are slightly smaller than normal and may occasionally have seizures. Histologically, homozygotes show severe dysgenesis of hindbrain and spinal cord, myelin deficiency that is more marked the more caudad the CNS region, and demyelination and axonal dystrophy in selective fiber systems including the spinocerebellar and vestibulospinal tracts. There is a deficit of cerebrosides in the hindbrain and spinal cord, but other lipid classes are present in normal amounts relative to the size of the CNS. Viability is somewhat less than normal. Males living to maturity may be fertile, but are poor breeders. Females rarely breed. In mice homozygous for either Cacna2d2^du or Cacna2d2^du-2J, no loss of Purkinje cells or granular cells was seen by immunohistochemistry for calbindin or calretinin r ..... For more information please see the full phenotype on the strain data sheet
001274	BALB/c-Krt71^Ca-9J/J	Cryopreserved - Ready for recovery

001548	BALB/cBy x A/J-Crm^J/J	Cryopreserved - Ready for recovery
	Hemizygotes, and homozygotes have a pale yellow coat color and hemizygotes have a mottled pale yellow and albino white coat.
001755	BALB/cBy-Krt71^Ca-10J/J	Cryopreserved - Ready for recovery

007971	BALB/cJ-Ppp1r13l^wa3-J/J	Cryopreserved - Ready for recovery
	Homozygotes have a coat that is sparse but not wavy. They are born with their eyelids open and develop vascular corneas. They also develop early-onset cardiomyopathy, which leads to congestive heart failure. Female homozygotes have not successfully bred and male homozygotes have significantly reduced fertility, producing one or two litters in their lifetime at best.
013715	BALB/cJ-psds1l/GrsrJ	Cryopreserved - Ready for recovery
	psds1l homozygotes can be identified when their first coat grows in by the dirty white coat color and sparse hair. Hair is usually absent from around the eyes, which often have a crusty growth around them, and hair loss is commonly found around the cervical area.
000652	BDP/J	Cryopreserved - Ready for recovery

005736	BKS(Cg)-calre/GrsrJ	Cryopreserved - Ready for recovery
	The curly coat of this spontaneous homozygous mutant mouse (BKS.Cg m +/+ Lepr^db /J-calre/J) is recognized at 10-12 days of age when hair is fully covering the body. At 2 weeks of age the coat of homozygous mutants looks very curly, and the mutants also have curly vibrissae. After several weeks, the curly phenotype is reduced; the hair becomes fuzzy in appearance, and the vibrissae straighten out and appear normal. Some mutant mice have no whiskers at wean age. Also, in older homozygous and heterzygous mice more whiskers are lost, and homozygous mutants lose more hair as they age. Homozygous mutant mice live normal life spans and breed normally.
000700	BKS.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS Lepr^db homozygotes. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Lepr^db/+) also have increased metabolic ..... For more information please see the full phenotype on the strain data sheet
001049	BKS.Cg-mea^2J Dock7^m/+ +/J	Cryopreserved - Ready for recovery
	Mice homozygous for the meander tail 2J spontaneous mutation (mea^2J) have a phenotype that is very similar to the original meander tail (mea) and meander tail J mice (mea^J). Homozygous mutant mice have variably shortened and kinked tails. At about 2 weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygotes are smaller and less vigorous than wiltype controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This strain is maintained in linkage with the misty coat color mutation (Dock7^m).
001192	BKS.Cg-mea^J Lepr^db +/+ + Dock7^m/J	Cryopreserved - Ready for recovery
	Mice homozygous for the meander tail-J spontaneous mutation (mea^J) have variably shortened and kinked tails. At about two weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wild-type controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Lepr^db +/+ Dock7^m strain so it is also segregating for the diabetes (Lepr^db) and misty (Dock7^m) mutations. See strain description for Stock No. 000642 for more information.
000081	BXD25/TyJ	Cryopreserved - Ready for recovery
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
002662	C.Cg-Fech^m1Pas/J	Cryopreserved - Ready for recovery
	Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age.
008228	C3.129S7(B6)-Ifng^tm1Ts/J	Cryopreserved - Ready for recovery
	Leukocytes do not respond to and Th1 cells are not activated by skin grafts in homozygous mice. Homozygotes are resistant to experimentally induced alopecia areata with diminished T cell infiltration in skin and reduced MHC class I and II molecule expression in the hair follicle infrainfundibular site. No gene product (protein) is detected by ELISA analysis of splenocyte supernatants from homozygous animals. Mice that are homozygous 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 immune response, inflammation and autoimmunity.
000509	C3.Cg-Lyst^bg-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige 2J spontaneous mutation (Lyst^bg-2J) display characteristics very similar to the original beige mutation (Lyst^bg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet
000232	C3Fe.C3-Ap3b1^pe/J	Cryopreserved - Ready for recovery
	The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness.
002758	C3Fe.Cg-scb/J	Cryopreserved - Ready for recovery
	Scabby is a recessive mutation that maps to chromosome 8. Homozygotes display scar tissue on the skin and tail shortly after birth with defects in hair growth in these areas. Transverse stripes particularly over the rump may be seen in the juvenile coat, but are generally absent in the adult. Webbed feet and a short and kinky or constricted tail may also be seen. Homozygotes are viable and fertile although males breed better than females. (Searle and Beechey, 1977.)
000200	C3FeB6 A/A^w-J-Ank^ank/J	Cryopreserved - Ready for recovery
	The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting i ..... For more information please see the full phenotype on the strain data sheet
000225	C3FeLe.B6 a/a-Ptpn6^me/J	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000511	C3H/HeJ-Ap3d1^mh-2J/J	Cryopreserved - Ready for recovery
	The mh-2J allele of Ap3d causes a similar yet less severe pigment dilution than that caused by the mh allele, but each causes a different neurological phenotype. These homozygotes are recognizable by a lighter coat color and decreased pigmentation in the eyes. For the Ap3d^mh allele, this coat color dilution has been shown to result from smaller and fewer melanin granules in the hairs. While both alleles cause similar degrees of hyperactivity, the cochlear degeneration and accompanying head tilt is observed less frequently in the Ap3d^mh-2J homozygotes and the auditory evoked brain responses in these mice are similar to wildtype. At three months of age, mice homozygous for the Ap3d^mh allele have significantly increased auditory evoked potentials after the first of two paired tones. Ap3d^mh-2J homozygotes also show an increased response to the first tone, but this has not been proven with stat ..... For more information please see the full phenotype on the strain data sheet
001232	C3H/HeJ-Eda^Ta-5J/J	Cryopreserved - Ready for recovery

003161	C3H/HeJ-Hps3^coa-6J/J	Cryopreserved - Ready for recovery

000627	C3H/HeJ-Kit^W-x/J	Cryopreserved - Ready for recovery

003401	C3H/HeJ-Lpin1^fld-2J/J	Cryopreserved - Ready for recovery
	Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot analysis of sciatic nerve from two-to-three month old fld/fld mice showed a 7-13-fold reduction in myelin P₀, a vast increase in apoE, an increase in GAP-43, and no detectable myelin P₂. It was also noted that a ..... For more information please see the full phenotype on the strain data sheet
004806	C3H/HeJ-Mfs/J	Cryopreserved - Ready for recovery
	Both male and female mice homozygous or heterozygous for the Mfs mutation have a striped pattern in their coats that is visible by 3 weeks of age.
000809	C3H/HeJ-Mgrn1^md-2J/J	Cryopreserved - Ready for recovery

000223	C3H/HeJ-Mgrn1^md/J	Cryopreserved - Ready for recovery

002460	C3H/HeJ-Oca2^p-J Is(7;1)40H/J	Cryopreserved - Ready for recovery

000513	C3H/HeJ-Oca2^p-J/J	Cryopreserved - Ready for recovery
	Oca2^p-J/Oca2^p-J mice exhibit significant dilution of coat color with pink eyes, a phenotype similar to that produced by Oca2^p/Oca2^p. The Oca2^p-J mutation is a partial deletion of the gene that completely ablates Oca2^p function (Oakey et al. 1996).
000339	C3H/HeJ-Tyr^c-9J/J	Cryopreserved - Ready for recovery

001294	C3H/HeJ-Tyr^c-a/J	Cryopreserved - Ready for recovery

002441	C3H/HeJ-jal/J	Cryopreserved - Ready for recovery
	Mice homozygous for the juvenile alopecia mutation have curled vibrissae shortly after birth, are runted and have wavy hair. Foci of alopecia appear on the dorsal trunk by 18 days of age and hairs are bifurcated, grossly distorted and lack a cuticle. Hairs from heterozygotes have focal distortions and breaks.
001588	C3H/HeJ-jd/J	Cryopreserved - Ready for recovery

001544	C3H/HeJ-ruf/J	Cryopreserved - Ready for recovery

001529	C3H/HeSn-Paf/J	Cryopreserved - Ready for recovery
	X^Paf/X females have patchy or striped coats; X^Paf/Y males have a dark, shiny coat until hair loss begins between 12 and 30 days of age when the underfur is lost and the coat becomes sparse and bristly. X^Paf/X^Paf females initially have a dark shiny coat which looks like that of X^Paf/Y males although less bristly and sparse and appears more striped or patched than heterozygous females. Due to X-Y nondisjunction, approximately 1% of offspring from Paf/Y males are XXY phenotypic males and 19% are XO phenotypic females.
000120	C3H/HeSn-Rab27a^ash/J	Cryopreserved - Ready for recovery
	Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5a^d) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t ..... For more information please see the full phenotype on the strain data sheet
001551	C3H/HeSnJ x STOCK dds/J	Cryopreserved - Ready for recovery

001272	C3H/HeSnJ-A^hvy/J	Cryopreserved - Ready for recovery
	The dominant A^hvy allele has the broadest array of expressivity of any of the agouti alleles. Carriers' coat colors range from mostly yellow to almost completely black and the color is usually patchy or striped. Mice with coats on the yellow end of the spectrum tend to develop obesity while those with more black coats do not. Homozygotes are viable and fertile, and are more likely to have yellow or mostly yellow coats than are heterozygotes. A^hvy is recessive to A^y, dominant to a and a^e, and results in an increase in the yellow pigment in the belly coat of A^hvy/a^t and A^hvy/A^w mice.
001310	C3H/HeSnJ-Slc7a11^sut/J	Cryopreserved - Ready for recovery

002261	C3H/HeSnJ-Sox18^Ra-J/J	Cryopreserved - Ready for recovery
	The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18^Ra/+ coats have l ..... For more information please see the full phenotype on the strain data sheet
002333	C3H/HeSnJ-gri/J	Cryopreserved - Ready for recovery
	On an agouti background gri homozygotes resemble Tyr^c-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.)
001434	C3HeB/FeJ x STX/Le-Mc1r^E-so Gli3^Xt-J Zeb1^Tw/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the twirler mutation (Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1r^E-so) and extra toes-Jackson (Gli3^St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E ..... For more information please see the full phenotype on the strain data sheet
000099	C3HeB/FeJ-A^vy/J	Cryopreserved - Ready for recovery
	Homozygotes (A^vy/A^vy) and heterozygotes (A^vy/A and A^vy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. A^vy resembles AP^y in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in A^vy/a mice of mottled phenotype but not in those of agout ..... For more information please see the full phenotype on the strain data sheet
000069	C3HeB/FeJ-Atrn^mg-3J/J	Cryopreserved - Ready for recovery
	Attractin (ATRN) deficiencies cause darkened pigmentation, increased locomotor activity, decreased body weight, and vacuolization and myelination defects in the central nervous system. Agouti protein competes with alpha-melanocyte stimulating hormone (a-MSH) for binding of melanocortin 1 receptor (MC1R), and this in turn signals pigment type switching from eumelanin production to pheomelanin production. ATRN interacts with agouti possibly to facilitate the interaction with MC1R. In mice, ATRN deficiencies result in decreased pheomelanin production causing darkened ears, tail, feet, and coat color which becomes dark reddish brown as these mice age. Thus, the initial Atrn mutation reported by Lane and Green was called mahogany (mg). ATRN deficiencies darken the coloring caused by nonagouti such that these mice are coal black with no white hairs behind the ears or around the perineum and have blacker ears, tail, and feet. ATRN deficiency can suppress the impact on coat co ..... For more information please see the full phenotype on the strain data sheet
006045	C3HeB/FeJ-Eif3c^Xsl/GrsrJ	Cryopreserved - Ready for recovery
	Xsl heterozygotes are smaller than normal at 3 weeks of age but catch up to normal size by 6 weeks of age. They have a belly spot and extra digits at the thumb position on one or both front paws.
001533	C3HeB/FeJ-Mc1r^E-so Gli3^Xt-J/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the extra toes-J spontaneous mutation (Gli3^Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. This strain is homozygous for the sombre mutation (Mc1r^E-so).
001292	C3HeB/FeJ-vs/J	Cryopreserved - Ready for recovery

000847	C3Sn.B6-Kit^W-39J/J	Cryopreserved - Ready for recovery

004135	C3Sn.CAST-Atrn^mg-6J/J	Cryopreserved - Ready for recovery
	Attractin (ATRN) deficiencies cause darkened pigmentation, increased locomotor activity, decreased body weight, and vacuolization and myelination defects in the central nervous system. Agouti protein competes with alpha-melanocyte stimulating hormone (a-MSH) for binding of melanocortin 1 receptor (MC1R), and this in turn signals pigment type switching from eumelanin production to pheomelanin production. ATRN interacts with agouti possibly to facilitate the interaction with MC1R. In mice, ATRN deficiencies result in decreased pheomelanin production causing darkened ears, tail, feet, and coat color which becomes dark reddish brown as these mice age. Thus, the initial Atrn mutation reported by Lane and Green was called mahogany (mg). ATRN deficiencies darken the coloring caused by nonagouti such that these mice are coal black with no white hairs behind the ears or around the perineum and have blacker ears, tail, and feet. ATRN deficiency can suppress the impact on coa ..... For more information please see the full phenotype on the strain data sheet
001380	C3Sn.Cg-Kitl^Sl-con/J	Cryopreserved - Ready for recovery
	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.
001517	C3Sn.Peru-rs^grc/J	Cryopreserved - Ready for recovery

003100	C3Sn;129-Del(10AI646023-Ggt5)1Bayer/J	Cryopreserved - Ready for recovery
	The dwarf-Bayer mutation (dwg^Bayer) occurred spontaneously in an embryonic stem cell line during genetic targeting of the insulin receptor gene. The phenotype of the mice resemble drawf grey (dwg, Stock No. 001743) and subsequent characterization determined that the two mutations are allelic. Homozygous mutant mice are grey and smaller in size than wildtype littermates.
001942	C57BL-Bloc1s3^rp/J	Cryopreserved - Ready for recovery
	The reduced pigmentation (rp) mutation causes defects in organelle biogenesis. On a non-agouti background, mice homozygous for the recessive rp mutation have lighter coat color, pale ears and tail, and the eyes are dark. This coat color is similar in intensity to that caused by the cocoa or ruby eye-2 mutations, and there is no change in coloration with age. Homozygotes are viable and fertile, but have an increased bleed time, decreased splenic NK cell activity, and the melanosomes fail to properly mature (Gibb et al., 1981; Ahmed et al., 1989). There are fewer ellipsoidal type IV melanosomes, and the striated melanosomes are elongated but irregularly shaped indicating that rp disrupts the melanosomal maturation step II (Nguyen et al., 2002). These pigment granules are smaller than normal, but they are not found clumped together. Increased beta-galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase activities are found in kidney homogenates of > ..... For more information please see the full phenotype on the strain data sheet
001002	C57BL/10SnJ-Tyr^c-11J/J	Cryopreserved - Ready for recovery

002566	C57BL/6-Atp7a^Mo-br/J	Cryopreserved - Ready for recovery
	Heterozygous females carrying the brindled allele (Atp7a^Mo-br) are very similar to mottled heterozygous females (Atp7a^Mo/+) in appearance but have normal viability. They have curly vibrissae, but the coat is not noticeably waved. Hemizygous males are almost devoid of pigment except in the eyes and ears. The vibrissae are strongly curled, and the coat is wavy. Males usually die by two weeks of age, but a few have lived and been fertile. They have a behavioral abnormality consisting of a slight tremor, uncoordinated gait, and clasping of the hindfeet when held up by the tail. Histological examination of the brain of brindled males shows widespread neuronal degeneration in the cerebral cortex and thalamic nuclei and scattered degeneration in the cerebellum. Heterozygous females have been shown to have neurochemical abnormalities as well. In contrast to mice bearing other Atp7a alleles, brindled mice have no aortic lesions and no defect in crossli ..... For more information please see the full phenotype on the strain data sheet
002197	C57BL/6-Col1a1^Mov13/J	Cryopreserved - Ready for recovery
	The integration of the M-MuLV genome near the 5' end of the Col1a1 gene blocks transcription of the gene from this locus. Mice homozygous for this mutation suffer from arrested development at day 12 and die at about embryonic day 13-14. Heterozygotes in our colony rarely survived to 8 months of age. Many died at less than 3 months of age.
000338	C57BL/6J A^w-J-Eda^Ta-6J/J	Cryopreserved - Ready for recovery

000258	C57BL/6J-Aⁱ/a/J	Cryopreserved - Ready for recovery

000774	C57BL/6J-A^sy/a/J	Cryopreserved - Ready for recovery

000569	C57BL/6J-A^w-J-Eda^Ta +/+ Ar^Tfm/J	Cryopreserved - Ready for recovery
	Testicular feminization (Ar^Tfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby mutation (Eda^Ta) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
000519	C57BL/6J-Dsg3^bal/J	Cryopreserved - Ready for recovery

007711	C57BL/6J-Hps3^coa-8J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the cocoa 8 Jackson mutation have hypopigmentation resulting in a diluted coat color and pale ears, feet and tail.
000542	C57BL/6J-Hps5^ru2-J/J	Cryopreserved - Ready for recovery

000166	C57BL/6J-Kit^W-17J/J	Cryopreserved - Ready for recovery

000167	C57BL/6J-Kit^W-18J/J	Cryopreserved - Ready for recovery

000169	C57BL/6J-Kit^W-20J/J	Cryopreserved - Ready for recovery

000117	C57BL/6J-Kit^W-34J/J	Cryopreserved - Ready for recovery

000128	C57BL/6J-Kit^W-35J/J	Cryopreserved - Ready for recovery

000134	C57BL/6J-Kit^W-37J/J	Cryopreserved - Ready for recovery

000062	C57BL/6J-Kit^W-39J/J	Cryopreserved - Ready for recovery

000121	C57BL/6J-Kit^W-40J/J	Cryopreserved - Ready for recovery

000119	C57BL/6J-Kit^W-41J/J	Cryopreserved - Ready for recovery

000127	C57BL/6J-Kit^W-42J/J	Cryopreserved - Ready for recovery

000129	C57BL/6J-Kit^W-43J/J	Cryopreserved - Ready for recovery

000990	C57BL/6J-Kit^W-55J/J	Cryopreserved - Ready for recovery

001179	C57BL/6J-Kit^W-62J/J	Cryopreserved - Ready for recovery

003252	C57BL/6J-Kitl^Sl-20J/J	Cryopreserved - Ready for recovery
	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.
000529	C57BL/6J-Lbr^ic-J/J	Cryopreserved - Ready for recovery
	Lbr^ic-J/Lbr^ic-J homozygotes can be identified at 2 weeks of age due to sparse fur and at 3-4 weeks of age scales develop on the tail and, to a lesser degree, on the trunk. These mutants are smaller than their wild type siblings. The mutants develop mild epidermal hyperplasia with orthokeratotic hyperkeratosis and dilation of the piliary canals. Homozygotes have an increased incidence of syndactyly and hydrocephaly, and a high prenatal mortality rate. Aberrant morphology of nuclear heterochromatin occurs in lymphocytes, neutrophils, eosinophils, intestinal epithelium, and cerebellar granule cells. Electron microscopy reveals clumps of heterochromatin at the periphery of the nucleus within splenic lymphocytes. These mice are a model for Pelger-Huet anomaly, which is associated with mutations in LBR, although the skin pathology is specific to the mouse mutation. (Eicher, 1976; Hoffmann et al., 2002; Shultz et al., 2003.)
000060	C57BL/6J-Mc1r^e/J	Cryopreserved - Ready for recovery

002611	C57BL/6J-Mitf^mi-bws/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption.
000540	C57BL/6J-Mpzl3^rc/J	Cryopreserved - Ready for recovery
	The rough coat (Mpzl3^rc) mutation is recessive and fully penetrant. Homozygotes have an unkempt coat appearance and gradual hair loss that becomes extensive. As early as two weeks of age, thinning fur can be seen, and the hair becomes brittle, clumpy and oily in appearance. Homozygotes are fertile. (Lane 1966; Ruvinsky et al., 2002.)
001136	C57BL/6J-Oca2^p-un+2J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001506	C57BL/6J-Oca2^p-un+3J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001810	C57BL/6J-Oca2^p-un+4J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001513	C57BL/6J-Oca2^p-un+5J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001499	C57BL/6J-Oca2^p-un+6J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001033	C57BL/6J-Oca2^p-un+J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes of this revertant allele are phenotypically indistinguishable from wild-type.
000028	C57BL/6J-Oca2^p-un/J	Cryopreserved - Ready for recovery
	The pink-eyed unstable (Oca2^p-un) mutation comprises a 70-kb, head-to-tail duplication of a transcribed region of the Oca2^p gene. Oca2^p-un homozygotes have a greatly diluted coat color and pink eyes; however, approximately 3.5% of Oca2^p-un/Oca2^p-un mice are mosaic for wild-type coat color (Melvold et al., 1971) because of somatic reversion of the mutation involving loss of the duplicated segment (Brilliant et al.1991, Gondo et al. 1993).
001672	C57BL/6J-Otc^spf-J/J	Cryopreserved - Ready for recovery

000565	C57BL/6J-Pax3^Sp-d/J	Cryopreserved - Ready for recovery
	Mice homozygous for the splotch-delayed spontaneous mutation (Pax3^Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3^Sp, Stock No. 002469). Splotch-delayed homozygous embryos survive to birth, compared to splotch mutant embryos that die at E13 due to neural tube defects. Homozygous splotch-delayed mutant embryos display caudal rachischisis only. Heterozygous splotch-delayed have a white belly spot. Delayed splotch is a point mutation within the paired domain of Pax3. This impairs DNA binding of this domain and also, suprisingly, of the homeodomain, not directly affected in the mutant gene.
000118	C57BL/6J-Ph/J	Cryopreserved - Ready for recovery

010825	C57BL/6J-Ptpn6^me/SzJ	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
000976	C57BL/6J-Rab38^cht/J	Cryopreserved - Ready for recovery
	On the C57BL/6J background Rab38^cht/Rab38^cht mice have a rich dark chocolate coat color instead of the normal black coat. This can be difficult to distinguish, but is made easier by the lightened color in the ear pinnae and tail. At birth the eyes of Rab38^cht/Rab38^cht mice are lighter in color than wild type C57BL/6J mice. The melanosomes in melanocytes cultured from newborn C57BL/6J mice are oval and intensely black while those of chocolate mice are circular and brown. The end-stage melanosomes of chocolate mice contain less TYRP1 than do wild type mice. Mutations in Tyrp1 result in increased brown rather than black pigment. Thus, Loftus et al. have hypothesized that the chocolate mutation results in decreased black pigmentation because RAB38 is important in the vesicular trafficking that moves TYRP1 from the trans-Golgi network to the end-stage melanosome. Many of the pigment diluting mutations with ..... For more information please see the full phenotype on the strain data sheet
000110	C57BL/6J-Rabggta^gm/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Rabggta^gm allele are grayish-black on a non-agouti background due to pigment dilution. Eye color is not affected. Homozygotes have reduced viability and do not breed well. These mutants have a prolonged bleeding time. Although gunmetal mice have an increased number of megakariocytes, they have about half the number platelets found in wildtype siblings. This decrease in platelet number results from a slower rate of platelet synthesis. These platelets are heterogeneous in size and are larger than normal, but have fewer dense granules per platelet and approximately half of the normal level of serotonin. The prolonged bleeding time and decreased platelet count and volume can be transferred to wildtype mice through bone marrow transplantion. Likewise bone marrow transplants from wildtype mice reversed the platelet deficiency in gunmetal recipients. Western blots of platelet extracts showed a decrease in fibrinogen, von Willebrand factor, and platel ..... For more information please see the full phenotype on the strain data sheet
005482	C57BL/6J-Shar/J	Cryopreserved - Ready for recovery
	By 3 weeks of age mice carrying the dominant Shar mutation have a shiny and rough coat that has a greasy appearance.
000219	C57BL/6J-Slc30a4^lm/J	Cryopreserved - Ready for recovery
	Female mice homozygous for the lethal milk mutation (Slc30a4^lm, formerly Znt4^lm) produce milk that is lethal to mice nursed during the first week of life and detrimental to mice nursed thereafter. The lethal and detrimental effects are due to a deficiency of zinc in the milk. If foster nursed on normal dams, lethal milk homozygotes survive and become reproductively mature. Zinc supplementation of the drinking water of dams enables them to nurse their young successfully. All homozygous mutant mice lack utricular otoliths and this defect is not prevented by zinc supplementation. They have varying loss of saccular otoliths and show mild behavioral abnormalities related to the otolith defect. Homozygotes over eight months of age show progressive hair loss, dermatitis, and skin lesions, symptoms of zinc deficiency.
000570	C57BL/6J-Slc45a2^uw Adamts20^bt-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive Adamts20^bt-2J mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt.
000003	C57BL/6J-Slc45a2^uw/J	Cryopreserved - Ready for recovery

005135	C57BL/6J-Sls/GrsrJ	Cryopreserved - Ready for recovery

000068	C57BL/6J-Tyrp1^b-J/J	Cryopreserved - Ready for recovery

000520	C57BL/6J-Vps33a^bf/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive buff (Vps33a^bf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33^bf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al. found n ..... For more information please see the full phenotype on the strain data sheet
000055	C57BL/6J-a^t-33J/J	Cryopreserved - Ready for recovery

000070	C57BL/6J-a^td/J	Cryopreserved - Ready for recovery

006107	C57BL/6J-rslk^2J/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes have white spotting and a diluted gray coat color.
000108	C57BL/6J-sea/J	Cryopreserved - Ready for recovery
	Mice homozygous for the sepia (sea) mutation have a pigment dilution that is similar to but not as severe as that of beige (Lyst^bg) mutants. On a nonagouti background sea/sea mice have lighter colored coat, ears and tail relative to their heterozygous and wildtype siblings, but do not have a detectable dilution in eye pigment at birth (Sweet and Lane, 1977). Unlike other coat color dilution mutations (including beige, reduced pigmentation, pallid, and pale ear) sepia mice do not have a diminution in NK cell activity (Orn et al., 1982).
001009	C57BL/6J-tp^3J/J	Cryopreserved - Ready for recovery
	Taupe is a recessive spontaneous mutation that causes a lightening of the coat color such that a/a tp/tp mice are slate grey. The coat color is similar to that of the ruby (ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. tp/tp females do not have normal nipple development, although the mammary ducts and alveoli develop normally. These females also have difficulty with pregnancy and birth. They can not rear their pups even if the pups are born alive so this strain is maintained by breeding heterozygous females to homozygous males. (Fielder, 1952; Fielder, 1950.)
003655	C57BL/6JEi-wn^J/J	Cryopreserved - Ready for recovery
	Homozygotes have white spots on a black coat background. The hair, skin, and tail have the large white spots.
007599	C57BL/KaLawRij-Sharpin^cpdm/RijSunJ	Cryopreserved - Ready for recovery
	Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. Mice appear runted and life span is shortened. In addition to dermatitis, homozygotes exhibit multi-organ inflammation with eosinophilia, defective TH1 cytokine production, splenomegaly, absent Peyer's patches (adult), diminished serum immunoglobulins, and an absence of B cell follicles, follicular dendritic cells, and germinal centers in secondary lymph organs. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation, and secondary lymphoid organ deveopment.
000144	C57BLKS-sch/J	Cryopreserved - Ready for recovery

000707	CBA.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	Lepr^db/Lepr^db mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months (Leiter EH et al, 1981). Because of the sterility of Lepr^db homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Lepr^db +/+ Dock7^m) facilitates identification of heterozygotes for breeding, while the coupling ..... For more information please see the full phenotype on the strain data sheet
000813	CBA/J-Atp7a^Mo-pew/J	Cryopreserved - Ready for recovery
	The Atp7 genes encode Cu2⁺ ATPases. Atp7a is the mouse ortholog of the human ATP7A gene, which is mutated in children with Menke's syndrome. The range of defects in both Menke's syndrome and in mice having mutations of Atp7a--the mottled series of mutants--are due to deficiencies in a number of copper-requiring enzymes, in turn attributed to an intracellular copper transport defect. Thus, it is likely that the Atp7a gene product functions as a copper transport protein. (For brief review and references, see Levinson et al., 1994.) Atp7a^Mo-pew, the mottled-pewter mutation, has the mildest effect of the known mutations at this locus. The sole phenotype noted in hemizygous males and homozygous females is their pale, silvery gray coat color. The coats of affected mice of both sexes are initially agouti; males become pewter by about 4 weeks and females at 5-6 weeks of age. Heterozygous females have normal, agouti coats throug ..... For more information please see the full phenotype on the strain data sheet
001006	CBA/J-Tyr^c-10J/J	Cryopreserved - Ready for recovery

003398	CBA/J-dal/GrsrJ	Cryopreserved - Ready for recovery
	Dark-like dal is a recessive mutation causing a darkened coat color, smaller size, gonad abnormalities, and dark staining urine. dal maps to Chromosome 7 and a previously described mutation named dark da maps to the same chromosomal region. Dark-like may be a remutation to dark da.However a test for allelism is not possible because dark is thought to be extinct. Mice homozygous for the dal mutation are easily recognized by 14 days of age by their darkened coats and smaller size. Some homozygotes appear, both phenotypically and pathologically (dense bones), to have skeletal abnormalities however X-rays appear normal. At 7 months of age females had no follicles and many corpora lutea and males mild testicular degeneration with increased Leydig cells. Serum assays for Albumin, BUN, Creatine, Bilirubin, and iron showed no significant differences from controls.
000965	CBACa.C3-Kit^W-x/J	Cryopreserved - Ready for recovery

005274	CBACaGnLe.Cg-Xls/GrsrJ	Cryopreserved - Ready for recovery
	The dominant mutation X-linked stripe seems to be a hemizygous lethal mutation since no affected males have been observed. On this CBA background, heterozygous females have an agouti coat color with stripes and a white patch on the left hind flank.
001723	CByJ.A-Ttc7^fsn/J	Cryopreserved - Ready for recovery
	Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G ..... For more information please see the full phenotype on the strain data sheet
000711	CByJ.Cg-Foxn1^nu/J	Cryopreserved - Ready for recovery
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d ..... For more information please see the full phenotype on the strain data sheet
002839	CByJ.LAH-Dsg4^lah/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Dsg4^lah mutation have thicker, stiffer skin and a fine scale within a few days of birth. The epidermal keratinocytes have a hyperproliferative phenotype. These mice fail to develop normal fur, and have alopecia and shortened vibrissae. Although all hair types are found, the hair is very sparse and is shorter and more rough than normal. Rather than the normal gradual transition of keratinocytes from proliferation to differentiation in the lower hair follicle, the lanceolate hair mice show a premature, abrupt switch. Above the melanogenic zone, a swelling forms that subsequently is pushed out by continued growth of the hair shaft to become the distal tip of the hair. Lanceolate hair mice take their name from the resulting lance-head shape of the hair. Homozygotes can breed, but heterozygous females are better mothers than homozygotes. Unlike Dsg4^lah-J homozygotes, Dsg4^lah homozygotes do not have growth re ..... For more information please see the full phenotype on the strain data sheet
000293	CHMU/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the congenital hydrocephalus (Foxc1^ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Muted^mu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldn^pa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths ..... For more information please see the full phenotype on the strain data sheet
000284	CWD/LeJ	Cryopreserved - Ready for recovery

002922	D2.HRS-Hr^hr/J	Cryopreserved - Ready for recovery

002531	DBA/1LacJ-Ap3b1^pe-7J/J	Cryopreserved - Ready for recovery

002838	DBA/1LacJ-Dsg4^lah-J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Dsg4^lah-J mutation completely lack vibrissae and develop only very short hair that resembles peach fuzz. This is lost by a few months of age, leaving these mice bald. They are runted from birth throughout life. These mice have hyperplasia in the interfollicular epidermis that leads to thickened skin, and their skin wrinkles as they age. Transmission electron micrographs of epidermis from Dsg4^lah-J homozygotes reveals acantholysis with small, poorly formed, and dislodged desmosomes. Rather than the normal gradual transition of keratinocytes from proliferation to differentiation in the lower hair follicle, the lanceolate hair mice show a premature, abrupt switch. Above the melanogenic zone a swelling forms that subsequently is pushed out by continued growth of the hair shaft to become the distal tip of the hair. Lanceolate hair mice take their name from the resulting lance-head shape of the hair. The less severely affect ..... For more information please see the full phenotype on the strain data sheet
002304	DBA/1LacJ-Scd1^ab-2J/J	Cryopreserved - Ready for recovery
	The overall appearance of mice homozygous for either the Scd1^ab-J allele or the Scd1^ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1^ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1^ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an i ..... For more information please see the full phenotype on the strain data sheet
002510	DBA/2J-Ap3b1^pe-8J/J	Cryopreserved - Ready for recovery
	Appearance: Ap3b1^pe-8J/Ap3b1^pe-8J, lighter brown than normal DBA/2J mice.
001594	DBA/2J-Dtnbp1^sdy/J	Cryopreserved - Ready for recovery
	The autosomal recessive mutation sandy (sdy) takes its name from the lightened coat color first identified on the DBA/2J background. As early as 7-8 days of age the pinnae, feet, tail and fur are lighter in color than those of wildtype littermates and the lack of eye pigment is a defining trait at birth. The eye color does not darken with age unlike muted (mu) homozygotes. On the agouti C3H background, sandy homozygotes look like muted homozygotes, but on the non-agouti C57BL/6J or DBA/2J backgrounds, sandy homozygotes look like pallid (Pldn^pa) homozygotes. The reduced pigmentation is linked to a storage pool deficiency. Sandy homozygotes have a prolonged bleeding time, in excess of 15 minutes, yet have normal platelet counts and normal sized platelets. Electron microscopy detects very few, if any, dense granules present in individual platelets of sandy homozygotes. Those that are detected are of normal size. Platelet serotonin levels are 7% that ..... For more information please see the full phenotype on the strain data sheet
000963	DBA/2J-Myo5a^d+17J/Myo5a^d/J	Cryopreserved - Ready for recovery

000964	DBA/2J-Myo5a^d+18J/Myo5a^d/J	Cryopreserved - Ready for recovery

000067	DBA/2J-Myo5a^d+2J/Myo5a^d/J	Cryopreserved - Ready for recovery

001789	DBA/2J-ge/J	Cryopreserved - Ready for recovery

000252	DC/LeJ	Cryopreserved - Ready for recovery
	Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004).
000253	DLS/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the dilute-lethal spontaneous mutation (Myo5a^d-l) display a severe neuromuscular disorder characterized by convulsions and opisthotonus. Homozygous mutant mice usually die by approximately 3 weeks of age. Dilute lethal homozygotes lack smooth endoplasmic reticulum in the dendritic spine of Purkinje cells causing an absence of intracellular calcium. Loss of this intracellular calcium may be the cause of dilute-lethal neurological symptoms. Homozygous dilute-neurological mutant mice (Myo5a^d-n, Stock No. 001013) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal homozygotes. In this DLS/Le inbred strain the dilute-lethal mutation is maintained in repulsion with short ear (Bmp^se), closely linked mutations on Chromosome 9.
000643	DW/J Mlph^ln Pou1f1^dw/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1^dw) are characterized by severe dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary.
001595	DW/J-Acd^acd/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
000092	FL/1Re-Kit^W/J	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
000023	FL/1ReJ	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
000619	FS/EiJ	Cryopreserved - Ready for recovery
	The FS/Ei strain was originally used as a linkage testing stock for gene mapping. It is homozygous for several visible recessive mutations including brown (Tyrp1^b), pink-eyed dilution (Oca2^p), chinchilla (Tyr^c-ch), frizzy (fr), and the neurological mutation shaker 1 (Myo7a^sh1). It is also homozygous for a couple allelic variants that can be easily typed (Mod2^b and Hbb^d). Mice homozygous for the shaker 1 show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist ..... For more information please see the full phenotype on the strain data sheet
006125	FVB-Tg(H2-D-Il15)3304Clgr/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this transgene are viable and fertile. The transgene was designed to optimize the overexpression of secreted, mature interleukin-15. Transgenic IL-15 expression has a similar tissue distribution as the endogenous gene, but at a significantly higher level. IL-15 protein is detectable in the serum from most mutant, but not from wildtype, mice. Mutant mice develop a progressive alopecia by as early as 5-6 weeks of age, with skin lesions appearing over time. While all transgenic mice exhibit early polyclonal/benign expansion of natural killer and memory CD8⁺ T lymphocytes (T/NK), two distinct phenotypes emerge over time: approximately 70% of the transgenic mice will exhibit polyclonal T/NK progression in multiple tissues, while the remaining 30% are characterized by T/NK clonal expansion in multiple tissues and acute lymphoblastic leukemia (T/NK ALL). Both T/NK phenotypes are fatal within the first year of life. Mice harboring this transgene may be useful in ..... For more information please see the full phenotype on the strain data sheet
006822	FVB-Tg(KRT14-MAP2K1/Esr1)12Pkha/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this "K14-Mek1:ER" transgene are viable and fertile, with expression of the Mek1:ER fusion protein (a constitutively active mutant region from human mitogen activated protein kinase-kinase 1 (Mek1^R4F; containing an amino-terminal deletion of aa 32-51 and the S218E/S222D substitutions) fused at its carboxy terminal with the G525R mutant murine estrogen receptor ligand binding domain (ER^TM)) directed to epidermis by the human keratin 14 promoter. Because of the ER^TM region of the fusion protein, Mek1:ER is restricted to the cytoplasm and the biochemical activity of the Mek1:ER fusion gene can be induced following tamoxifen administration. For example, induction of this constitutively active form of human Map2k1 (Mek1^R4F) promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal neoplasia in as few as 5 days (including hyperplasia, increased levels of phosphorylated ERK1/2, increased mitot ..... For more information please see the full phenotype on the strain data sheet
005705	FVB-Tg(KRT14-Vegfa)3Dtm/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the transgene are viable and fertile. Transgene expression is demonstrated in the basal keratinocyte layer of the epidermis and outer root sheath keratinocytes of hair follicles. Homozygous mice spontaneously develop severe psoriasis-like lesions between 3-6 months of age, where hemizygous mice do not. Transgenic mice have increased density of tortuous cutaneous blood capillaries with elevated expression of select VEGF receptors, most prominently in neonates. Dermal mast cell localization and capillary hyperpermeability are also increased. Postcapillary venules exhibit significantly enhanced leukocyte rolling and adhesion. Transgenic expression promotes lymphangiogenesis associated not only with delayed-type hypersensitivity induced psoriasis-like skin inflammation but also with cutaneous tissue repair after wounding. Further, transgenic mice have accelerated chemically induced skin carcinogenesis with tumor associated lymphangiogenesis and angiogenesis. Elevated me ..... For more information please see the full phenotype on the strain data sheet
011032	FVB/N-Tg(Hoxc13)61B1Awg/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the transgene mice are viable, fertile and overexpress HOXC13. At birth, transgenic mice can be identified by a short tail (reduced number of verterbrae), taut skin, kinky whiskers and small size. By 4.5 months, mice exhibit retarded coat hair growth, followed by progressive alopecia and a hyperproliferative disorder resembling ichthyosis. Both cellular and squamous epidermal layers appear thickened, irregular and disorganized. Hair follicles are enlarged, and, in older mice, many follicles degenerate into cyst-like structures.
002961	FVB/N-Tg(KRT10BMP6)VI632Mbl Chr Y^FVB/N/J	Cryopreserved - Ready for recovery
	Male mice carrying the VI632 transgene incorporated on the Y chromosome appear normal at birth, but begin to show skin abnormalities at about 6 days of age. Inflammatory lesions develop by 2-3 weeks of age. The skin condition progressively worsens and is characterized by hair loss, flaky skin, and nail abnormalities.
002714	FVB/NJ-Crm^3J/J	Cryopreserved - Ready for recovery
	Hemizygous males and homozygous females are pale yellow and heterozygous females are mosaic, pale yellow and albino. Under long wave ultraviolet light the coats of these mutants fluoresce and heterozygous females show a mosaic fluorescence. This mutation is only visible on mice with an otherwise white coat.
000255	GL/Le Edar^dl-J +/+ Ostm1^gl/J	Cryopreserved - Ready for recovery
	Mice homozygous for the grey-lethal spontaneous mutation (Ostm1^gl) are characterized by osteopetrosis. Homozygous mutant mice are anemic, have a reduced white cell count, early thymic involution, and deficient calcium regulation. Homozygotes lack the power of secondary bone resorption. Consequently, the bones cannot grow normally, they do not form normal marrow cavities, and the teeth do not erupt.
001057	HPT/LeJ	Cryopreserved - Ready for recovery

000673	HRS/J	Cryopreserved - Ready for recovery
	Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an ather ..... For more information please see the full phenotype on the strain data sheet
001103	HRS/J-Hr^hr Esd^b/+ Esd^b/J	Cryopreserved - Ready for recovery
	Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization.
000494	J.Cg-Oca2⁺ Tyr⁺ Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
000259	JE/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the jerker spontaneous mutation (Espn^je) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes ar ..... For more information please see the full phenotype on the strain data sheet
000260	JGBF/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive buff (Vps33a^bf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33a^bf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al.> ..... For more information please see the full phenotype on the strain data sheet
000072	JGBF/LeTyJ	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive buff (Vps33a^bf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33a^bf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al. ..... For more information please see the full phenotype on the strain data sheet
000572	JIGR/DnJ	Cryopreserved - Ready for recovery
	JIGR/Dn is maintained with jittery (Atcay^ji) and grizzled (gr) in repulsion. Atcay^ji homozygotes can first be identified at approximately 12 days of age by a leaning, zig-zag gait when they attempt to run and by the difficulty they have righting themselves when placed on their backs. Disease progression is rapid such that within two more days mutants are found to crouch on their heels in a squatting position and can not run without falling. Within three to four days of the first symptoms, tetany is seen during exertion or excitement. This is initially most pronounced in the forelegs, which the mice beat up and down during these two- to three-second spasms. Failure to gain weight is seen by the third week of life and it is unclear whether this results from an inability to take in food. The severity and frequency of tetany increases, and during the fourth week weight loss and increased weakness precede death. The mean age of death is approxi ..... For more information please see the full phenotype on the strain data sheet
000289	LDJ/LeJ	Cryopreserved - Ready for recovery
	Attractin (ATRN) deficiencies cause darkened pigmentation, increased locomotor activity, decreased body weight, and vacuolization and myelination defects in the central nervous system. Agouti protein competes with alpha-melanocyte stimulating hormone (a-MSH) for binding of melanocortin 1 receptor (MC1R), and this in turn signals pigment type switching from eumelanin production to pheomelanin production. ATRN interacts with agouti possibly to facilitate the interaction with MC1R. In mice, ATRN deficiencies result in decreased pheomelanin production causing darkened ears, tail, feet, and coat color which becomes dark reddish brown as these mice age. Thus, the initial Atrn mutation reported by Lane and Green was called mahogany (Atrn^mg). ATRN deficiencies darken the coloring caused by nonagouti such that these mice are coal black with no white hairs behind the ears or around the perineum and have blacker ears, tail, and feet. ATRN deficiency can suppress the i ..... For more information please see the full phenotype on the strain data sheet
000262	LS/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the lethal spotting mutation (Edn3^ls) resemble piebald mice (Ednrb^s/Ednrb^s) mice. Homozygous mutant mice exhibit considerable white spotting and like homozygotes for the piebald-lethal allele (Ednrb^s-l) usually develop megacolon. Lethal spotting mutant mice usually die in the third week of life from the megacolon abnormality, which is associated with deficiency of intrinsic ganglion cells in the lower colon. A few homozygotes may survive and breed. This strain is also homozygous for the black and tan coat color mutation (a^t).
001850	MEV-Q/TyJ	Cryopreserved - Ready for recovery
	In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. This strain is also homozygous for nonagouti (a). Further analysis of MEV/1Ty progeny identified subsequent MuLV provirus re-insertions that were used to ..... For more information please see the full phenotype on the strain data sheet
001855	MEV-V/TyJ	Cryopreserved - Ready for recovery
	In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. This strain is also homozygous for nonagouti (a). Further analysis of MEV/1Ty progeny identified subsequent MuLV provirus re-insertions that were used to ..... For more information please see the full phenotype on the strain data sheet
003345	MEV/2Ty-Emv64/J	Cryopreserved - Ready for recovery
	In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. MEV/1Ty is also homozygous for nonagouti (a). Because Emv13 and Emv25 could not be distinguished using PvuII digests, thus requiring instead Hind ..... For more information please see the full phenotype on the strain data sheet
003896	MRL/MpJ Fas^lpr-Foxq1^sa-J/J	Cryopreserved - Ready for recovery
	MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/M ..... For more information please see the full phenotype on the strain data sheet
013782	MRL/MpJ-aphl/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes can be identified as early as 7 to 8 days of age when the first coat comes in. The hair growth is sparse and grows in stripes with bald areas between. The areas around the eyes often develop a mild, crusty growth and rash. All four hair types are present. Of two homozygotes tested both display a low cone response by electroretinograph.
000265	MY/HuLeJ	Cryopreserved - Ready for recovery

002281	NFS.C58-Tyr⁺/J	Cryopreserved - Ready for recovery

003091	NH/KiPtJ	Cryopreserved - Ready for recovery

016897	NOD.129S7(B6)-Itgb2^tm2Bay/CgkJ	Cryopreserved - Ready for recovery
	Commonly called NOD.CD18, mice homozygous for the Itgb2^tm2Bay targeted mutation are viable and fertile. Homozygous females are poor breeders, often producing 1 litter prior to becoming non-productive. Examination, of uterine horns, indicates poor healing post partum (unpublished communication). Unlike C57BL/6 mutant (Stock No. 003329) mice, congenic NOD Itgb2 mutant mice do not develop dermatitis or facial submandibular erosions. Similar to the C57BL/6 mutant, the congenic NOD Itgb2 mutant displays splenomegaly and lymphadenopathy. Splenic cells of NOD mutant mice exhibit significantly increased levels of CD29 and significantly decreased levels of Cd62L and the absence of CD11a and CD18. NOD mutant mice are resistant to diabetes to 34 weeks of age. Histological evaluation of the pancreas, at 18 weeks of age, reveals no insulitis. This strain may be useful for in vivo analysis of leukocyte integrin-dependent adhesion in inflammatory d ..... For more information please see the full phenotype on the strain data sheet
004304	NOD.CBALs-Tyr⁺/LtJ	Cryopreserved - Ready for recovery
	This Chr 7 congenic strain in which the tyrosinase allele Tyr⁺ of the CBA/JLsLt strain is fixed on the NOD/Lt background, therefore making the strain agouti in color. This strain should be a good donor for blastocysts in which to microinject targeted NOD ES cells, and may alleviate unwanted genome integration experienced with use of the C57BL/6 blastocysts. The congenic segment on Chromosome 7 slightly supresses spontaneous T1D development which is an asset when these females are used as blastocyst recipients.
006775	NOD.Cg-Foxp3^sf/DoiJ	Cryopreserved - Ready for recovery
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
006935	NOD.Cg-H2^b thnh/J	Cryopreserved - Ready for recovery
	Thin hair homozygotes have a sparse coat discernible by two weeks of age. By three weeks of age the pelt has fewer zigzag hairs than normal and by four weeks of age skin follicles are somewhat dilated with degeneration of the deepest portions of the anagen hair follicles. Hair fragments from degenerating follicles are found in the connective tissue and granulomatous inflammation develops.
006956	NOD.Cg-Vdr^tm1Ska/CmatJ	Cryopreserved - Ready for recovery
	Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles. Homozygous mice exhibit normal pancreatic islet archite ..... For more information please see the full phenotype on the strain data sheet
004774	NOD/ShiLtJ-wly/J	Cryopreserved - Ready for recovery
	Mice develop curly hair by 4 weeks of age; whiskers are normal (straight). Giant hair follicles in anagen and a paucity of subdermal fat were found in histology of the skin at 5 weeks of age.
002345	NXSMC/Ei-Dct^slt-2J/J	Cryopreserved - Ready for recovery

000993	NZB/BlNJ-Kit^W-59J/J	Cryopreserved - Ready for recovery

008777	NZG/KgmJ	Cryopreserved - Ready for recovery
	The New Zealand Ginger (NZG) mouse is characterized by rapid growth and a large body size as a result of excessive lean body mass. This inbred strain is not obese, diabetic or insulin resistant. Both sexes exhibit a rapid growth rate which plateaus at 60 days, however, males are heavier than females. ELISA assay indicates that mice have higher levels of circulating insulin-like growth factor I (IGF1) than C57BL/6 mice, but comparable levels of insulin and growth hormone. Mice have an unusual pattern of fat distribution compared to C57BL/6 mice with higher percentages of retroperitoneal, gonadal and inguinal fat rather than visceral fat. NZG mice have less total body fat (6%) than C57BL/6 mice (13.8%). These mice are susceptible to high fat (45%) diet-induced obesity, but not diet-induced diabetes. Genetic analysis indicates that the yellow (ginger) coat is not the result of alleles at either agouti or the melanocortin 1 receptor (Mc1r) genes. The fur is described ..... For more information please see the full phenotype on the strain data sheet
000267	ROP/GnLeJ	Cryopreserved - Ready for recovery
	The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18^Ra/+ coats have l ..... For more information please see the full phenotype on the strain data sheet
000268	RSV/LeJ	Cryopreserved - Ready for recovery
	Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3^Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3^Va-J> ..... For more information please see the full phenotype on the strain data sheet
000269	SB/LeJ	Cryopreserved - Ready for recovery
	The SB/Le inbred strain is homozygous for both the satin (Foxq1^sa) and beige (Lyst^bg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full phenotype on the strain data sheet
010968	SB;C3Sn-Lrp4^mdig-2J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Lrp4^mdig-2J mutation have toes missing from each foot, have a coarse tail, and some, but not all, have one or two extra upper incisors.
000271	SH1/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the shaker 1 spontaneous mutation (Myo7a^sh1) show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist of degeneration of the organ of Corti, the spiral ganglion, and the stria vascularis in the cochlea, and of the saccular macula and the vestibular ganglion in the vestibular labyrinth.
000622	SHR/GnEiJ	Cryopreserved - Ready for recovery

001045	SI/Col Tyrp1^b Dnahc11^iv/J	Cryopreserved - Ready for recovery
	DNAHC11 is important for developmental control of organ positioning in the left-right axis such that homozygosity for the situs inversus viscerum (iv) mutant allele can result not only in inverse placement of the visceral and thoracic organs, but also in anomalous positioning and interactions of blood vessels (including the hepatic portal, inferior vena cava, and azygos vein) and modified shape of organs and blood vessels, including abnormal lobation of lungs or liver. Approximately 50% of mice homozygous for Dnahc11^iv have situs inversus, and the likelihood of situs inversus is not impacted by whether the homozygous parent has situs inversus. This indicates that wild type Dnahc11 instructs left-right asymmetry, and in the absence of functional Dnahc11 the direction of this asymmetry is random. Heterotaxia is found in less than half of homozygotes and occurs equally in those that do and do not have situs inversus. W ..... For more information please see the full phenotype on the strain data sheet
001910	SJL/J-Crm^2J/J	Cryopreserved - Ready for recovery

002335	SKH2/J	Cryopreserved - Ready for recovery
	Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa ..... For more information please see the full phenotype on the strain data sheet
000308	SSL/LeJ	Cryopreserved - Ready for recovery
	This inbred strain carries both the piebald (Ednrb^s) and piebald lethal (Ednrb^s-l) alleles. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. Homozygous piebald lethal mice are almost completely white with dark eyes and only an occasional small pigmented spot on the head or rump. Piebald-piebald lethal heterozygotes (Ednrb^s/Ednrb^s-l) mice resemble piebald mice in the degree of spotting. The piebald mutations disrupt the development of melanocytes derived from the neural crest. All piebald lethal homozygotes develop megacolon with a lack of enteric ganglion cells in the posterior end of the colon. On the SSL/Le background, although many Ednrb^s-l homozygotes die between 2 and 4 weeks of age, significant numbers survive and may breed. The incidence of megacolon is reduced in piebald and piebald-piebald lethal ..... For more information please see the full phenotype on the strain data sheet
001759	STOCK A Tyr^c Sha/J	Cryopreserved - Ready for recovery

003118	STOCK Ces1c^e Foxn1^nu/J	Cryopreserved - Ready for recovery
	Mice homozygous for Ces1c^e are viable and fertile and exhibit no apparent defect. Ces1c^e was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Ces1c^e was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Ces1c^e was shown to be a hypomorphic electrophoretic variant (Soares 1979). The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly <> ..... For more information please see the full phenotype on the strain data sheet
000306	STOCK Dll3^pu + Tyr^c-ch/+ Oca2^p Tyr^c-ch/J	Cryopreserved - Ready for recovery

003112	STOCK Eda^Ta-5J/J	Cryopreserved - Ready for recovery

004711	STOCK Ednrb^s-52Pub	Cryopreserved - Ready for recovery

002857	STOCK Egfr^tm1Mag/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Egfr^tm1Mag targeted mutation are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Fertile mutant females have impaired lactation.
001743	STOCK Gtg1^dwg/J	Cryopreserved - Ready for recovery
	Mice homozgyous for the dwarf grey spontaneous mutation (Gtg1^dwg) are viable but do not breed. Homozygous mutant mice have grey coats, are smaller than littermates, and develop cataracts by 3-4 weeks of age. Additional characteristics include increased numbers of osteoclasts, reduced bone mass, reduced red pulp area of the spleen, and slightly reduced thyroxin levels.
000006	STOCK Hk Tyr^c/J	Cryopreserved - Ready for recovery
	While mice carrying the Hk mutation often have a hooked curl at the end of a shortened tail, this mutation may more consistently result in a displaced anus that is positioned posterior to the normal site and is more slit-shaped than circular. In some instances the anus has been located in the beginning of the tail and a depression was found to extend partway down the ventral side of the tail (Holman, 1951). The Hk mutation is semidominant with homozygotes often showing a shorter, more affected tail than heterozygotes (P.W. Lane Personal Communication).
000979	STOCK Kitl^Sl-16J/J	Cryopreserved - Ready for recovery
	The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two 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.
001610	STOCK Krt27^Re-wc/J	Cryopreserved - Ready for recovery

001277	STOCK Mgrn1^md Igl-1^b Igl1-r^lo/J	Cryopreserved - Ready for recovery

001253	STOCK Mitf^Mi-wh +/+ Wnt7a^px/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (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 diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7a^px) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet
000390	STOCK Myo5a^d Ds/J	Cryopreserved - Ready for recovery

001584	STOCK Oca2^p-J/Oca2^p-bs/J	Cryopreserved - Ready for recovery
	Oca2^p-J/Oca2^p-J mice exhibit significant dilution of coat color with pink eyes, a phenotype similar to that produced by Oca2^p/Oca2^p. The Oca2^p-J mutation is a partial deletion of the gene that completely ablates Oca2^p function (Oakey et al. 1996). Oca2^p-bs/Oca2^p-bs mice show a less extreme coat color dilution and have black eyes from birth; the phenotype of Oca2^p-bs homozygotes also includes stunted growth, jerky gait, male sterility, female semisterility, and impaired maternal behavior, and the smaller-than-expected proportion of Oca2^p-bs homozygous intercross offspring implies reduced prenatal viability (Lyon et al. 1992). The Oca2^p-bs mutation comprises a deletion that begins about 10 kb 5' of the Oca2^p locus and extends for about 8 kb in the proximal direc ..... For more information please see the full phenotype on the strain data sheet
001585	STOCK Oca2^p-d/Oca2^p-25H/J	Cryopreserved - Ready for recovery
	Oca2^p-25H/Oca2^p-25H mice exhibit significant dilution of coat color with pink eyes, similar in appearance to Oca2^p/Oca2^p mice. The Oca2^p-25H phenotype also includes a slightly jerky gait with some tremor, small body size compared to control littermates, male sterility, female semisterility, and impaired maternal behavior, and the smaller-than-expected proportion of Oca2^p-25H homozygous intercross offspring implies reduced prenatal viability (Lyon et al. 1992, Phillips et al. 1977). The Oca2^p-25H mutation comprises an inversion of a segment of Chromsome 7 that alters the 5' end of the Oca2^p gene so that no detectable ptranscript is produced, accounting for the pigment-dilution phenotype (Gardner et al. 1992). The deletion also disrupts the Herc2/rjs gene proximal to Oca2^p so the transcript seq ..... For more information please see the full phenotype on the strain data sheet
000823	STOCK Oca2^p-d/Oca2^p-6H/J	Cryopreserved - Ready for recovery

001747	STOCK Oca2^p-d/Oca2^p-cp/J	Cryopreserved - Ready for recovery
	Mice homozygous for Oca2^p-d (dark pink-eye) are born with lightly pigmented eyes, darker than those of Oca2^p/Oca2^p mice, which darken by weaning and a coat color "considerably darker than that of Oca2^p/Oca2^p mice, somewhat resembling that of brown [Tyrp1^b/Tyrp1^b] mice"; both sexes are fertile (Gardner et al. 1977, Lyon et al. 1992). A normal-sized Oca2^p transcript is present in eyes of Oca2^p-d/Oca2^p-d mice (Gardner et al. 1992), and Southern blot analysis revealed no gross alteration of the Oca2^p gene (Gardner et al. 1992, Lyon et al. 1992); thus, the molecular nature of the defect is unknown. Most Oca2^p-cp (p-cleft palate, formerly p^11H) homozygotes die soon after birth with cleft palate; the few that survive to adulthood exhibit significant dilution of coat co ..... For more information please see the full phenotype on the strain data sheet
002902	STOCK Pax3^Sp Mlph^ln/J	Cryopreserved - Ready for recovery

006135	STOCK Sgk3^fz-ica/McirJ	Cryopreserved - Ready for recovery

003318	STOCK Shh^tm1Amc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Shh^tm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e ..... For more information please see the full phenotype on the strain data sheet
000994	STOCK a Myo5a^d Mreg^dsu/J	Cryopreserved - Ready for recovery

000064	STOCK a Tyrp1^b Pmel^si/J	Cryopreserved - Ready for recovery
	Several proteins have been characterized as being critical for melanogenesis, including tyrosinase and its related proteins tyrosinase related protein 1 and 2 (TRP-1 and TRP-2). The silver locus protein (SI) is also crucial to the normal melanogenic pathway and it is believed that the interactions of these, and probably other, proteins are necessary for proper melanin pigment production within melanocytes. Nonagouti mice (a/a) homozygous for the recessive si mutation display a range of coat color variations, including all black and all white. Also, single hairs can be both black and white as the tips contain no pigment while the base retains pigmentation. Black and white banding patterns in individual hairs is also observed. It is noted that similar si/si hair color variation is also seen on the agouti background. Young a/a mice typically have black hairs, with some silver/grey hair present on the head, behind the ears and around the posterior. The hai ..... For more information please see the full phenotype on the strain data sheet
002238	STOCK a Tyrp1^b shmy/J	Cryopreserved - Ready for recovery
	Shimmy homozygotes can generally be identified by 12-14 days of age by a hesitant, wobbly gait with swaying hindquarters and slightly smaller overall body size as compared with unaffected littermates. There can be a delay in the opening of the eyes such that one or both remain closed until 15 to 20 days of age.
000579	STOCK a tp/J	Cryopreserved - Ready for recovery
	Taupe is a recessive spontaneous mutation that causes a lightening of the coat color such that a/a tp/tp mice are slate grey. The coat color is similar to that of the ruby (Hps5^ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. The homozygous females do not have normal nipple development, although the mammary ducts and alveoli develop normally. These females also have difficulty with pregnancy and birth. They can not rear their pups even if the pups are born alive so this strain is maintained by breeding heterozygous females to homozygous males. (Fielder, 1952; Fielder, 1950.)
000317	STOCK a/a Egfr^wa2/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the waved 2 spontaneous mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation.
000302	STOCK a/a Mitf^Mi-wh +/+ Itpr1^opt/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (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 diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalities of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the opisthotonus spontaneous mutation (Itpr1^opt) display a characteristic upward arching of head and tail. Homozygous mutant mice can be recognized at about 10 days of age by their loss of balance when standing or moving. Typical behavior of 15 to 20 day old homozygotes consists of falling over and struggling to get up. Agitation and s ..... For more information please see the full phenotype on the strain data sheet
000286	STOCK a/a Myo5a^d fd/+ +/J	Cryopreserved - Ready for recovery

000206	STOCK a/a Tyr^c-h/J	Cryopreserved - Ready for recovery

001432	STOCK a/a Tyrp1^b sks/Tyrp1^b +/J	Cryopreserved - Ready for recovery

000281	STOCK a/a ma Flg^ft/J	Cryopreserved - Ready for recovery

003148	STOCK chky/J	Cryopreserved - Ready for recovery
	Mice homozygous for the chick yellow mutation on an albino background have a pale yellow coat color evident by approximately 10 days of age when the first coat of hair comes in. Cataracts, lens extrusion, and retinal degeneration develop. Independent of the chick yellow mutation, mice of this background, which is an inbred of an ICR outbred population, may develop polydipsia with age.
000279	STOCK gr +/+ Ap3d1^mh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the mocha spontaneous mutation (Ap3d1^mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1^mh allele have si ..... For more information please see the full phenotype on the strain data sheet
013132	STOCK slck/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the slick hair mutation can be identified by 3 weeks of age by a disheveled coat, which is less evident by 5 weeks of age.
001874	STOCK t^w82 tf/J	Cryopreserved - Ready for recovery

000594	STOCK T(2;8)26H a/T(2;8)26H a Tyrp1⁺/Tyrp1^b/J	Cryopreserved - Ready for recovery

001101	STOCK T(3;4)5Rk Tyrp1^b/J	Cryopreserved - Ready for recovery

000583	STOCK T(X;16)16H +/+ Eda^Ta	Cryopreserved - Ready for recovery

000588	TF/GnLe-T(1;17)190Ca +/+ tf/J	Cryopreserved - Ready for recovery

000623	TR/DiEiJ	Cryopreserved - Ready for recovery

000275	V/LeJ	Cryopreserved - Ready for recovery
	This strain was originally used as a linkage stock for gene mapping. It is homozygous for several visible recessive mutations all located on different chromosomes including nonagouti (a), fuzzy (fz), leaden (Mlph^ln), and piebald (Ednrb^s) and is segregating for the neurological mutation, waltzer (Cdh23^v). Homozygous waltzer mice show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. Homozygous piebald mice have dark eyes. The white areas of the coat are completely lacking in melanocytes and there is a reduction in the number of melanocytes in the choroid layer of the eye.
000791	WB.Cg-f/J	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
000161	WB.D2-Kitl^Sl-d/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000147	WLHR/LeJ	Cryopreserved - Ready for recovery
	WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v ..... For more information please see the full phenotype on the strain data sheet
016926	BTBR T⁺ tf-Fbxl3^Ovtm/J	Under Development - Now Accepting Orders
	Ovtm ENU-induced mutants contain an A to G transition at nucleotide in exon 5 of the F-box and leucine-rich repeat protein 3 (Fbxl3) gene that defines an amino acid change from isoleucine to threonine at residue 364. While homozygous males are viable, fertile, and normal in size, homozygous females are viable and normal in size, but are often infertile. FBXL3 is part of the SKP1-CUL1-F-box-protein (SCF) ubiquitin protein ligase complex which mediates phosphorylation-dependent ubiquitination. Homozygotes have a long circadian period of ~26 hours. These mice may be useful for studying circadian rhythm modulation.
014173	STOCK Tyr^c-2J Omp^{tm1.1(COP4/EYFP)Tboz}*/J	Under Development - Now Accepting Orders
	These OMP-ChR2-YFP (OCY-58) mice express a ChR2(H134R)-EYFP fusion gene from the olfactory marker protein locus (Omp). Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. ChR2(H134R)-EYFP is expressed in all mature olfactory sensory neurons, rendering them light sensitive. Light directed at the olfactory epithelium or the glomeruli can elicit activity in mitral/tufted (M/T) cells of the olfactory bulb and can drive odor guided behavior. These mutant mice thus allow precise, timed delivery of stimuli input to the olfactory system. The Donating Investigator reports that this this targeted mutation creates a null allele. Due to possible olfactory deficits, analysis should be performed in heterozygous mice. The Donating Investigator recommends keeping the strain on the albino B6 background to avoid possible interference by pigmented melanocytes. The ChR2(H134R)-EYFP fusio ..... For more information please see the full phenotype on the strain data sheet

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New Strains Awaiting Transfer

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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
017614	B6(Cg)-Tyr^c-2J Tg(UBC-mCherry)1Phbs/J	Awaiting Transfer from the Donor
These transgenic mice express monomeric red fluorescent protein (mCherry) under the direction of the human ubiqutin C promoter. Expression is observed in almost all tissues examined and may be useful as a bright and photostable means for visualizing morphogenesis and tissue rearrangements alone or in combination with mice expressing eGFP.
009355	SAMP1/YitFcsJ	Awaiting Transfer from the Donor
SAMP1/YitFcs (also called SAMP1/YitFc or SAMP1/Fc) mice develop a spontaneous ileitis that is similar in many features to the human Crohn's disease (a type of inflammatory bowel disease).

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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.
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New Strains Awaiting Transfer

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