JAX Mice Database - Color and White Spotting Defects

Search Criteria: Research Area is "Dermatology Research: Color and White Spotting Defects"

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
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.
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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).
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
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.
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.
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
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

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

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
000419	B10.UW-H3^b we Pax1^un a^t/SnJ	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

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

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.
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).
003533	B6.129P-B2m^tm1Unc-rs^2J/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.
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
000977	B6.B10(PL)-Slc45a2^Uw-dbr/J	Cryopreserved - Ready for recovery

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

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

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
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

000035	B6.Cg-Tyr^c-J/J	Cryopreserved - Ready for recovery

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

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

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

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.
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.
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).
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

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

000290	B6C3Fe a/a-Sox10^Dom/J	Cryopreserved - Ready for recovery

002018	B6C3Fe a/a-din/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.
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).
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

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
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

000652	BDP/J	Cryopreserved - Ready for recovery

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.
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.
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

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

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

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
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.
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.
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.
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).
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

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
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.
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.
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

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

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
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
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
000265	MY/HuLeJ	Cryopreserved - Ready for recovery

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

003091	NH/KiPtJ	Cryopreserved - Ready for recovery

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.
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
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.
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

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

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

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.
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

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.)
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

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
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

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
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.

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

New Strains Awaiting Transfer

JAX^® Mice Strains