Search Criteria: Research Area is "Dermatology Research: Color and White Spotting Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000671 | DBA/2J | Level 1 |
| 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. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral
..... For more information please see the full descriiption on the strain data sheet | ||
| 000058 | B6(Cg)-Tyrc-2J/J | Level 2 |
| Mice homozygous for Tyrc-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 Tyrc-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-m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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-Leprdb 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 descriiption 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). | ||
| 002468 | KK.Cg-Ay/J | Level 2 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and
..... For more information please see the full descriiption on the strain data sheet | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW 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. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 000697 | B6.Cg-m +/+ Leprdb/J | Level 3 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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 (Leprdb/+) 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 Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabet
..... For more information please see the full descriiption on the strain data sheet | ||
| 000676 | LP/J | Level 3 |
| 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 (Ednrbs). 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. | ||
| 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-Aw-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 Aw-J is dominant to the nonagouti a. Since a to Aw is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin. | ||
| 000049 | C57BL/6J-KitW-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. KitW-v homozygotes resemble KitW 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. | ||
| 000629 | C57BL/6J-Lystbg-J/J | Level 4 |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). 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 descriiption on the strain data sheet | ||
| 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). 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. | ||
| 000692 | WB/ReJ KitW/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. | ||
| 002565 | A.B6-Tyr+/J | Repository- Live |
| 000199 | AEJ/GnLeJ | Repository- Live |
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) 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 Myo6sv 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
..... | ||
| 004684 | B6(129P2) Nos2tm1Lau-chtl/J | 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. | ||
| 005071 | B6(Cg)-DctSlt-lt3J/J | Repository- Live |
| DctSlt-lt3J heterozygous mice are diluted to a dark brown and homozygous mice are diluted to a light brown. | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Repository- Live |
| 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. | ||
| 001809 | B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J | Repository- Live |
| Testicular feminization (ArTfm) 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 (EdaTa-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. | ||
| 008115 | B6.129X1-Pomctm2Ute/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 003625 | B6.C-H2-Ab1bm12/KhEg-Mc1re-J/J | Repository- Live |
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Repository- Live |
| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of
..... For more information please see the full descriiption on the strain data sheet | ||
| 000305 | B6.Cg-Fbn1Tsk +/+ Pldnpa/J | Repository- Live |
| Mice homozygous for the pallid spontaneous mutation Pldnpa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldnpa/Pldnpa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2p/Oca2p). 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 descriiption on the strain data sheet | ||
| 005051 | B6.Cg-KitW-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 KitW-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). KitW-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the KitW and KitW-v mutations, KitW-sh germ cells and erythrocytes are not affected. Homozygtes have some
..... For more information please see the full descriiption on the strain data sheet | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Repository- Live |
| On an albino background Tg(Tyr)3412ARpw permits the identification of gender as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-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 female brain (Dewing et al., 20
..... | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) 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 (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu
..... For more information please see the full descriiption on the strain data sheet | ||
| 001573 | B6C3Fe a/a-MitfMi/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the MitfMi 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. | ||
| 000314 | B6CBACa Aw-J/A-EdaTa/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. | ||
| 002044 | B6Ei.Cg-Atp7aMo-blo/J | Repository- Live |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-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 descriiption on the strain data sheet | ||
| 003215 | B6Pin.C3-Ap3b1pe/J | Repository- Live |
| 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. | ||
| 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 Amy1a allele to an allele that has an electrophoretic mobility closer to that of Amy1b. 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/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. | ||
| 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+ Hbbs/J | Repository- Live |
| 000198 | C3FeLe.B6-a/J | Repository- Live |
| 004806 | C3H/HeJ-Mfs/J | Repository- Live |
| 002134 | C57BL/6J-Mitfmi-vit/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitfmi-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. | ||
| 000565 | C57BL/6J-Pax3Sp-d/J | Repository- Live |
| Mice homozygous for the splotch-delayed spontaneous mutation (Pax3Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3Sp, 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. | ||
| 002469 | C57BL/6J-Pax3Sp/J | Repository- Live |
| Mice homozygous for the splotch spontaneous mutation (Pax3Sp) 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 Pax3Sp 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 (Pax3Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. | ||
| 005135 | C57BL/6J-Sls/J | Repository- Live |
| 000516 | C57BLKS-Rpl24Bst/J | Repository- Live |
| Belly spot and tail (Rpl24Bst) 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 Rpl24Bst 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 descriiption on the strain data sheet | ||
| 000643 | DW/J Mlphln Pou1f1dw/J | Repository- Live |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) 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. | ||
| 004828 | FVB.129P2-Pde6b+ Tyrc-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-Fmr1tm1Cgr/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 Tyrc-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-Fmr1tm1Cgr/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. 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 (Ednrbs). 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 complet
..... For more information please see the full descriiption 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 (Tyrp1b), pink-eyed dilution (Oca2p), short ear (Bmp5se), dilute Myo5ad), and retinal degeneration 1 (Pdeb1rd1). | ||
| 000268 | RSV/LeJ | Repository- Live |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) 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 (Mcoln3Va-J
>
..... For more information please see the full descriiption on the strain data sheet | ||
| 000644 | SEA/GnJ | Repository- Live |
| 001618 | STOCK Oca2p/Oca2p Prop1df/J | Repository- Live |
| Mice homozygous for the Ames dwarf spontaneous mutation (Prop1df) resemble mice homozygous for the Snell's dwarf mutation (Pit1dw). 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. | ||
| 001743 | STOCK dwg/J | Repository- Live |
| Mice homozgyous for the dwarf grey spontaneous mutation (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. | ||
| 003100 | STOCK dwgBayer/J | Repository- Live |
| The dwarf-Bayer mutation (dwgBayer) 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. | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) 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. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing
..... For more information please see the full descriiption on the strain data sheet | ||
| 100401 | WCB6F1/J KitlSl KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) 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., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall
..... For more information please see the full descriiption on the strain data sheet | ||
| 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.). | ||
| 002516 | 129-Edn3tm1Ywa/J | Repository-Cryopreserved |
| 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+ KitlSl-J/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) 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. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000091 | 129T1/Sv-Oca2+ Tyrc-ch Dnd1Ter/J | Repository-Cryopreserved |
| 001279 | 129T1/Sv-Oca2+ Tyrc-ch-Aft/J | Repository-Cryopreserved |
| Aft is a dominant mutation that causes increased postnatal lethality in heterozygotes and nearly 100% embryonic or perinatal lethality in homozygotes. Aft/+ mice can be identified by tail kinks near the tail tip and syndactyly of the third and fourth digits of the hind feet, a trait which is often unilateral. This syndactyly does not result from bone fusion, but rather from the persistence of the skin web that normally is removed via apoptosis during development. The tail kinks appear to result from cartilage overgrowth and fusion. Alopecia is found at six to eight months of age and can progress into bleeding ulcerations. Histology of Aft/+ skin shows fewer follicles, fibrosis, and an increase in the number of mast cells. The penetrance of this mutation is only approximately 65% on the 129/Sv and C57BL/6J backgrounds and the expressivity is variable. The most prevalent trait in Aft/+ mice is tail kinks, followed by syndactyly then skin lesions. The
..... For more information please see the full descriiption on the strain data sheet | ||
| 005445 | A.B6 Tyr+-Cybanmf333/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry. | ||
| 005012 | A.B6 Tyr+-Myo5ad-l31J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page. | ||
| 000004 | ABP/LeJ | Repository-Cryopreserved |
| Mice homozygous for the Tgfawa1 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 Adamts20bt 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
..... | ||
| 000251 | AEJ.Cg-ae +/a Gdf5bp-H/J | Repository-Cryopreserved |
| 000202 | AEJ/Gn-bd/J | Repository-Cryopreserved |
| 001005 | AKXD1/TyJ | Repository-Cryopreserved |
| 001017 | AKXD10/TyJ | Repository-Cryopreserved |
| 001003 | AKXD11/TyJ | Repository-Cryopreserved |
| 000765 | AKXD13/TyJ | Repository-Cryopreserved |
| 000779 | AKXD14/TyJ | Repository-Cryopreserved |
| 000954 | AKXD15/TyJ | Repository-Cryopreserved |
| 000958 | AKXD16/TyJ | Repository-Cryopreserved |
| 001093 | AKXD18/TyJ | Repository-Cryopreserved |
| 000776 | AKXD2/TyJ | Repository-Cryopreserved |
| 001062 | AKXD21/TyJ | Repository-Cryopreserved |
| 000947 | AKXD22/TyJ | Repository-Cryopreserved |
| 000969 | AKXD24/TyJ | Repository-Cryopreserved |
| 000949 | AKXD25/TyJ | Repository-Cryopreserved |
| 000764 | AKXD27/TyJ | Repository-Cryopreserved |
| 000959 | AKXD3/TyJ | Repository-Cryopreserved |
| 000777 | AKXD6/TyJ | Repository-Cryopreserved |
| 000763 | AKXD9/TyJ | Repository-Cryopreserved |
| 000409 | B10.129P-H1b Hbbd Tyrc Ea7a/(5M)oSnJ | Repository-Cryopreserved |
| 000418 | B10.129P-H1b Tyrc Hbbd/(5M)nSnJ | Repository-Cryopreserved |
| 002472 | B10.A/SgSnJ-Hps3coa-5J/J | Repository-Cryopreserved |
| 000432 | B10.C-H1b Hbbd Tyrc/(41N)SnJ | Repository-Cryopreserved |
| 000427 | B10.CE-H13b Aw/(30NX)SnJ | Repository-Cryopreserved |
| 000580 | B10.D2/nSn-Tyrc-4J/J | Repository-Cryopreserved |
| 001013 | B10.D2/nSnJ-Myo5ad-n/J | Repository-Cryopreserved |
| Mice homozygous for the dilute-neurological spontaneous mutation (Myo5ad-n) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal mutant mice (Myo5ad-l, Stock No. 000253). | ||
| 000420 | B10.LP-H13b Aw/Sn | Repository-Cryopreserved |
| 000422 | B10.LP-H3b H13b/(36NS)Sn | Repository-Cryopreserved |
| 000477 | B10.PA-Pldnpa H3e at/SnJ | Repository-Cryopreserved |
| This minor histocompatibility 3 (H3e) congenic strain is also carrying the closely linked pallid mutation (Pldnpa) 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 descriiption on the strain data sheet | ||
| 000419 | B10.UW-H3b we Pax1un at/SnJ | Repository-Cryopreserved |
| 000234 | B10Gn.Cg-Rn/J | Repository-Cryopreserved |
| 000822 | B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J | Repository-Cryopreserved |
| 000593 | B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J | Repository-Cryopreserved |
| Mice homozygous for the MitfMi 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 Aw-J/A-T(5;13)264Ca KitW-v/J | Repository-Cryopreserved |
| 002048 | B6 x C57BLKS-m Leprdb Myo15sh2-J/J | Repository-Cryopreserved |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wildtype mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (m) and diabetes (Leprdb) spontaneous mutations. | ||
| 002542 | B6 x CByJ.Cg-Crm/J | Repository-Cryopreserved |
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Repository-Cryopreserved |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease
..... For more information please see the full descriiption on the strain data sheet | ||
| 002016 | B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ | Repository-Cryopreserved |
| 005565 | B6(V)-chtl2J/J | Repository-Cryopreserved |
| 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-Aw-J-EdaTa-6J.Cg-Sxr | Repository-Cryopreserved |
| 001730 | B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J | Repository-Cryopreserved |
| 000841 | B6-Aw-J.CBy-EdaTa-By/J | Repository-Cryopreserved |
| 000311 | B6-Pax3Sp.Cg-N/J | Repository-Cryopreserved |
| Mice homozygous for the splotch spontaneous mutation (Pax3Sp) 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 (Pax3Sp-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-B2mtm1Unc-rs2J/J | Repository-Cryopreserved |
| 000977 | B6.B10(PL)-Slc45a2Uw-dbr/J | Repository-Cryopreserved |
| 000495 | B6.C-H38c/By-KitW-56J/J | Repository-Cryopreserved |
| 000560 | B6.C-H7b/By KitW-50J/J | Repository-Cryopreserved |
| 000383 | B6.C-Tyrc H1b Hbbd/ByJ | Repository-Cryopreserved |
| 000769 | B6.C/(HZ18)By-at-44J/J | Repository-Cryopreserved |
| 000001 | B6.C3 A/a Mgrn1md/J | Repository-Cryopreserved |
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Repository-Cryopreserved |
| 000203 | B6.C3-Aiy/a/J | Repository-Cryopreserved |
| 000102 | B6.C3-Ap3b1pe/J | Repository-Cryopreserved |
| 000122 | B6.C3-KitW-44J/J | Repository-Cryopreserved |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* 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 KitW-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 KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t
..... For more information please see the full descriiption on the strain data sheet | ||
| 000309 | B6.C3-Mgrn1md/J | Repository-Cryopreserved |
| 001572 | B6.C3-am-J/J | Repository-Cryopreserved |
| 000449 | B6.C3-rs/J | Repository-Cryopreserved |
| 000017 | B6.C3Fe-Avy/J | Repository-Cryopreserved |
| Homozygous (Avy/Avy) and heterozygotes (Avy/A and Avy/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. Avy resembles Ay 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 Avy/a mice of mottled phenotype but not in those of agouti phenotype. | ||
| 000050 | B6.C3Fe-H51 Hps1ep /ByJ | Repository-Cryopreserved |
| 000525 | B6.C3Fe-Hps1ep/J | Repository-Cryopreserved |
| 000991 | B6.C58-KitW-57J/J | Repository-Cryopreserved |
| 000535 | B6.Cg-Atp7aMo-blo/J | Repository-Cryopreserved |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-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 descriiption on the strain data sheet | ||
| 001381 | B6.Cg-Atp7aMo-pew2J/J | Repository-Cryopreserved |
| 000053 | B6.Cg-Atp7aMo-to/J | Repository-Cryopreserved |
| 000131 | B6.Cg-Dctslt/J | Repository-Cryopreserved |
| 006429 | B6.Cg-Dwh/J | Repository-Cryopreserved |
| 000103 | B6.Cg-Hps6ru/J | Repository-Cryopreserved |
| 002283 | B6.Cg-KitW-19H/EiJ | Repository-Cryopreserved |
| 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 YAKR/J Chromosome (available from Stock No. 007250), KitW-19H heterozygosity results in sex reversed XY females. | ||
| 000133 | B6.Cg-KitW-24J/J | Repository-Cryopreserved |
| 000139 | B6.Cg-KitW-25J/J | Repository-Cryopreserved |
| 000164 | B6.Cg-KitW/J | Repository-Cryopreserved |
| 002993 | B6.Cg-KitlSl-18H/EiJ | Repository-Cryopreserved |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) 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. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva
..... For more information please see the full descriiption on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW 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 KitW-v/
..... | ||
| 000204 | B6.Cg-Lystbg/J | Repository-Cryopreserved |
| Mice homozygous for the beige spontaneous mutation (Lystbg) 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 descriiption on the strain data sheet | ||
| 000158 | B6.Cg-MitfMi-wh/MitfMi/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-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 (MitfMi) 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 descriiption on the strain data sheet | ||
| 000184 | B6.Cg-MitfMi-wh/Mitfmi-rw/J | Repository-Cryopreserved |
| 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 Mitfmi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (MitfMi-wh/Mitfmi-rw) are mostly white with tan spots and red eyes. | ||
| 000157 | B6.Cg-MitfMi-wh/Mitfmi-sp/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-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 (Mitfmi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (MitfMi-wh/Mitfmi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes. | ||
| 000057 | B6.Cg-MitfMi-wh/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-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 (MitfMi-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-Pldnpa/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 000285 | B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J | Repository-Cryopreserved |
| Mice homozygous for the staggerer spontaneous mutation (Rorasg) 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 Rorasg/Rorasg mice on the C57BL/6J background relative to wild type siblings.
In this congenic strain the staggerer mutation is maintain
..... | ||
| 001176 | B6.Cg-Rw/J | Repository-Cryopreserved |
| 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
..... | ||
| 000112 | B6.Cg-Sgk3fz H54 Mlphln/+ H54 +/J | Repository-Cryopreserved |
| 000035 | B6.Cg-Tyrc-J/J | Repository-Cryopreserved |
| 000104 | B6.Cg-Tyrc-h/J | Repository-Cryopreserved |
| 000571 | B6.Cg-Whrnwi Tyrp1b/+ +/J | Repository-Cryopreserved |
| At 9 to 10 days of age Whrnwi 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
..... | ||
| 000699 | B6.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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 (Leprdb/+) 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 Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabe
..... For more information please see the full descriiption on the strain data sheet | ||
| 000027 | B6.D-Tyrp1b m/J | Repository-Cryopreserved |
| 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-Hps5ru2-hz/J | Repository-Cryopreserved |
| 000171 | B6.D2-KitW-45J/J | Repository-Cryopreserved |
| 001563 | B6.D2-KitW-73J/J | Repository-Cryopreserved |
| 000054 | B6.D2-Tyrc-p/J | Repository-Cryopreserved |
| 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-KitW-49J/J | Repository-Cryopreserved |
| 002550 | B6.TF-Slc45a2uw-d/J | Repository-Cryopreserved |
| 003295 | B6;129-Ednrbtm1Ywa/J | Repository-Cryopreserved |
| Mice homozygous for the Ednrbtm1Ywa 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-Hps3coa/J | Repository-Cryopreserved |
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW 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 (MitfMi-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 (MitfMi-wh/+) have a dilut
..... For more information please see the full descriiption on the strain data sheet | ||
| 001059 | B6By.Cg-Oca2p/J | Repository-Cryopreserved |
| A normal-size Oca2p mRNA is present in the skin of mice homozygous for the Oca2p mutation, but in greatly reduced amounts; thus, this appears to be a hypomorphic rather than a null allele. B6By.Cg-Oca2p/Oca2p/J mice are grey with pink eyes. The Oca2p 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 Mcoln3Va-J Krt25Re/J | Repository-Cryopreserved |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-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 (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying two other mutations, rex (Krt25Re) and Danforth's short tail (Sd). | ||
| 000505 | B6C3 Aw-J/A-Mutedmu/J | Repository-Cryopreserved |
| Mice homozygous for the muted spontaneous mutation (Mutedmu) 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 (Pldnpa). 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 (Ap3d1mh), and is also seen in human Hermansky-Pudlak syndrome. | ||
| 000604 | B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J | Repository-Cryopreserved |
| 000278 | B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J | Repository-Cryopreserved |
| 001750 | B6C3Fe a/a-XsJ/J | Repository-Cryopreserved |
| 002018 | B6C3Fe a/a-din/J | Repository-Cryopreserved |
| 000065 | B6C3Fe a/a-we Pax1un at/J | Repository-Cryopreserved |
| The affected mutant (we Pax1un at/we Pax1un a?) has a wavy coat, wavy tail, and is black and tan. | ||
| 000296 | B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J | Repository-Cryopreserved |
| Mice heterozygous for the varitint-waddler Jackson spontaneous mutation (Mcoln3Va-J) are more pigmented than the original varitint waddler mice (Mcoln3Va) 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 (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced. This strain is also carrying the semidominant hypodactyly spontaneous mutation (Hoxa13Hd). Heterozygous hyp
..... For more information please see the full descriiption on the strain data sheet | ||
| 000956 | B6CB-Mitfmi-rw/J | Repository-Cryopreserved |
| 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 Mitfmi-rw have some pigmentation around the neck and have small red eyes. | ||
| 000287 | B6CBACa Aw-J/A-Plp1jp EdaTa/J | Repository-Cryopreserved |
| Hemizygous males carrying the X-linked jimpy spontaneous mutation (Plp1jp) 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. The stock is also carrying the X-linked tabby mutation (EdaTa). | ||
| 002622 | B6Ei.Cg-pwk/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 000971 | B6EiC3 a/A-Och/J | Repository-Cryopreserved |
| 001548 | BALB/cBy x A/J-CrmJ/J | Repository-Cryopreserved |
| 001755 | BALB/cBy-Krt71Ca-10J/J | Repository-Cryopreserved |
| 000652 | BDP/J | Repository-Cryopreserved |
| 000700 | BKS.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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. 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 Leprdb homozygotes. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and
..... For more information please see the full descriiption on the strain data sheet | ||
| 001049 | BKS.Cg-mea2J m/+ +/J | Repository-Cryopreserved |
| Mice homozygous for the meander tail 2J spontaneous mutation (mea2J) have a phenotype that is very similar to the original meander tail (mea) and meander tail J mice (meaJ). 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 (m). | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + m/J | Repository-Cryopreserved |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about 2 weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice 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 mutation occurred in the BKS.Cg-Leprdb +/+ m strain so it is also segregating for the diabetes (Leprdb) and misty (m) mutations. See strain description for BKS.Cg-Leprdb +/+ m (Stock No. 000642) for more information. | ||
| 000081 | BXD25/TyJ | Repository-Cryopreserved |
| 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. | ||
| 000232 | C3Fe.C3-Ap3b1pe/J | Repository-Cryopreserved |
| 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 KitlSl Krt71Ca-J/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) 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, | ||