JAX Mice Database - Bone/Bone Marrow Defects

Search Criteria: Research Area is "Endocrine Deficiency Research: Bone/Bone Marrow Defects"

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

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
100410	WBB6F1/J-Kit^W/Kit^W-v/J	Level 2
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
000049	C57BL/6J-Kit^W-v/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
004104	FVB.Cg-Mmp9^tm1Tvu/J	Level 4
	Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
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.
006133	B6.129S4-Vdr^tm1Mbd/J	Repository- Live
	Heterozygous mice are phenotypically indistinguishable from wildtype siblings. Homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days. ..... For more information please see the full descriiption on the strain data sheet
000528	B6.Cg-Phex^Hyp/J	Repository- Live
	Hypophosphatemia (Phex^Hyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (Phex^Gy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males.
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet
007084	B6.FVB(Cg)-Mmp9^tm1Tvu/J	Repository- Live
	Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain de ..... For more information please see the full descriiption on the strain data sheet
000231	B6C3Fe a/a-Csf1^op/J	Repository- Live
	Mice homozygous for the osteopetrosis spontaneous mutation (Csf1^op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.
001573	B6C3Fe a/a-Mitf^Mi/J	Repository- Live
	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.
002134	C57BL/6J-Mitf^mi-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 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.
000811	C57BL/6J-Ptpn6^me-v/J	Repository- Live
	Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6^me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo ..... For more information please see the full descriiption on the strain data sheet
006956	NOD.Cg-Vdr^tm1Ska/CmatJ	Repository- Live
	Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles. Homozygous mice exhibit normal pancreatic islet archite ..... For more information please see the full descriiption on the strain data sheet
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 dwg^Bayer/J	Repository- Live
	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.
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full descriiption on the strain data sheet
100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full descriiption on the strain data sheet
004166	129-Itgb5^tm1Des/J	Repository-Cryopreserved
	Mice that are homozygous for the Itgb5^tm1Des targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgb5 gene product (mRNA or protein) is detected. Homozygotes display defects in VEGF-mediated vascular permeability. Cultured keratinocytes derived from homozygous mutant animals display impaired adhesion and migration on vitronectin-coated surfaces.
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full descriiption on the strain data sheet
000593	B6 x B6CBCa A^w-J/A-Grid2^Lc T(2;6)7Ca Mitf^Mi-wh/J	Repository-Cryopreserved
	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	Repository-Cryopreserved

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Repository-Cryopreserved
	Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous Kit^W-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease ..... For more information please see the full descriiption on the strain data sheet
003142	B6.129P2-Prlr^tm1Cnp/J	Repository-Cryopreserved
	There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants.
002612	B6.129S2-Bmp4^tm1Blh/J	Repository-Cryopreserved
	Mice homozygous for the Bmp4^tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities.
000495	B6.C-H38^c/By-Kit^W-56J/J	Repository-Cryopreserved

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

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

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

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

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

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
000194	B6.Cg-Lx Kit^W-v/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter. Although homozygous Kit^W-v/ ..... For more information please see the full descriiption on the strain data sheet
000158	B6.Cg-Mitf^Mi-wh/Mitf^Mi/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 (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 descriiption on the strain data sheet
000184	B6.Cg-Mitf^Mi-wh/Mitf^mi-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 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	Repository-Cryopreserved
	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	Repository-Cryopreserved
	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.
000171	B6.D2-Kit^W-45J/J	Repository-Cryopreserved

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

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

006086	B6.SJL-Tg(HBB-GH1)420King/J	Repository-Cryopreserved
	Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly.
003728	B6;129S-Sparc^tm1Hwe/J	Repository-Cryopreserved
	Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. The development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia.
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Repository-Cryopreserved
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (Mitf^Mi-wh/+) have a dilut ..... For more information please see the full descriiption on the strain data sheet
000230	B6C3Fe a/a-Tcirg1^oc/J	Repository-Cryopreserved
	Mice homozygous for the osteosclerotic spontaneous mutation (oc) can be recognized at about 10 days by failure of eruption of the incisors, clubbed feet, and circling behavior. Homozygous mutant mice may also have a kinked tail. They grow normally for about the first 10 days of life, then lose weight or at least fail to gain.
000956	B6CB-Mitf^mi-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 Mitf^mi-rw have some pigmentation around the neck and have small red eyes.
000503	B6EiC3Sn a/A-Gy/J	Repository-Cryopreserved
	Gyro (Gy) is an X-linked dominant mutation that causes circling behavior and defects in phospate metabolism. It is allelic with the hypophosphatemia mutation (Phex^Hyp). Hemizygous males and heterozygous females are characterized by hypophosphatemia, rickets, circling behavior, and inner ear abnormalities. Affected males are also sterile.
000225	C3FeLe.B6 a/a-Ptpn6^me/J	Repository-Cryopreserved
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
000627	C3H/HeJ-Kit^W-x/J	Repository-Cryopreserved

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

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

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

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

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

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

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

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

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

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

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

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

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

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

003252	C57BL/6J-Kitl^Sl-20J/J	Repository-Cryopreserved
	Kitl^Sl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile.
002611	C57BL/6J-Mitf^mi-bws/J	Repository-Cryopreserved
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption.
006422	C57BL/6J-hlb324B/J	Repository-Cryopreserved
	For information on hlb324B view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
000965	CBACa.C3-Kit^W-x/J	Repository-Cryopreserved

001723	CByJ.A-Ttc7^fsn/J	Repository-Cryopreserved
	Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G ..... For more information please see the full descriiption on the strain data sheet
000092	FL/1Re-Kit^W/J	Repository-Cryopreserved

005710	FVB.129S-Mmp13^tm1Werb/J	Repository-Cryopreserved
	Mice that are homozygous for this loxP-flanked ("floxed") allele are viable and fertile with normal endogenous gene function. Cre-mediated recombination results in replacement of exons 3-5 of targeted gene with a single loxP site. When bred to cre-expressing transgenic strains, these floxed mutant mice may be used to generate whole mouse or tissue-specific targeted mutants that may be useful in examining extracellular matrix remodeling and bone development. Of note: when these floxed mice are bred to mice containing a beta-actin promoter-driven cre transgene the resulting cre-positive, homozygous-null mice show robust accumulation of cartilage matrix caused by a transient expansion of the hypertrophic zone and increased trabecular bone mass that persists for months.
000993	NZB/BlNJ-Kit^W-59J/J	Repository-Cryopreserved

000979	STOCK Kitl^Sl-16J/J	Repository-Cryopreserved
	The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two Mgf^Sl mutants (e.g. Mgf^Sl/Mgf^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable Mgf^Sl/ Mgf^Sl homozygotes and deficient in the Mgf^Sl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.
001253	STOCK Mitf^Mi-wh +/+ Wnt7a^px/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 (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 descriiption on the strain data sheet
000302	STOCK a/a Mitf^Mi-wh +/+ Itpr1^opt/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 (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 descriiption on the strain data sheet
000161	WB.D2-Kitl^Sl-d/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet

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Strains from the Research Colonies of Jackson Laboratory Scientists

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

Stock Number	Strain Name Strain Description	Standard Supply
000810	C57BL/6J-Ptpn6^me/J	Research Strain
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to a autoimmune pneumonitis.

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New Strains Under Development

(See informational text following listing of strains)

How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
000255	GL/Le Edar^dl-J +/+ Ostm1^gl/J	On Hold
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.
008172	BKS(HRS)-Ddr2^slie/JngJ	Under Development for Production
Mice homozygous for this mutation appear normal at birth. By weaning, they exhibit a reduced body mass, gain weight slower and display minor craniofacial abnormalities such as protruding eyes and a shortened snout. Bone mineral content, but not density is reduced in homozygotes. Plasma glucose levels are significantly increased while blood urea nitrogen levels are decreased in homozygotes. By six weeks, it can be seen that homozygous females lack a corpora lutea. By four months, homozygous males exhibit atrophy of spermatogonia, Sertoli and Leydig cells. This mutant mouse strain has characteristics similar to human Levi type dwarfism and may be useful in studies related to dwarfism and infertility.

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New Strains Under Development
Receive periodic updates on the status of the colony UNDER DEVELOPMENT
Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
Provide input affecting speed and quantity of availability
The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"
Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
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JAX® Mice Strains

Strains from the Research Colonies of Jackson Laboratory Scientists

New Strains Under Development

JAX^® Mice Strains