Search Criteria: Research Area is "Developmental Biology Research: Neural Crest Defects"

Additional Register Interest Strains

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
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.
000676 LP/J
Level 4
LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (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.
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.
100410 WBB6F1/J-KitW/KitW-v/J
Level 4
Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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.
016588 A.B6-KitW-v/BeiMmjax
Repository- Live
Homozygote: 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. On the A/J background, the classic black-eyed albino phenotype cannot be used to assess genotype. The donating investigator reports that mice on this background exhibit poor viability, mast cell defects, decreased airway hyperresponsiveness and sterility. On the hybrid (C57BL/6 x A/J)F1 background, KitW homozygotes are viable and exhibit decreased airway hyperresponsiveness.

Heterozygote: Not evaluated. On the albino A/J background, coat color markings are not visible.

006084 B6.129P2(Cg)-Foxg1tm1(cre)Skm/J
Repository- Live
This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma .....
For more information please see the full phenotype on the strain data sheet
005317 B6.Cg-Tg(BAT-lacZ)3Picc/J
Repository- Live
Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These "BAT-GAL" transgenic mice are a reporter strain that express beta-galactosidase in the presence of activated beta-catenin. The transgene expresses the lacZ gene under the control of a regulatory sequence consisting of seven consensus LEF/TCF-binding motifs upstream of the Xenopus siamois gene minimal promoter. Transgenic mice display beta-galactosidase activity beginning at embryonic day 6.0 in the posterior side of the proximal epiblast. Beta-galactosidase expression is detectable in the posterior primitive streak and node at gastrulation, and progresses to the paraxial mesoderm and notochord. Beta-galactosidase activity in developing and adult nervous tissue mimics the pattern of Wnt signaling. When bred to other mutant strains, this reporter strain may be useful for identifying mutations that affect the Wnt-signalling pa .....
For more information please see the full phenotype on the strain data sheet
018354 B6;129S4-Ror2tm1.1Meg/J
Repository- Live
These Ror2f/f mutant mice possess loxP sites flanking exons 3-4 of the receptor tyrosine kinase-like orphan receptor 2 (Ror2) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. ROR2 is a cell surface tyrosine-protein kinase receptor expressed during development of the facial primordia, limb mesenchyme, neural crest-derived tissues, and the genital tubercle. ROR2 is involved in cartilage and bone formation, and growth plate development, and is required for Wnt5a-mediated signaling. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 3-4 deleted in the cre-expressing tissues.

For example, when bred to Tg(EIIa-cre)C5379Lmgd transgenic mice, ROR2 null mice exhibit facial malformations, and truncation of the limbs and posterior region of the embryo. ROR2 null mice die soon after birth. This .....
For more information please see the full phenotype on the strain data sheet

000674 I/LnJ
Repository- Live
I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> .....
For more information please see the full phenotype on the strain data sheet
003720 JF1/Ms
Repository- Live
JF1/Ms (Japanese Fancy Mouse) was derived from a mouse stock purchased from a market in Denmark, and has been identifed as belonging to species M. m. molossinus. JF1 carries the piebald allele, a retroposon-like insertion in intron 1 of the endothelin receptor type B (Ednrb) gene, which results in a white coat with black spots and black eyes. The white areas of the coat are lacking in neural crest-derived melanocytes. In addition to alterations in coat color, JF1 mice exhibit a decreased amount of enteric innervation and neuronal density predominantly in the distal colon, but do not exhibit any of the megacolon symptoms often associated with mutations in Ednrb. Wild-derived mice are genetically distinct from common laboratory mice for a number of complex phenotypic characteristics and are valuable tools for genetic mapping, evolution and systematics research.
023412 B6N(Cg)-Pax7tm1.1(KOMP)Vlcg/J
Under Development - Now Accepting Orders
This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Pax7 (paired box gene 7) gene encodes a transcription factor involved in neural crest development and gastrulation. A beta-galactosidase-containing cassette disrupts the Pax7 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website.
023405 STOCK Tfap2atm1.1Hsv/J
Under Development - Now Accepting Orders
The AP-2alphaki knock-in/knockout allele has an IRES-lacZ cassette inserted into exon 7 of the transcription factor AP-2α gene; both abolishing endogenous gene function and placing lacZ expression under direction of the Tfap2a promoter/enhancer regions. Wildtype mice have AP-2alpha expression in the neural tube, and in cranial and cardiac neural crest cells in the developing embryo, as well as in the progress zone of the limb bud, the developing kidney, the eye, and surface ectoderm. Most homozygotes exhibit prenatal or postnatal lethality due to neural tube, craniofacial, body wall, and cardiac malfomation, while the majority of heterozygotes are viable and fertile. In these mice, β-gal labels the ectoderm, and cranial and cardiac neural crest populations during the E8.5-10.5. Homozygous mice exhibit failure of neural tube closure by E9.5, and outflow tract abnormalities from E14.5-15.5.
004337 129(Cg)-Foxg1tm1(cre)Skm/J
Cryopreserved - Ready for recovery
This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development.
002516 129-Edn3tm1Ywa/J
Cryopreserved - Ready for recovery
This mutation is alleleic with the lethal spotting spontaneous mutation. Homozygous mice are viable at birth, but most die within about a month. They show a disruption in neural crest lineage development. They die from peritonitis subsequent to aganglionic megacolon. They may serve as a model for human Hirschsprung's disease.
009085 129S/Sv-Rettm1Cos/J
Cryopreserved - Ready for recovery
The Ret- allele (also called ret-k-, ret-k minus, or c-ret-) disrupts the region of the ret proto-oncogene (Ret; also called ret-k or c-ret) locus harboring the invariant lysine codon required for Ret kinase activity. Homozygous mice die around 16-24 hours after birth, exhibiting abnormalities in kidney/urinary (renal agenesis/hypodysplasia) and peripheral nervous system development (including sympathetic, parasympathetic, and enteric ganglia), as well as abnormal enteric neural crest cell migration. Because homozygous mice lack enteric ganglia from the hindgut, these mice are also a model of Hirschsprung's Disease.
000090 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J
Cryopreserved - Ready for recovery
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 phenotype on the strain data sheet
000599 B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
Cryopreserved - Ready for recovery
000577 B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
Cryopreserved - Ready for recovery
006564 B6(C)-KitW-41J Gusbmps/BrkJ
Cryopreserved - Ready for recovery
Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They .....
For more information please see the full phenotype on the strain data sheet
002463 B6.129S-Itga4tm1Hyn/J
Cryopreserved - Ready for recovery
Mice homozygous for the Itga4tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4.
002274 B6.129S-Itga5tm1Hyn/J
Cryopreserved - Ready for recovery
Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches.
000495 B6.C-H38c/By-KitW-56J/J
Cryopreserved - Ready for recovery
000560 B6.C-H7b/By KitW-50J/J
Cryopreserved - Ready for recovery
000122 B6.C3-KitW-44J/J
Cryopreserved - Ready for recovery
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 phenotype on the strain data sheet
000991 B6.C58-KitW-57J/J
Cryopreserved - Ready for recovery
000133 B6.Cg-KitW-24J/J
Cryopreserved - Ready for recovery
000139 B6.Cg-KitW-25J/J
Cryopreserved - Ready for recovery
000164 B6.Cg-KitW/J
Cryopreserved - Ready for recovery
000124 B6.Cg-KitlSl Krt71Ca/J
Cryopreserved - Ready for recovery
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 phenotype on the strain data sheet
000194 B6.Cg-Lx KitW-v/J
Cryopreserved - Ready for recovery
Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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/> .....
For more information please see the full phenotype on the strain data sheet

000158 B6.Cg-MitfMi-wh/MitfMi/J
Cryopreserved - Ready for recovery
Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (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 phenotype on the strain data sheet
000311 B6.Cg-Pax3Sp N/J
Cryopreserved - Ready for recovery
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).
000171 B6.D2-KitW-45J/J
Cryopreserved - Ready for recovery
001563 B6.D2-KitW-73J/J
Cryopreserved - Ready for recovery
001177 B6.LP-KitW-49J/J
Cryopreserved - Ready for recovery
003295 B6;129-Ednrbtm1Ywa/J
Cryopreserved - Ready for recovery
In this strain, a neo cassette replaces exon 3 of the endothelin receptor type B (Ednrb) gene, abolishing gene function. Ednrb encodes a G protein-coupled receptor expressed in vascular endothelial cells where it is involved in vasoconstriction, vasodilation, bronchoconstriction and cell proliferation. Mutations have been associated with Waardenburg syndrome type 4 (Waardenburg-Shah syndrome) characterized by deafness, neural crest defects, pigmentation changes, and Hirschsprung's disease. Hirschsprung's disease is an intestinal disorder that causes intestinal blockage. Homozygotes are viable but usually die within the first month of life. They show a disruption of neural crest lineage development, which is characterized by a lack of hair or skin pigmentation on 90% of their body. They die due to peritonitis from distention caused by an aganglionic megacolon. The phenotype is less severe on this B6/129 hybrid background than on the congenic C57BL/6J background (Stoc .....
For more information please see the full phenotype on the strain data sheet
012373 B6;129S-Hoxb1tm1(cre)Og/J
Cryopreserved - Ready for recovery
Mice that are heterozygous for the targeted mutation are viable, fertile, and normal in size. The Cre recombinase expression pattern matches the endogenous gene expression pattern in heterozygous animals. Cre mediated recombination is detected in almost all tissues caudal to the hindbrain at age embryonic day 10.5 (spinal cord, peripheral nervous system, axial and appendicular musculature, and mesenchymal tissues). Mice that are homozygous for this targeted mutation allele are deficient (null) for HOXB1 and exhibit a phenotype similar to other null mutants (craniofacial defects, abnormal facial neurogenesis, facial muscle degeneration).

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify .....
For more information please see the full phenotype on the strain data sheet

000350 B6By.Cg-KitW-v MitfMi-wh T/J
Cryopreserved - Ready for recovery
Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. 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 phenotype on the strain data sheet
001573 B6C3Fe a/a-MitfMi/J
Cryopreserved - Ready for recovery
Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the 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.
000291 C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
Cryopreserved - Ready for recovery
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 phenotype on the strain data sheet
000627 C3H/HeJ-KitW-x/J
Cryopreserved - Ready for recovery
000847 C3Sn.B6-KitW-39J/J
Cryopreserved - Ready for recovery
001380 C3Sn.Cg-KitlSl-con/J
Cryopreserved - Ready for recovery
Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-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-KitW-17J/J
Cryopreserved - Ready for recovery
000167 C57BL/6J-KitW-18J/J
Cryopreserved - Ready for recovery
000169 C57BL/6J-KitW-20J/J
Cryopreserved - Ready for recovery
000117 C57BL/6J-KitW-34J/J
Cryopreserved - Ready for recovery
000128 C57BL/6J-KitW-35J/J
Cryopreserved - Ready for recovery
000134 C57BL/6J-KitW-37J/J
Cryopreserved - Ready for recovery
000062 C57BL/6J-KitW-39J/J
Cryopreserved - Ready for recovery
000121 C57BL/6J-KitW-40J/J
Cryopreserved - Ready for recovery
000119 C57BL/6J-KitW-41J/J
Cryopreserved - Ready for recovery
000127 C57BL/6J-KitW-42J/J
Cryopreserved - Ready for recovery
000129 C57BL/6J-KitW-43J/J
Cryopreserved - Ready for recovery
000990 C57BL/6J-KitW-55J/J
Cryopreserved - Ready for recovery
001179 C57BL/6J-KitW-62J/J
Cryopreserved - Ready for recovery
003252 C57BL/6J-KitlSl-20J/J
Cryopreserved - Ready for recovery
KitlSl-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.
000565 C57BL/6J-Pax3Sp-d/J
Cryopreserved - Ready for recovery
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.
000118 C57BL/6J-Ph/J
Cryopreserved - Ready for recovery
000965 CBACa.C3-KitW-x/J
Cryopreserved - Ready for recovery
000092 FL/1Re-KitW/J
Cryopreserved - Ready for recovery
Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been .....
For more information please see the full phenotype on the strain data sheet
000262 LS/LeJ
Cryopreserved - Ready for recovery
Mice homozygous for the lethal spotting mutation (Edn3ls) resemble piebald mice (Ednrbs/Ednrbs) mice. Homozygous mutant mice exhibit considerable white spotting and like homozygotes for the piebald-lethal allele (Ednrbs-l) usually develop megacolon. Lethal spotting mutant mice usually die in the third week of life from the megacolon abnormality, which is associated with deficiency of intrinsic ganglion cells in the lower colon. A few homozygotes may survive and breed. This strain is also homozygous for the black and tan coat color mutation (at).
000993 NZB/BlNJ-KitW-59J/J
Cryopreserved - Ready for recovery
000308 SSL/LeJ
Cryopreserved - Ready for recovery
This inbred strain carries both the piebald (Ednrbs) and piebald lethal (Ednrbs-l) alleles. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. Homozygous piebald lethal mice are almost completely white with dark eyes and only an occasional small pigmented spot on the head or rump. Piebald-piebald lethal heterozygotes (Ednrbs/Ednrbs-l) mice resemble piebald mice in the degree of spotting. The piebald mutations disrupt the development of melanocytes derived from the neural crest. All piebald lethal homozygotes develop megacolon with a lack of enteric ganglion cells in the posterior end of the colon. On the SSL/Le background, although many Ednrbs-l homozygotes die between 2 and 4 weeks of age, significant numbers survive and may breed. The incidence of megacolon is reduced in piebald and piebald-piebald lethal .....
For more information please see the full phenotype on the strain data sheet
004711 STOCK Ednrbs-52Pub
Cryopreserved - Ready for recovery
009063 STOCK Ednrbtm1Nrd/J
Cryopreserved - Ready for recovery
Mice heterozygous for this Ednrbflex3 allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 3, as well as a loxP site downstream of exon 3 of the Ednrb (endothelin receptor type B or ET-B receptor) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 3 deleted, or both the neo selection cassette and exon 3 deleted. The two latter genotypes are expected to result in a frameshifted transcript that is reported to confer the null phenotype. These mutant mice may be useful in generating conditional mutations for studying the role of Ednrb in development of melanocytes, development of neurons and glia of the enteric nervous system, neural crest-derived cells, mesenchymal-derived smooth muscle cells, vasodilation, mitogen signaling and cancer, and human Hirschsprung's dis .....
For more information please see the full phenotype on the strain data sheet
000979 STOCK KitlSl-16J/J
Cryopreserved - Ready for recovery
The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-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 MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ 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.
002902 STOCK Pax3Sp Mlphln/J
Cryopreserved - Ready for recovery
000275 V/LeJ
Cryopreserved - Ready for recovery
This strain was originally used as a linkage stock for gene mapping. It is homozygous for several visible recessive mutations all located on different chromosomes including nonagouti (a), fuzzy (fz), leaden (Mlphln), and piebald (Ednrbs) and is segregating for the neurological mutation, waltzer (Cdh23v). Homozygous waltzer mice show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. Homozygous piebald mice have dark eyes. The white areas of the coat are completely lacking in melanocytes and there is a reduction in the number of melanocytes in the choroid layer of the eye.
000693 WC/ReJ KitlSl/J
Cryopreserved - Ready for recovery
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 phenotype on the strain data sheet

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Stock
Number
Strain Name
 
Strain Description
Standard Supply
024843STOCK Foxi3tm1.1Akg/J
Under Development for Cryo
These Foxi3flox mice may be useful for studying the development of branchial arch and neural crest derivatives.

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