Overview

Also Known As:Kit^Wv, viable dominant spotting

These mice carry a spontaneous remutation at the Kit locus with homozygotes characterized by having better viability than the Kit^W mutants, macrocytic anemia, and a classic 'black-eyed-white' phenotype. Heterozygotes have mild, normochromic, macrocytic anemia and a white belly spot.

Genetic overview

Genetic Background	Generation

Kit^W-v

Allele Type	Gene Symbol	Gene Name
Spontaneous	Kit	KIT proto-oncogene receptor tyrosine kinase

View Genetics

Research Applications

Cancer Research
Dermatology Research
Developmental Biology Research
Endocrine Deficiency Research
Immunology, Inflammation and Autoimmunity Research
Reproductive Biology Research
Mouse/Human Gene Homologs
Research Tools

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. Heterozygous Kit^W-v mice produce a mid-ventral spot of variable size on the trunk, and very frequently a small mid-dorsal spot on the head as well. Homozygotes produce black-eyed white mice. Kit^W-v homozygotes survive significantly longer than Kit^W homozygotes. The inner ears of homozygotes have marked abnormalities in the cochlea (the most striking abnormalities occur in the organ of Corti and the stria vascularis) and many have severe abnormalities in the saccule as well. Female homozygotes possess very few ovarian follicles at any time and these cease to grow and develop after the age of 2 months. 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. Adult male homozygotes have abnormal testes, being almost devoid of spermatogenesis.

Development

The viable dominant spotting mutation (Kit^W-v) was observed by C.C Little and A.M. Cloudman in crosses made with dominant spotting mice and reported in 1937. The mutant mice were subsequently crossed to "C57 black" mice and have been continually backcrossed to C57BL/6J since. The Jackson Laboratory production colony was obtained from the research colony of Dr. E.S.Russell in 1969.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Arguello F; Furlanetto RW; Baggs RB; Graves BT; Harwell SE; Cohen HJ; Frantz CN. 1992. Incidence and distribution of experimental metastases in mutant mice with defective organ microenvironments (genotypes Sl/Sld and W/Wv). Cancer Res 52(8):2304-9PubMed: 1559233 MGI: J:468
Murphy ED. 1972. Hyperplastic and early neoplastic changes in the ovaries of mice after genic deletion of germ cells. J Natl Cancer Inst 48(5):1283-95PubMed: 4337905 MGI: J:5274
Nocka K; Tan JC; Chiu E; Chu TY; Ray P; Traktman P; Besmer P. 1990. Molecular bases of dominant negative and loss of function mutations at the murine c-kit/white spotting locus: W37, Wv, W41 and W. EMBO J 9(6):1805-13PubMed: 1693331 MGI: J:10528
Reis MM; Tsai MC; Schlegel PN; Feliciano M; Raffaelli R; Rosenwaks Z; Palermo GD. 2000. Xenogeneic transplantation of human spermatogonia. Zygote 8(2):97-105PubMed: 10857580 MGI: J:109890
Shyu H; Hsu S; Hsieh-Li H; Li H. 2001. A novel member of the RBCC family, Trif, expressed specifically in the spermatids of mouse testis. Mech Dev 108(1-2):213-6PubMed: 11578878 MGI: J:71914

View All References

Genetics

Kit^W-v

Allele Symbol: Kit^W-v

Allele Name	viable dominant spotting
Allele Type	Spontaneous
Allele Synonym(s)	Kit^Wv; W^'; W²; W^v; Wv
Gene Symbol and Name	Kit, KIT proto-oncogene receptor tyrosine kinase
Gene Synonym(s)
Strain of Origin	silvered black strain
Chromosome	5
Molecular Note	A C-to-T point mutation at coding nucleotide 1979 (transcript NM_021099) results in a threonine to methionine substitution at amino acid 660 (p.T660M).

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

macrocytic anemia

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Kit^W-v related

Cancer Research
- Growth Factors/Receptors/Cytokines
- Oncogenes
- Increased Tumor Incidence
  - Gonadal Tumors: ovarian
  - Gonadal Tumors
Dermatology Research
- Color and White Spotting Defects
Developmental Biology Research
- Neural Crest Defects
Endocrine Deficiency Research
- Bone/Bone Marrow Defects
- Gonad Defects
- Skin Defects
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - Mast Cell Deficiency
Reproductive Biology Research
- Gonadal Tumors
  - ovarian
- Developmental Defects Affecting Gonads
  - germ cell deficient
- Fertility Defects
Mouse/Human Gene Homologs
- piebaldism
- synpolydactyly
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - Mast Cell Deficiency
Neurobiology Research
- Receptor Defects
- Hearing Defects
Sensorineural Research
- Hearing Defects

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Kit^W-v/Kit⁺
Not Specified

pigmentation phenotype

diluted coat color
- slightly diluted coat color

variable body spotting
- variable amounts of white spotting

abnormal coat/hair pigmentation

integument phenotype

diluted coat color
- slightly diluted coat color

abnormal coat/hair pigmentation

variable body spotting
- variable amounts of white spotting

mammalian phenotype

reproductive system phenotype
- Normal - fertile

Genotype: Kit^W-v/Kit^W-v
involves: CBA/Ca

cardiovascular system phenotype

abnormal stria vascularis vasculature morphology
- the capillary network is poorly developed

integument phenotype

abnormal ear pigmentation
- no strial pigmentation in mutants that lack an endocochlear potential
- about half of the pinnae are pigmented and 21% of inner ears show some pigmentation of the vestibular region

pigmentation phenotype

abnormal ear pigmentation
- no strial pigmentation in mutants that lack an endocochlear potential
- about half of the pinnae are pigmented and 21% of inner ears show some pigmentation of the vestibular region

absent strial intermediate cells
- 89% lack melanocytes within the stria vascularis
- no pigment is present

abnormal melanocyte morphology
- no melanocytes detected in dorsal skin or in hair follicles

abnormal melanosome morphology
- in mutants that do have endocochlear potential, melanin granules were rarely observed and no melanosomes were detected in marginal or basal cells

craniofacial phenotype

abnormal ear pigmentation
- no strial pigmentation in mutants that lack an endocochlear potential
- about half of the pinnae are pigmented and 21% of inner ears show some pigmentation of the vestibular region

growth/size/body region phenotype

abnormal ear pigmentation
- about half of the pinnae are pigmented and 21% of inner ears show some pigmentation of the vestibular region
- no strial pigmentation in mutants that lack an endocochlear potential

hearing/vestibular/ear phenotype

abnormal ear pigmentation
- no strial pigmentation in mutants that lack an endocochlear potential
- about half of the pinnae are pigmented and 21% of inner ears show some pigmentation of the vestibular region

abnormal strial marginal cell morphology
- marginal cells have poorly developed basolateral projections

abnormal strial basal cell morphology
- basal cells have no cytoplasmic projections
- basal cells of the stria vascularis do not contain premelanosomes or melanosomes

absent strial intermediate cells
- 89% lack melanocytes within the stria vascularis
- no pigment is present

abnormal stria vascularis vasculature morphology
- the capillary network is poorly developed

abnormal stria vascularis morphology

absent endocochlear potential
- 89% of homozygous mutants lack an endocochlear potential

thin stria vascularis
- strias are noticeably thinner and are reduced to a two-layered tissue composed only of marginal and basal cells

Genotype: Kit^W-v/Kit^W-v
Not Specified

cardiovascular system phenotype

abnormal stria vascularis vasculature morphology
- vascularity was reduced

integument phenotype

abnormal ear pigmentation
- abnormal pigmentation in the inner ear such as unpigmented stria

abnormal coat/hair pigmentation
- mice are white with contrasting but normal black eye color

craniofacial phenotype

abnormal ear pigmentation
- abnormal pigmentation in the inner ear such as unpigmented stria

nervous system phenotype

abnormal cochlear outer hair cell morphology
- outer hair cells in the organ of Corti were mostly missing or malformed

vestibular hair cell degeneration
- some hair cells in the macula were lost and many others became enlarged and spherical

abnormal cochlear ganglion morphology
- about 50% had abnormal spiral ganglion, with cells appearing immature and occurring in clumps in certain regions

cochlear ganglion degeneration
- reduced cell density and severe degeneration in mutants over 140 days old so that spiral canal was virtually empty

pigmentation phenotype

abnormal coat/hair pigmentation
- mice are white with contrasting but normal black eye color

abnormal ear pigmentation
- abnormal pigmentation in the inner ear such as unpigmented stria

reproductive system phenotype

reduced fertility

growth/size/body region phenotype

abnormal ear pigmentation
- abnormal pigmentation in the inner ear such as unpigmented stria

hearing/vestibular/ear phenotype

abnormal organ of Corti morphology
- form of the organ of Corti was completely changed with no recognizable structure remaining in mutants older than 300 days

abnormal tectorial membrane morphology
- the tectorial membrane grew thicker and was usually attached to Reissner's membrane by 300 days of age
- the tectorial membrane was distorted and no longer in contact with the organ of Corti

abnormal cochlea morphology
- variable cochlea defects that increased in severity as mutants aged

abnormal cochlear outer hair cell morphology
- outer hair cells in the organ of Corti were mostly missing or malformed

enlarged otoliths
- otolith granules were larger

abnormal ear pigmentation
- abnormal pigmentation in the inner ear such as unpigmented stria

thin stria vascularis
- thinner than normal

abnormal otolith morphology
- increase in the amount of otoliths

abnormal stria vascularis morphology

abnormal vestibular saccule morphology
- variable saccule defects that increased in severity as mutants aged

vestibular hair cell degeneration
- some hair cells in the macula were lost and many others became enlarged and spherical

abnormal stria vascularis vasculature morphology
- vascularity was reduced

Genotype: Kit^W-v/Kit⁺
involves: C57BL * C57BL/6

hematopoietic system phenotype

decreased mast cell number
- mice exhibit fewer mast cells in the skin than wild-type mice

decreased erythrocyte cell number

immune system phenotype

decreased mast cell number
- mice exhibit fewer mast cells in the skin than wild-type mice

integument phenotype

diluted coat color

white spotting

pigmentation phenotype

white spotting

diluted coat color

Genotype: Kit^W-v/Kit⁺
involves: C57BL

integument phenotype

variable body spotting
- variable amount of white spotting

diluted coat color
- slightly diluted coat color

mammalian phenotype

reproductive system phenotype
- Normal - fertile

pigmentation phenotype

variable body spotting
- variable amount of white spotting

diluted coat color
- slightly diluted coat color

Genotype: Kit^W-v/Kit⁺
involves: C57BL * DBA

hematopoietic system phenotype

macrocytic anemia
- mild macrocytic anemia

integument phenotype

diluted coat color

head spot
- a head spot frequently but not always occurs

belly spot
- a spot is always present on the belly

pigmentation phenotype

diluted coat color

belly spot
- a spot is always present on the belly

head spot
- a head spot frequently but not always occurs

The following phenotype relates to a compound genotype created using this strain

Genotype: Kit^W-v/Kit^W-v
C57BL/6J-Kit/J

growth/size/body region phenotype

decreased body weight
- weights are normal at embryonic day 16 but by birth the body weight is retarded behind that of wildtype siblings and by 14 days of age there is more than a gram difference in average total body weight and this growth impairment continues to keep these homozygotes smaller than wild-type littermates in the adult

hematopoietic system phenotype

macrocytic anemia
- identified as early as embryonic day 16, the earliest timepoint assessed, and the severity is milder than in W/W homozygotes or compound heterozgyotes

Genotype: Kit^W-v/Kit^W-v
involves: C57BL/6

hematopoietic system phenotype

macrocytic anemia

homeostasis/metabolism phenotype

increased bleeding time
- bleed time of 6.9 minutes on average after tail nick is longer than the 3.8 minutes in C57BL/6J controls

Genotype: Kit^W/Kit^W-v
involves: C57BL/6J

growth/size/body region phenotype

decreased body weight
- weights are normal at embryonic day 16 but by birth the body weight is retarded behind that of wildtype siblings and by 14 days of age the average weight is almost 2 grams less than wildtype siblings

hematopoietic system phenotype

macrocytic anemia
- identified as early as embryonic day 16, the earliest timepoint assessed, and the severity is slighly less than in W homozygotes and more severe than in W-v homozygotes

liver/biliary system phenotype

hepatic steatosis
- seen in P7.5 mutants and adults

mortality/aging

preweaning lethality, incomplete penetrance
- only 65% of compound heterozygotes identified at birth survived to 21 days of age

Genotype: Kit^W-v/Kit⁺
involves: C57BL/6

hematopoietic system phenotype

macrocytic anemia
- slightly macrocytic

References

Arguello F; Furlanetto RW; Baggs RB; Graves BT; Harwell SE; Cohen HJ; Frantz CN. 1992. Incidence and distribution of experimental metastases in mutant mice with defective organ microenvironments (genotypes Sl/Sld and W/Wv). Cancer Res 52(8):2304-9PubMed: 1559233 MGI: J:468
Murphy ED. 1972. Hyperplastic and early neoplastic changes in the ovaries of mice after genic deletion of germ cells. J Natl Cancer Inst 48(5):1283-95PubMed: 4337905 MGI: J:5274
Nocka K; Tan JC; Chiu E; Chu TY; Ray P; Traktman P; Besmer P. 1990. Molecular bases of dominant negative and loss of function mutations at the murine c-kit/white spotting locus: W37, Wv, W41 and W. EMBO J 9(6):1805-13PubMed: 1693331 MGI: J:10528
Reis MM; Tsai MC; Schlegel PN; Feliciano M; Raffaelli R; Rosenwaks Z; Palermo GD. 2000. Xenogeneic transplantation of human spermatogonia. Zygote 8(2):97-105PubMed: 10857580 MGI: J:109890
Shyu H; Hsu S; Hsieh-Li H; Li H. 2001. A novel member of the RBCC family, Trif, expressed specifically in the spermatids of mouse testis. Mech Dev 108(1-2):213-6PubMed: 11578878 MGI: J:71914

Additional References

Ingram DA; Wenning MJ; Shannon K; Clapp DW. 2003. Leukemic potential of doubly mutant Nf1 and Wv hematopoietic cells. Blood 101(5):1984-6PubMed: 12393498 MGI: J:82128
Ito CY; Li CY; Bernstein A; Dick JE; Stanford WL. 2003. Hematopoietic stem cell and progenitor defects in Sca-1/Ly-6A-null mice. Blood 101(2):517-23PubMed: 12393491 MGI: J:81387
Kitamura Y; Kasugai T; Ebi Y; Nomura S. 1991. Fibroblast-dependent differentiation/proliferation of mast cells. Skin Pharmacol 4 Suppl 1:2-7PubMed: 1764248 MGI: J:619
Lai YL; Li H; Chiang HS; Hsieh-Li HM. 2002. Expression of a novel TGIF subclass homeobox gene, Tex1, in the spermatids of mouse testis during spermatogenesis. Mech Dev 113(2):185-7PubMed: 11960710 MGI: J:76545
Ross AJ; Amy SP; Mahar PL; Lindsten T; Knudson CM; Thompson CB; Korsmeyer SJ; MacGregor GR. 2001. BCLW Mediates Survival of Postmitotic Sertoli Cells by Regulating BAX Activity. Dev Biol 239(2):295-308PubMed: 11784036 MGI: J:72582
Takaki S; Morita H; Tezuka Y; Takatsu K. 2002. Enhanced hematopoiesis by hematopoietic progenitor cells lacking intracellular adaptor protein, Lnk. J Exp Med 195(2):151-60PubMed: 11805142 MGI: J:76219

Additional - Kit^W-v related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Restriction Enzyme Digest:Kit-
- Pyrosequencing:KitPYRO
- End Point Analysis:KitAlternate1
- Genotyping resources and troubleshooting
Coat color is used to determine genotypes of our C57BL/6J-Kit^W-v/J colony. This strain is maintained by breeding heterozygote x C57BL/6J (or reciprocal). Heterozygous (Kit^W-v/+) mutants have a gray with light belly and white spot, light tail and feet. The wild-type animals have a black coat color.
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Mating System
- heterozygote x C57BL/6J or reciproca
Appearance
- gray with light belly and white spot, light tail and feet, affected
  Related Genotype: a/a Kit^W-v/+
  
  black
  Related Genotype: a/a +/+
Citation
When using the viable dominant spotting mouse strain in a publication, please cite the originating article(s) and include JAX stock #000049 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous or wildtype for Kit<W-v>

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:KitWv, viable dominant spotting

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

KitW-v

Allele Symbol: KitW-v

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: KitW-v related

Mammalian Phenotype Terms by Genotype

Genotype: KitW-v/Kit+Not Specified

pigmentation phenotype

integument phenotype

mammalian phenotype

Genotype: KitW-v/KitW-vinvolves: CBA/Ca

cardiovascular system phenotype

integument phenotype

pigmentation phenotype

craniofacial phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

Genotype: KitW-v/KitW-vNot Specified

cardiovascular system phenotype

integument phenotype

craniofacial phenotype

nervous system phenotype

pigmentation phenotype

reproductive system phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

Genotype: KitW-v/Kit+involves: C57BL * C57BL/6

hematopoietic system phenotype

immune system phenotype

integument phenotype

pigmentation phenotype

Genotype: KitW-v/Kit+involves: C57BL

integument phenotype

mammalian phenotype

pigmentation phenotype

Genotype: KitW-v/Kit+involves: C57BL * DBA

hematopoietic system phenotype

integument phenotype

pigmentation phenotype

Genotype: KitW-v/KitW-vC57BL/6J-Kit/J

growth/size/body region phenotype

hematopoietic system phenotype

Genotype: KitW-v/KitW-vinvolves: C57BL/6

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: KitW/KitW-vinvolves: C57BL/6J

growth/size/body region phenotype

hematopoietic system phenotype

liver/biliary system phenotype

mortality/aging

Genotype: KitW-v/Kit+involves: C57BL/6

hematopoietic system phenotype

References

Additional References

Additional - KitW-v related

Genotyping Protocols

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Also Known As:Kit^Wv, viable dominant spotting

Kit^W-v

Allele Symbol: Kit^W-v

Genotype: Kit^W-v related

Genotype: Kit^W-v/Kit⁺
Not Specified

Genotype: Kit^W-v/Kit^W-v
involves: CBA/Ca

Genotype: Kit^W-v/Kit^W-v
Not Specified

Genotype: Kit^W-v/Kit⁺
involves: C57BL * C57BL/6

Genotype: Kit^W-v/Kit⁺
involves: C57BL

Genotype: Kit^W-v/Kit⁺
involves: C57BL * DBA

Genotype: Kit^W-v/Kit^W-v
C57BL/6J-Kit/J

Genotype: Kit^W-v/Kit^W-v
involves: C57BL/6

Genotype: Kit^W/Kit^W-v
involves: C57BL/6J

Genotype: Kit^W-v/Kit⁺
involves: C57BL/6

Additional - Kit^W-v related