Estimated Removal of Live Colony date: 17 April 2020.KitW/KitW-v double heterozygotes are mast cell deficient, and lack intermediate cells derived from melanoblasts in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. Read More +
This strain is heterozygous for the retinal degeneration allele Pde6brd1.
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.
|Allele Name||dominant spotting|
|Gene Symbol and Name||Kit, KIT proto-oncogene receptor tyrosine kinase|
|Strain of Origin||old mutant of the mouse fancy|
|General Note||This is an old mutant of the mouse fancy. KitW mutants are a potential model for human inherited pure red cell anemia, called Diamond-Blackfan anemia (OMIM 205900), but mouse mutants do not respond to corticosteroid treatment as do human patients. Thus, the mechanism of anemia causation in the two conditions must be different (J:14286).|
|Molecular Note||A guanosine to adenosine substitution at the first nucleotide at the 5' boundary of the intron following the transmembrane exon results in two different aberrantly spliced transcripts putatively expressed in a tissue specific manner. A deletion of 107 bp was found in transcripts from mast cells of mutant mice. A deletion of 234 was found in transcripts from brain or bone marrow cells. The GT to AT point mutation probably disrupted a splice donor site, thereby causing exon skipping. The 107 bp deletion could have resulted from skipping of a transmembrane region exon and the 234 bp deletion from skipping 3 exons. The 107 bp deletion would generate a stop codon 12 bp downstream because of a frame shift, whereas the larger deletion would still be in frame. Northern blot analysis indicated that mast cells from mutants have only 31-37% of the transcripts as mast cells derived from normal bone marrow, suggesting that the mutation may reduce efficiency and authenticity of transcription and splicing.|
|Allele Name||viable dominant spotting|
|Allele Synonym(s)||KitWv; W'; W2; Wv; Wv|
|Gene Symbol and Name||Kit, KIT proto-oncogene receptor tyrosine kinase|
|Strain of Origin||silvered black strain|
|Molecular Note||A C to T point mutation at nucleotide 2007 results in a threonine to methionine substitution at amino acid 660.|
The Jackson Laboratory uses phenotype to determine genotypes for the WBB6F1/J-KitW/KitW-v/J mouse strain. See appearances for this strain under the Description tab.
When using the W/Wv mouse strain in a publication, please cite the originating article(s) and include JAX stock #100410 in your Materials and Methods section.
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