The KitW-sh (or "sash") mutation results in an embryonic deficit and eventual abolishment of mast cells soon after birth. There is also a deficit of melanocytes and interstitial cells in these mice. Reduced numbers of melanocytes results in some hearing impairment in homozygotes. The KitW-sh mutation is a inversion in regulatory elements upstream of the c-kit element. Homozygous mice have white coat, black eyes, and some pigment around the ears. Heterozygotes have black coat with a white sash at the midline. Wildtype mice should have black coat (indistinguishable from C57BL/6J). Additionally, The Jackson Laboratory Stock Nos. 012861 and 030764 have historically/consistently exhibited longer white fur covering the body of homozygotes, while heterozygotes have longer white belt/sash fur but normal length black fur. For Stock No. 030764, the longer white fur coat is more prevalent in the 3-5 week age range, by 6 weeks the coat in the majority of homozygotes breeders starts to look smoothed out, and may proceed to become a more typical length over time. For Stock No. 012861, the longer white fur coat may persist throughout the life of the animal. Heterozygous and homozygous mice are fertile and not anemic. 2012: Findings of altered immune responses as a result of mast cell deficit in these mice include: &nbsp;&nbsp;&nbsp;&bull; &nbsp; heightened susceptibility to vaccinia virus skin infection; &nbsp;&nbsp;&nbsp;&bull; &nbsp; earlier and more severe experimental autoimmune encephalomyelitis disease (a model of multiple sclerosis) with extensive demyelination and inflammation in the CNS; &nbsp;&nbsp;&nbsp;&bull; &nbsp; exacerbated dermatitis upon repeated oxazolone challenge when compared to their wild-type; &nbsp;&nbsp;&nbsp;&bull; &nbsp; Ultra violet exposure in these mice does not induce immune suppression, as it does in wild type mice; &nbsp;&nbsp;&nbsp;&bull; &nbsp; lower serum IgE levels compared with wildtype mice under steady-state conditions and after N. brasiliensis (hookworm) infection; &nbsp;&nbsp;&nbsp;&bull; &nbsp; failure to elicit histamine release or contractile responses in trachea isolated from ovalbumin sensitized mast cell-deficient mice; &nbsp;&nbsp;&nbsp;&bull; &nbsp; development of ~50% more adenomas than littermate controls and with tumors being ~33% larger in KitW-sh mice; &nbsp;&nbsp;&nbsp;&bull; &nbsp; increased resistance to bacterial lipopolysaccharide injection; &nbsp;&nbsp;&nbsp;&bull; &nbsp; failure of ovalbumin sensitization to elicit histamine release or contractile responses in trachea isolated from sensitized KitW-sh mice. 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 description if necessary as published results become available. Also see Stock No. <a href="https://www.jax.org/strain/030764">030764</a> that has been backcrossed to C57BL/6J using a marker-assisted speed congenic protocol.

A C57BL/6J congenic version of this strain made via SNP marker-assisted speed congenic protocol is available as Stock No. <a href="https://www.jax.org/strain/030764">030764</a> (all 140+ tested markers outside the Kit genomic region were C57BL/6J). The spontaneous KitW-sh (or "sash") mutation affects melanoblast and mast cell survival, and may be useful in studying melanogenesis, hematopoiesis, gametogenesis and mast cell deficiency.

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