| First Author | Lamoreux ML | Year | 1992 |
| Journal | J Hered | Volume | 83 |
| Issue | 6 | Pages | 435-9 |
| PubMed ID | 1460250 | Mgi Jnum | J:3383 |
| Mgi Id | MGI:51896 | Doi | 10.1093/oxfordjournals.jhered.a111247 |
| Citation | Lamoreux ML, et al. (1992) The vit gene maps to the mi (microphthalmia) locus of the laboratory mouse. J Hered 83(6):435-9 |
| abstractText | The murine model for human vitiligo (the vit/vit mouse) develops progressive depigmentation of the pelage, skin, and eyes. The vit gene is inherited as an autosomal recessive. We have used classical breeding and isozyme marker analysis to map this vit gene that produces a vitiligo-like condition in the mouse. Crossbreeding the C57BL/6J-vit/vit mice with C57BL/6J mice carrying the Miwh and/or miws alleles at the microphthalmia locus resulted in mutant phenotypes, demonstrating absence of complementation. When vit is heterozygous with the Miwh allele, a blotched pigment pattern results. When it is heterozygous with the miws allele, a novel expression of the vitiliginous phenotype results. Further mating analysis of these crossbred populations demonstrates allelic inheritance between vit and the alleles at the microphthalmia locus. Other breeding studies using alleles at the agouti, belted, brown, dominant spotting, extension, mahogany, patch, and piebald loci did not demonstrate pigmentation explainable by allelic inheritance with the vit gene. Also, vit was tested for linkage with isozyme markers located on chromosomes 1, 4, 5, 7, 9, and 11, and results were negative. Therefore, the vit (vitiligo) gene of the laboratory mouse has been mapped to the mi (microphthalmia) locus on chromosome 6. The gene properly should be designated as mivit. |
