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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Identification of a Keratin 4 mutation in a chemically induced mouse mutant that models white sponge nevus.

With the goal of increasing the number of genetic entry points for studying physiologic processes and human disease, large-scale, systematic, chemical mutagenesis projects in mice have been initiated in several different centers. We have been studying mouse mutants that exhibit dominantly inherited defects in either skin and/or hair color. Here, we describe a bright coat color mutant, Bright coat color 1 (Bcc1), which develops light-colored hair at 4 weeks of age, and when homozygous exhibits oral leukoplakia and blistering, and growth retardation. We identified a missense mutation in mutant animals that predicts an N154S amino-acid substitution in the 1A domain of Keratin 4 (encoded by the Krt2-4 gene), a region known to be mutated in human patients with white sponge nevus (WSN). Bcc1 recapitulates the gross pathologic, histologic, and genetic aspects of the human disorder, WSN.[1]

References

  1. Identification of a Keratin 4 mutation in a chemically induced mouse mutant that models white sponge nevus. McGowan, K.A., Fuchs, H., Hrab?? de Angelis, M., Barsh, G.S. J. Invest. Dermatol. (2007) [Pubmed]
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