ABSTRACT
The bareskin mutation arose out of mutagenesis studies. Two mutant mice were found in a litter sired by a male mouse treated with 250 milligram/kilogram of ethylnitrosourea. Breakage of the zigzag hairs was common in the hairs collected from mutant mice but not of hairs collected in the same manner from the control mouse. Microscopically, the epidermis was moderately acanthotic and hair follicles were essentially absent in long stretches of truncal skin. Bareskin maps to mouse Chromosome 11. The clustering of mutations with similar phenotypes on mouse Chromosomes 11 and 15 led to the speculation that the genes coded proteins involved in hair structure. These genes were subsequently determined to be the type I (Chromosome 11) and type II (Chromosome 15) keratin genes. No human diseases have been compared with the mouse bareskin mutation. No domestic animal genodermatoses have been compared with the mouse bareskin mutation.
