| First Author | Taylor LA | Year | 2000 |
| Journal | Mamm Genome | Volume | 11 |
| Issue | 4 | Pages | 255-9 |
| PubMed ID | 10754100 | Mgi Jnum | J:61104 |
| Mgi Id | MGI:1354450 | Doi | 10.1007/s003350010050 |
| Citation | Taylor LA, et al. (2000) Whiskers amiss, a new vibrissae and hair mutation near the Krt1 cluster on mouse chromosome 11. Mamm Genome 11(4):255-9 |
| abstractText | Whiskers amiss (wam) is a new spontaneous recessive mutation in the SELH/Bc strain of mice that causes a phenotype of askew, sometimes kinked or curled, breakable whiskers and disheveled-appearing body hair, apparently owing to disoriented guard hairs. Heterozygotes on three genetic backgrounds are indistinguishable from normal. Using informative SSLPs in the F2 generation after crosses to two normal strains, we have mapped wam to the region of the type I keratin cluster on Chromosome (Chr) 11, within an approximately 6-cM segment according to the current Mouse Genome Database (MGD) map position of flanking SSLPs. Although several other hair mutations also map to the Krt1 region (Re, Rim3, Bdai, Bsk), none has a hair and whisker phenotype similar to that of wam, and, because all are transmitted as dominants, interpretable complementation tests could not be done. Scabbing and tissue loss occur on the rims of the pinnae and tail tip in some aging wam homozygotes, suggesting that wam may be an animal model of a genetic ectodermal disorder. The SELH/Bc strain background appears to have an unusually high rate of spontaneous mutation; wam is the sixth mutation to be described. |
