ANGORA MOUSE MUTATION - ALTERED HAIR CYCLE, FOLLICULAR DYSTROPHY, PHENOTYPIC MAINTENANCE OF SKIN-GRAFTS, AND CHANGES IN KERATIN EXPRESSION

Angora is an autosomal recessive mouse mutation caused by a deletion o f similar to 2 kilobases in the fibroblast growth factor 5 (Fgf5) gene . Phenotypically, homozygous angora (Fgf5(go)/FgfS(go)) mice have exce ssively long truncal hair and can be differentiated from heterozygous (+/Fgf5(go)) and wild-type (+/+) littermates by 21 days of age. Abnorm al hair length is due to a prolongation of the anagen phase of the hai r cycle of approximately 3 days. In addition, widely scattered hair fo llicles produce structurally defective hair shafts that twist within t he follicle, presumably causing secondary hyperplasia of the outer roo t sheath and epidermis adjacent to the follicle. These follicular abno rmalities were accentuated by immunohistochemical detection of mouse s pecific keratin 6, a nonspecific marker of epidermal hyperplasia. Thes e abnormalities could be identified from birth throughout life in ango ra mice genotyped by polymerase chain reaction techniques. Moreover, t he long truncal hair phenotype was maintained in skin grafted onto C.B -17/S-z-scid/scid mice that had normal pelage hairs and hair cycles, s uggesting that circulating or diffusible humoral factors regulating th e mouse hair cycle are not involved in this mutation. The angora mutat ion provides another useful mouse model for studying the hair cycle an d its modulation.