The expression of the gene asebia in the laboratory mouse: 2. Hair follicles

Abstract

SUMMARYMice homozygous for the asebia mutation (ab/ab) are char1acterized by defective sebaceous glands, a short sparse hair coat from 7 days and progressive alopecia. In addition, we have found that the initial hair follicle rudiments in the skin of these mice are able to differentiate into relatively normal anagen follicles which are often excessive in length and have minor abnormalities of the inner and outer root sheath components. The inner root sheath fails to form the typical transverse corrugations at the level of the sebaceous glands and its cells apparently remain, partially undegraded, plugging the hair canal and adhering to emerging hair shafts. Defects noted in the outer root sheath may be responsible for the failure of inner root sheath degradation. With increasing age, irregularities in hair cycle duration, loss of the originally parallel arrangement of hair follicles and further abnormalities of the individual follicular components are increasingly evident. Follicles in asebic mice have a tendency to form buds and branches which occasionally begin typical follicular differentiation. The consistent failure of the asebic follicles to pass normally through the catagen stage to the telogen stage results in long twisted follicles with abnormal and often loosely anchored hair clubs. The dermal papillae are often abnormal or absent from telogen follicles, while typical germ cells are not formed. Thus the lack of multiple hair follicles, the disorganization of follicles and the progressive alopecia observed in the asebic mice are accounted for. It is suggested that the altered dermal environment and outer root sheath abnormalities may be responsible for many of the follicular defects.