THE EXPRESSION AND INTERACTION OF HEREDITARY FACTORS PRODUCING HYPOTRICHOSIS IN THE MOUSE: HISTOLOGY AND EXPERIMENTAL RESULTS

Abstract

The first visible abnormality in the skins of homozygous rhino mice is a hyperkeratosis of the epidermis and follicle neck wall at the time when active growth of the hair ceases. This is associated with a widening of the hair canal (due to a lateral expansion of the hyperplastic layers of the follicle neck) and a subsequent irregular shortening of the follicle. The cause of hair loss is considered to be the widening of the hair canal and consequent lack of the support supplied by the normally tight-fitting follicle neck when shortening of the follicle raises the base of the hair to a level just below the proximal end of the hair canal. The hyperplastic tendencies of the epidermal derivatives are further expressed by (a) the development of hair canal cysts (utriculi), which leads to an increase in the surface area and a consequent wrinkling of the skin, (b) the formation of sebaceous-gland and follicle-end cysts, which cause the thickening of the epidermis, and (c) overgrowth of the nails.Hairless (hr hr) mice show a similar, but less extreme, tendency towards hyperplasia, and the histological character of the skins of hairless/rhino hybrids is intermediate between that of the rhino and hairless types.Mice of any of these types (hr hr, hrrhhr, hrrhhrrh), which are also heterozygous for the Naked factor, show an exaggeration of both the follicular keratosis and the Naked characteristics. In mice homozygous for the Naked factor the exaggeration is more extreme.Transplantation experiments show that rhino skin adjacent to normal skin behaves non-autonomously, indicating that rhino skin cells are able to utilize but cannot produce some substance necessary for the maintenance of normal stratified squamous epithelium; this substance is produced by normal skin cells but is not present in the blood stream of normal mice.Results of an attempt to discover a relationship between the mode of action of the rhino mutation and the metabolism of vitamin A by feeding rhino mice massive doses of vitamin A were inconclusive.