ABSTRACT
Asebia is maintained as an inbred strain. Abnormalities of the sebaceous glands appear to be the same between the two mutations. The asebia mutation is autosomal recessive and maps to mouse Chromosome 19. Homozygous asebia mice exhibit abnormalities of hair growth that can sometimes be detected as early as 7 days of age. Fine epidermal scaling may be mild but becomes more severe with age. Mutant mice also exhibit alterations of their epidermis, dermis, and hair follicles. The epidermis becomes moderately thicker (orthokeratotic), which increases in severity with age. The dermis is thicker and more vascular than littermate controls with various degrees of inflammation. Most publications utilizing the asebia mouse have been directed at characterizing the phenotype of the mutation or as a double mutation with hairless or rhino to help define the phenotype of those mutations. The asebia mutation has been used as a model for therapeutic regimens directed at hyperkeratotic diseases.
