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The expression of the gene asebia in the laboratory mouse: 3. Sebaceous glands

Published online by Cambridge University Press:  14 April 2009

Wendy J. Josefowicz  and
Margaret H. Hardy
Wendy J. Josefowicz
Affiliation:
Department of Biomedical Sciences, University of Guelph, Guelph, Canada NIG 2W2
Margaret H. Hardy
Affiliation:
Department of Biomedical Sciences, University of Guelph, Guelph, Canada NIG 2W2
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Summary

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Contrary to what their name asebia implies, mice homozygous for the ab gene do possess actively secreting sebaceous glands which develop normally from the follicular outer root sheath, at 18 days post-conception. However, by the 20th day post-conception, these mice exhibit the abnormal sebaceous cytodifferentiation which remains typical of the asebic glands throughout life. Nests of outer root sheath cells below the sebaceous glands also undergo atypical sebaceous differentiation. The smooth membrane system and mitochondria, which appear to be responsible for the orderly accumulation of lipid droplets and sebum production in normal mice, become increasingly abnormal in asebic mice. Fewer lipid droplets form, the smooth endoplasmic reticulum becomes distorted and dilated, and the normal transformation of mitochondria does not occur. Atypical differentiation occurs randomly and ‘differentiated’ cells often degenerate within the asebic sebaceous glands. Of the larger specialized sebaceous-type glands studied, only the Meibomian glands are similarly affected by the asebia mutation, while the anal and preputial glands appear to undergo a more normal cytological differentiation. The abnormalities seen in the asebic sebaceous glands seem to be due to defective regulation of the synthetic or degenerative processes necessary for completion of normal sebum production. Both the defects of sebaceous glands and the unusual characteristics of the epidermis and hair follicles in asebic mice may be initiated by the abnormal underlying dermis or the apparently abnormal endocrine system.

Type
Research Article
Information
Genetics Research , Volume 31 , Issue 2 , April 1978 , pp. 157 - 166
Copyright
Copyright © Cambridge University Press 1978

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