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Human Molecular Genetics Advance Access originally published online on September 23, 2003
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Human Molecular Genetics, 2003, Vol. 12, No. 22 2931-2940
DOI: 10.1093/hmg/ddg325
© 2003 Oxford University Press

Inducible mEDA-A1 transgene mediates sebaceous gland hyperplasia and differential formation of two types of mouse hair follicles

Chang-Yi Cui1, Meredith Durmowicz1, Chris Ottolenghi1, Tsuyoshi Hashimoto1, Bradley Griggs2, Anand K. Srivastava2 and David Schlessinger1,*

1Laboratory of Genetics, NIH/National Institute on Aging, Baltimore, MD 21224, USA and 2JC Self Research Institute of Human Genetics, Greenwood Genetic Center, Greenwood, SC 29646, USA

Received June 25, 2003; Accepted September 15, 2003

EDA splice isoforms EDA-A1 and EDA-A2 belong to the TNF ligand family and regulate skin appendage formation by activating NF-kB- and JNK- promoted transcription. To analyze their action further, we conditionally expressed the isoforms as tetracycline (‘Tet’)-regulated transgenes in Tabby (EDA-negative) and wild-type mice. Expression of only the mEDA-A1 transgene had two types of effects during embryogenesis: (1) determinative effects on sweat glands and hair follicles. In Tabby mice, one type of hair follicle (‘guard hair’) was restored, whereas a second type, the dominant undercoat hair follicle (‘zigzag’) was not; furthermore, the transgene sharply suppressed zigzag hair formation in wild-type mice, with the overall numbers of back hair follicles remaining the same; and (2) trophic effects on sebaceous and Meibomian glands. Marked hyperplasia resulted from expansion of the sebocyte-producing zone in sebaceous glands, with particularly high expression of the transgene and the replication marker PCNA, and correspondingly high production of sebum. The phenotypic effects of mEDA-A1 on sebaceous glands, but not on hair follicles, were reversed when the gene was repressed in adult animals. The results thus reveal both initiating and trophic isoform-specific effects of the EDA gene, and suggest a possible balance of isoform interactions in skin appendage formation.

* To whom correspondence should be addressed at: Laboratory of Genetics, NIH/National Institute on Aging, 333 Cassell Dr., Suite 3000, Baltimore, MD 21224, USA. Tel: +1 4105588337; Fax: +1 4105588331; Email: schlessingerd{at}grc.nia.nih.gov


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