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J. Cell Biol.,
Volume 142, Number 4, August 24, 1998 1035-1051
Department of Biological Chemistry and Department of Dermatology, The Johns Hopkins University School of Medicine,
Baltimore, Maryland 21205
We previously hypothesized that the type I
keratin 16 (K16) plays a role in the process of keratinocyte activation that occurs in response to skin injury
(Paladini, R.D., K. Takahashi, N.S. Bravo, and P.A.
Coulombe. 1996. J. Cell Biol. 132:381-397). To further
examine its properties in vivo, the human K16 cDNA
was constitutively expressed in the progenitor basal
layer of transgenic mouse skin using the K14 gene promoter. Mice that express approximately as much K16
protein as endogenous K14 display a dramatic postnatal phenotype that consists of skin that is hyperkeratotic, scaly, and essentially devoid of fur. Histologically,
the epidermis is thickened because of hyperproliferation of transgenic basal cells, whereas the hair follicles
are decreased in number, poorly developed, and hypoproliferative. Microscopically, the transgenic keratinocytes are hypertrophic and feature an altered keratin
filament network and decreased cell-cell adhesion. The
phenotype normalizes at ~5 wk after birth. In contrast,
control mice expressing a K16-K14 chimeric protein to
comparable levels are normal. The character and temporal evolution of the phenotype in the K16 transgenic mice are reminiscent of the activated EGF receptor-
mediated signaling pathway in skin. In fact, tyrosine
phosphorylation of the EGF receptor is increased in
the newborn skin of K16 transgenic mice. We conclude
that expression of K16 can significantly alter the response of skin keratinocytes to signaling cues, a distinctive property likely resulting from its unique COOH-terminal tail domain.
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