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J. Cell Biol.,
Volume 143, Number 2, October 19, 1998 469-486
Department of Biological Chemistry and Department of Dermatology, The Johns Hopkins University School of Medicine,
Baltimore, Maryland 21205
The type I keratin 17 (K17) shows a peculiar
localization in human epithelial appendages including
hair follicles, which undergo a growth cycle throughout
adult life. Additionally K17 is induced, along with K6
and K16, early after acute injury to human skin. To gain
further insights into its potential function(s), we cloned the mouse K17 gene and investigated its expression
during skin development. Synthesis of K17 protein first
occurs in a subset of epithelial cells within the single-layered, undifferentiated ectoderm of embryonic day
10.5 mouse fetuses. In the ensuing 48 h, K17-expressing
cells give rise to placodes, the precursors of ectoderm-derived appendages (hair, glands, and tooth), and to
periderm. During early development, there is a spatial
correspondence in the distribution of K17 and that of
lymphoid-enhancer factor (lef-1), a DNA-bending protein involved in inductive epithelial-mesenchymal interactions. We demonstrate that ectopic lef-1 expression induces K17 protein in the skin of adult transgenic
mice. The pattern of K17 gene expression during development has direct implications for the morphogenesis
of skin epithelia, and points to the existence of a molecular relationship between development and wound repair.
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