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Published 24 April 2006. doi:10.1083/jcb.200508196
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 2, 253-264
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Article

 Ovol1 regulates the growth arrest of embryonic epidermal progenitor cells and represses c-myc transcription

Mahalakshmi Nair1,2, Andy Teng1, Virginia Bilanchone1, Anshu Agrawal3, Baoan Li1, and Xing Dai1,2

1 Department of Biological Chemistry, 2 Developmental Biology Center, and 3 Department of Medicine, University of California, Irvine, Irvine, CA 92697

Correspondence to Xing Dai: xdai{at}uci.edu

Transcriptional control plays a key role in regulating epidermal proliferation and differentiation. Although ample information has been obtained on how epidermal homeostasis is controlled in adult skin, less is known about the control of proliferation/differentiation of epidermal stem/progenitor cells in the developing embryo. Ovol1, encoding a zinc finger protein homologous to Drosophila melanogaster Ovo, is expressed in embryonic epidermal progenitor cells that are transiting from proliferation to terminal differentiation. In this study, we demonstrate a function for Ovol1 in interfollicular epidermal development. In its absence, developing epidermis fails to properly restrict the proliferative potential of progenitor cells, and cultured keratinocytes fail to efficiently undergo growth arrest in response to extrinsic growth-inhibitory signals. We present molecular evidence that c-myc expression is up-regulated in Ovol1-deficient suprabasal cells and that Ovol1 represses c-myc transcription by directly binding to its promoter. Collectively, our findings indicate that Ovol1 is required for proliferation exit of committed epidermal progenitor cells and identify c-myc as an Ovol1 target.

M. Nair and A. Teng contributed equally to this paper.

B. Li's present address is School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China.

Abbreviations used in this paper: ChIP, chromatin immunoprecipitation; EMSA, electrophoretic mobility shift assay; Id, inhibitor of differentiation; TG3, transglutaminase 3.


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