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J. Biol. Chem., Vol. 279, Issue 49, 51226-51233, December 3, 2004

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UV-induced Expression of Key Component of the Tanning Process, the POMC and MC1R Genes, Is Dependent on the p-38-activated Upstream Stimulating Factor-1 (USF-1)^*

Sébastien Corre, Aline Primot, Elena Sviderskaya, Dorothy C. Bennett, Sophie Vaulont¶, Colin R. Goding||, and Marie-Dominique Galibert**

From the CNRS UMR 6061 Laboratoire de Génétique et Développement, Faculté de Médecine, Université de Rennes-1, 2 Avenue du Pr. Léon Bernard, 35043 Rennes Cedex, France, St. Georges Hospital Medical School, Department of Basic Medical Sciences, London SW17 0RE, United Kingdom, the ^¶Département de Génétique, Développement et Pathologie Moléculaire, Institut Cochin, Faculté de Médecine Cochin-Port Royal, 75014 Paris, France, and the ^||Eukaryotic Transcription Laboratory, Marie Curie Research Institute, The Chart, Oxted, Surrey RH8 OTL, United Kingdom

Protection against UV-mediated DNA damage and the onset of oncogenesis is afforded by the tanning response in which UV irradiation triggers melanocytes to increase production of melanin that is then transferred to keratinocytes. A key component of the tanning process is the UV-mediated induction of the pro-opiomelanocortin (POMC) and MC1R genes encoding the -melanocyte-stimulating hormone and its receptor, respectively, which play a crucial role in pigmentation by regulating the intracellular levels of cAMP. How these genes are regulated in response to UV irradiation is not known. Here we have shown that UV-induced activation of the POMC and MC1R promoters is mediated by p38 stress-activated kinase signaling to the transcription factor, upstream stimulating factor-1 (USF-1). Importantly, melanocytes derived from USF-1 -/- mice exhibit a defective UV response and fail to activate POMC and MC1R expression in response to UV irradiation. The results define USF-1 as a critical UV-responsive activator of genes implicated in protection from solar radiation.

Received for publication, August 25, 2004

^* This work was supported by Marie Curie Cancer Care, the Ligue National contre le Cancer, and the Association pour la Recherche contre le Cancer. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^** To whom correspondence should be addressed. Tel.: 0033-223-234-705; Fax: 0033-223-234-607; E-mail: mgaliber{at}univ-rennes1.fr.

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