CLOCK-mediated acetylation of BMAL1 controls circadian function

Jun Hirayama, Saurabh Sahar, Benedetto Grimaldi, Teruya Tamaru, Ken Takamatsu, Yasukazu Nakahata and Paolo Sassone-Corsi ()
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Jun Hirayama: School of Medicine, University of California, Irvine, 92697-4625 Irvine, California, USA
Saurabh Sahar: School of Medicine, University of California, Irvine, 92697-4625 Irvine, California, USA
Benedetto Grimaldi: School of Medicine, University of California, Irvine, 92697-4625 Irvine, California, USA
Teruya Tamaru: Toho University, Faculty of Medicine, Tokyo 143-8540, Japan
Ken Takamatsu: Toho University, Faculty of Medicine, Tokyo 143-8540, Japan
Yasukazu Nakahata: School of Medicine, University of California, Irvine, 92697-4625 Irvine, California, USA
Paolo Sassone-Corsi: School of Medicine, University of California, Irvine, 92697-4625 Irvine, California, USA

Nature, 2007, vol. 450, issue 7172, 1086-1090

Abstract: The circadian regulator CLOCK has histone acetyltransferase (HAT) activity that contributes to chromatin-remodelling events during circadian control of gene expression. Here, CLOCK is shown to acetylate its heterodimerization partner BMAL1, a step which facilitates recruitment of CRY1 and promotes transcriptional repression.

Date: 2007
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DOI: 10.1038/nature06394

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