The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals

Author:

He Ying1,Jones Christopher R.2,Fujiki Nobuhiro3,Xu Ying1,Guo Bin4,Holder Jimmy L.1,Rossner Moritz J.5,Nishino Seiji3,Fu Ying-Hui1

Affiliation:

1. Department of Neurology, University of California at San Francisco, Mission Bay, 1550 Fourth Street, San Francisco, CA 94158, USA.

2. Department of Neurology, University of Utah, Salt Lake City, UT 84132, USA.

3. Sleep and Circadian Neurobiology Laboratory, Stanford University, 1201 Welch Road, P213, Palo Alto, CA 94304, USA.

4. Mechanical Engineering, University of California, Berkeley, Hesse Hall, Room 245, Berkeley, CA 94720, USA.

5. Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.

Abstract

Reducing Sleep Length Humans, like most animals, need their beauty sleep. But the preferred amount and quality of sleep varies between individuals—and some individuals exhibit a heritable, lifetime tendency to sleep less then 6 hours per night. He et al. (p. 866 ; see the Perspective by Hor and Tafti ) identified a mutation in humans associated with people who regularly require shorter than usual sleep duration. The mutation is found in the gene encoding a transcriptional repressor, DEC2, already implicated in regulation of circadian rhythms. Related mutations introduced into mice and flies similarly resulted in shortened sleep phases.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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