The mPer2 gene encodes a functional component of the mammalian circadian clock

Binhai Zheng, David W. Larkin, Urs Albrecht, Zhong Sheng Sun, Marijke Sage, Gregor Eichele, Cheng Chi Lee () and Allan Bradley
Additional contact information
Binhai Zheng: Department of Molecular and Human Genetics
David W. Larkin: Division of Neuroscience
Urs Albrecht: Verna and Marrs McLean Department of Biochemistry
Zhong Sheng Sun: Department of Molecular and Human Genetics
Marijke Sage: Department of Molecular and Human Genetics
Gregor Eichele: Verna and Marrs McLean Department of Biochemistry
Cheng Chi Lee: Department of Molecular and Human Genetics
Allan Bradley: Department of Molecular and Human Genetics

Nature, 1999, vol. 400, issue 6740, 169-173

Abstract: Abstract Circadian rhythms are driven by endogenous biological clocks that regulate many biochemical, physiological and behavioural processes in a wide range of life forms1. In mammals, there is a master circadian clock in the suprachiasmatic nucleus of the anterior hypothalamus. Three putative mammalian homologues (mPer1, mPer2 and mPer3) of the Drosophila circadian clock gene period (per) have been identified2,3,4,5,6,7,8. The mPer genes share a conserved PAS domain (a dimerization domain found in Per, Arnt and Sim) and show a circadian expression pattern in the suprachiasmatic nucleus. To assess the in vivo function of mPer2, we generated and characterized a deletion mutation in the PAS domain of the mouse mPer2 gene. Here we show that mice homozygous for this mutation display a shorter circadian period followed by a loss of circadian rhythmicity in constant darkness. The mutation also diminishes the oscillating expression of both mPer1 and mPer2 in the suprachiasmatic nucleus, indicating that mPer2 may regulate mPer1 in vivo. These data provide evidence that an mPer gene functions in the circadian clock, and define mPer2 as a component of the mammalian circadian oscillator.

Date: 1999
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DOI: 10.1038/22118

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