Mop3 is an essential component of the master circadian pacemaker in mammals

Maureen K. Bunger, Lisa D. Wilsbacher, Susan M. Moran, Cynthia Clendenin, Laurel A. Radcliffe, John B. Hogenesch, M. Celeste Simon, Joseph S. Takahashi, Christopher A. Bradfield

Research output: Contribution to journalArticlepeer-review

1090 Scopus citations


Circadian oscillations in mammalian physiology and behavior are regulated by an endogenous biological clock. Here we show that loss of the PAS protein MOP3 (also known as BMAL1) in mice results in immediate and complete loss of circadian rhythmicity in constant darkness. Additionally, locomotor activity in light-dark (LD) cycles is impaired and activity levels are reduced in Mop3-/- mice. Analysis of Period gene expression in the suprachiasmatic nucleus (SCN) indicates that these behavioral phenotypes arise from loss of circadian function at the molecular level. These results provide genetic evidence that MOP3 is the bona fide hetero-dimeric partner of mCLOCK. Furthermore, these data demonstrate that MOP3 is a nonredundant and essential component of the circadian pacemaker in mammals.

Original languageEnglish (US)
Pages (from-to)1009-1017
Number of pages9
Issue number7
StatePublished - Dec 22 2000

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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