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

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 heterodimeric partner of mCLOCK. Furthermore, these data demonstrate that MOP3 is a nonredundant and essential component of the circadian pacemaker in mammals.

Pubmed ID: 11163178


  • Bunger MK
  • Wilsbacher LD
  • Moran SM
  • Clendenin C
  • Radcliffe LA
  • Hogenesch JB
  • Simon MC
  • Takahashi JS
  • Bradfield CA



Publication Data

December 22, 2000

Associated Grants

  • Agency: NIEHS NIH HHS, Id: ES05703
  • Agency: NCI NIH HHS, Id: P30-CA07175
  • Agency: NIEHS NIH HHS, Id: R01 ES005703
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • ARNTL Transcription Factors
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors
  • Behavior, Animal
  • Cell Cycle Proteins
  • Circadian Rhythm
  • DNA Probes
  • DNA-Binding Proteins
  • Gene Expression
  • Mammals
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Motor Activity
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Period Circadian Proteins
  • Phenotype
  • Suprachiasmatic Nucleus
  • Transcription Factors