CLOCK and NPAS2 have overlapping roles in the suprachiasmatic circadian clock.
Heterodimers of CLOCK and BMAL1, bHLH-PAS transcription factors, are believed to be the major transcriptional regulators of the circadian clock mechanism in mammals. However, a recent study shows that CLOCK-deficient mice continue to exhibit robust behavioral and molecular rhythms. Here we report that the transcription factor NPAS2 (MOP4) is able to functionally substitute for CLOCK in the master brain clock in mice to regulate circadian rhythmicity.
DeBruyne
Jason P
JP
Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, Massachusetts 01605, USA.
Weaver
David R
DR
Reppert
Steven M
SM
D000704:Analysis of Variance; D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000172:deficiency / Q000378:metabolism*; D001522:Behavior, Animal; D056926:CLOCK Proteins; D002940:Circadian Rhythm / Q000502:physiology*; D005786:Gene Expression Regulation / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D009043:Motor Activity / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000172:deficiency / Q000378:metabolism*; D013493:Suprachiasmatic Nucleus / Q000502:physiology*; D015534:Trans-Activators / Q000172:deficiency / Q000378:metabolism*
D051792:Basic Helix-Loop-Helix Proteins; D056926:CLOCK Proteins; D009419:Nerve Tissue Proteins; D015534:Trans-Activators; C491259:Npas2 protein, mouse; C538944:Clock protein, mouse