期刊
CELL
卷 103, 期 7, 页码 1009-1017出版社
CELL PRESS
DOI: 10.1016/S0092-8674(00)00205-1
关键词
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资金
- Howard Hughes Medical Institute Funding Source: Medline
- NCI NIH HHS [P30-CA07175] Funding Source: Medline
- NIEHS NIH HHS [F32 ES005703, ES05703, R01 ES005703, R37 ES005703] Funding Source: Medline
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 revels 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.
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