Genetic insights on sleep schedules: this time, it's PERsonal.

Genetic insights on sleep schedules: this time, it's PERsonal.
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DOI:
10.1016/j.tig.2012.08.002
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发表时间:
2012-12
期刊:
影响因子:
11.4
通讯作者:
Fu, Ying-Hui
Fu, Ying-Hui
中科院分区:
生物学1区
文献类型:
--
作者:
Chong, S. Y. Christin;Ptacek, Louis J.;Fu, Ying-Hui

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昼夜节律的研究正在成为理解支配人类生理和行为的细胞机制的一个富有成效的机会,因为直接将睡眠障碍和影响昼夜节律分子通路的基因突变联系起来的证据推动了这一研究。家族性晚期睡眠时相障碍(FASPD)是第一个公认的孟德尔昼夜节律特征,并且受影响的个体由于时期同源物2(PER 2)的翻译后调节改变而表现出异常早的睡眠-觉醒发作。行为和细胞的昼夜节律受到类似的影响,因为在没有环境时间线索的情况下,行为的昼夜周期长度减少,并且分子钟的周期持续时间同样缩短。鉴于这些发现,我们回顾了PER 2的昼夜节律调节的背景下,揭示了睡眠时间调节的机制。了解PER 2的调节和功能可能会为我们的遗传组成如何影响我们的睡眠-觉醒行为提供新的线索。
The study of circadian rhythms is emerging as a fruitful opportunity for understanding cellular mechanisms that govern human physiology and behavior, as fueled by evidence directly linking sleep disorders and genetic mutations affecting circadian molecular pathways. Familial Advanced Sleep Phase Disorder (FASPD) is the first recognized Mendelian circadian rhythm trait, and affected individuals exhibit exceptionally early sleep-wake onset due to altered post-translational regulation of period homolog 2 (PER2). Behavioral and cellular circadian rhythms are analogously affected, as the circadian period length of behavior is reduced in the absence of environmental time cues, and cycle duration of the molecular clock is likewise shortened. In light of these findings, we review the PER2 dynamics in the context of circadian regulation to reveal the mechanism of sleep schedule modulation. Understanding PER2 regulation and functionality may shed new light on how our genetic composition can influence our sleep-wake behaviors.
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