Mouse period1 (mPER1) acts as a circadian adaptor to entrain the oscillator to environmental light/dark cycles by regulating mPER2 protein
Mouse period1 (mPER1) acts as a circadian adaptor to entrain the oscillator to environmental light/dark cycles by regulating mPER2 protein
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DOI：
10.1523/jneurosci.4761-04.2005
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发表时间：
2005-05-11
影响因子：
5.3
通讯作者：
Okamura, H
中科院分区：
文献类型：
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作者：
Masubuchi, S;Kataoka, N;Okamura, H
小鼠周期1(MPer1)和mPer2是果蝇时钟基因周期的哺乳动物同源基因，它们在视交叉上核(哺乳动物的主钟)中表现出强劲的振荡，被认为是核心时钟机制的重要组成部分。基因打靶研究表明，mPer2在行为节律的产生中起主导作用，但mPer1的作用尚未完全阐明。在这里，我们报告了延长光照周期(4-16小时)导致mPer1缺陷(mPer1(-/-))小鼠行为节律的较大延迟相移。在光延长任务中，mPer1(-/-)小鼠的mPER2蛋白衰减比野生型小鼠慢(接近4h)，从而导致更大的行为时相延迟。MPer1(-/-)小鼠在长全光暗周期或长骨骼光周期中不能适应环境光/暗周期。这些光周期条件模拟了高纬度地区的自然环境变化，表明mPer1可以作用于夜间小鼠的生物钟适应环境光/暗周期的大季节变化。
Mouse period1 ( mPer1) and mPer2 are mammalian homologs of the Drosophila clock gene period that show robust oscillation in the suprachiasmatic nucleus, the mammalian master clock, and have been implicated as essential components of the core clock mechanism. Gene- targeting studies have demonstrated that mPer2 plays a dominant function in behavioral rhythm generation, although the role of mPer1 has not been fully clarified. Here, we report that prolongation of the lighting period ( 4 - 16 h) induces a larger- delay phase shift of the behavioral rhythm in mPer1- deficient ( mPer1 (-/-)) mice. During the light- elongation task, mPER2 protein decay in mPer1 (-/-) mice is slower ( similar to 4 h) than in wild- type mice, which thereby causes larger behavioral phase delay. mPer1 (-/-) mice could not adapt to environmental light/ dark cycles in long complete photoperiods with dim light or in long skeleton photoperiods. These photoperiodic conditions mimic natural environmental changes present at high latitudes, indicating that mPer1 could operate in the adaptation of the circadian clock of nocturnal mice to large seasonal changes of environmental light/ dark cycles.