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首页> 外文期刊>Neuron >Differential functions of mPer1, mPer2, and mPer3 in the SCN circadian clock.
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Differential functions of mPer1, mPer2, and mPer3 in the SCN circadian clock.

机译：SCN昼夜节律时钟中mPer1，mPer2和mPer3的差分功能。

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The role of mPer1 and mPer2 in regulating circadian rhythms was assessed by disrupting these genes. Mice homozygous for the targeted allele of either mPer1 or mPer2 had severely disrupted locomotor activity rhythms during extended exposure to constant darkness. Clock gene RNA rhythms were blunted in the suprachiasmatic nucleus of mPer2 mutant mice, but not of mPER1-deficient mice. Peak mPER and mCRY1 protein levels were reduced in both lines. Behavioral rhythms of mPer1/mPer3 and mPer2/mPer3 double-mutant mice resembled rhythms of mice with disruption of mPer1 or mPer2 alone, respectively, confirming the placement of mPer3 outside the core circadian clockwork. In contrast, mPer1/mPer2 double-mutant mice were immediately arrhythmic. Thus, mPER1 influences rhythmicity primarily through interaction with other clock proteins, while mPER2 positively regulates rhythmic gene expression, and there is partial compensation between products of these two genes.
机译：通过破坏这些基因来评估mPer1和mPer2在调节昼夜节律中的作用。 mPer1或mPer2的目标等位基因纯合的小鼠在长期暴露于恒定黑暗中期间严重破坏了运动活动节律。在mPer2突变型小鼠的眼交叉上核中，时钟基因RNA节律变钝，而在mPER1缺陷型小鼠中，则没有。在两个系中，峰值mPER和mCRY1蛋白水平均降低。 mPer1 / mPer3和mPer2 / mPer3双突变小鼠的行为节律分别类似于单独破坏mPer1或mPer2的小鼠节律，这证实了mPer3在核心生物钟周围的位置。相反，mPer1 / mPer2双突变小鼠立即出现心律不齐。因此，mPER1主要通过与其他时钟蛋白相互作用来影响节律性，而mPER2积极调节节律性基因表达，并且这两个基因的产物之间存在部分补偿。

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