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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >LARK activates posttranscriptional expression of an essential mammalian clock protein, PERIOD1
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LARK activates posttranscriptional expression of an essential mammalian clock protein, PERIOD1

机译：LARK激活一种必需的哺乳动物时钟蛋白PERIOD1的转录后表达

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摘要

The mammalian molecular clock is composed of feedback loops to keep circadian 24-h rhythms. Although much focus has been on transcriptional regulation, it is dear that posttranscriptional controls also play important roles in molecular circadian clocks. In this study, we found that mouse LARK (mLARK), an RNA binding protein, activates the posttranscriptional expression of the mouse Period1 (mPer1) mRNA. A strong circadian cycling of the mLARK protein is observed in the suprachiasmatic nuclei with a phase similar to that of mPER1, although the level of the Lark transcripts are not rhythmic. We demonstrate that LARK causes increased mPER1 protein levels, most likely through translational regulation and that the LARK1 protein binds directly to a cis element in the 3′ UTR of the mPer1 mRNA. Alterations of mLark expression in cycling cells caused significant changes in circadian period, with mLark knockdown by si RNA resulting in a shorter circadian period, and the overexpression of mLARK1 resulting in a lengthened period. These data indicate that mLARKs are novel posttranscriptional regulators of mammalian circadian clocks.
机译：哺乳动物分子钟由反馈环组成，以保持昼夜24小时节律。尽管人们非常关注转录调控，但是亲爱的转录后调控在分子生物钟中也起着重要的作用。在这项研究中，我们发现小鼠LARK（mLARK）是一种RNA结合蛋白，可激活小鼠Period1（mPer1）mRNA的转录后表达。尽管Lark转录物的水平不是有节律的，但在裂口上核中观察到了mLARK蛋白的强昼夜节律循环，其相位与mPER1相似。我们证明LARK引起增加的mPER1蛋白水平，最有可能通过翻译调节，并且LARK1蛋白直接与mPer1 mRNA 3'UTR中的顺式元件结合。循环细胞中mLark表达的变化导致昼夜节律发生显着变化，siRNA敲除mLark导致昼夜节律周期缩短，而mLARK1的过表达导致周期延长。这些数据表明，mLARKs是哺乳动物生物钟的新型转录后调节因子。

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