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首页> 外文期刊>Plant signaling & behavior >Histone acetylation and the circadian clock: a role for the MYB transcription factor RVE8/LCL5.
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Histone acetylation and the circadian clock: a role for the MYB transcription factor RVE8/LCL5.

机译:组蛋白乙酰化和昼夜节律:MYB转录因子RVE8 / LCL5的作用。

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摘要

Most organisms have developed an internal timing mechanism or circadian clock that is able to generate 24-hour biological rhythms in synchronization with the diurnal environmental changes. Despite our increasing understanding of the molecular machinery underlying circadian clock function, a complete picture of the components and regulatory mechanisms governing the circadian system in Arabidopsis thaliana is still lacking. In a recent study, we have characterized the role of the MYB-like transcription factor REVEILLE8/LHY-CCA1-LIKE5 (RVE8/LCL5) within the Arabidopsis circadian clock. We have generated RVE8/LCL5 mutant and overexpressing plants and showed that similar to the MYB-like transcription factor CIRCADIAN CLOCK-ASSOCIATED1 (CCA1), RVE8/LCL5 binds to the promoter of key clock component TOC1 (Timing of CAB expression 1) and regulates its circadian expression. However, the mechanisms of RVE8/LCL5 and CCA1 circadian function seem to differ: while CCA1 represses TOC1 expression by facilitating a hypo-acetylated state of Histone H3, RVE8/LCL5 contributes to TOC1 expression by favouring H3 acetylation at the TOC1 locus. Although CCA1 has a more predominant role on this regulation, our results showing the opposing function of RVE8/LCL5 open interesting questions about the complex networks of transcriptional regulators and chromatin remodeling activities that need to be integrated in synergistic and antagonistic ways to generate the circadian periodicity.
机译:大多数生物体已经开发出一种内部计时机制或昼夜节律时钟,能够与昼夜环境变化同步地产生24小时生物节律。尽管我们对昼夜节律时钟功能的分子机制有了越来越多的了解,但仍缺乏对拟南芥(irabidopsis thaliana)的昼夜节律系统的组成部分和调控机制的完整描述。在最近的研究中,我们已经表征了拟南芥昼夜节律中MYB样转录因子REVEILLE8 / LHY-CCA1-LIKE5(RVE8 / LCL5)的作用。我们已经生成了 RVE8 / LCL5 突变体和过表达植物,结果表明,类似于MYB样转录因子CIRCADIAN CLOCK-ASSOCIATED1(CCA1),RVE8 / LCL5与关键时钟组件的启动子结合。 TOC1 (CAB表达1的时间)并调节其昼夜节律表达。但是,RVE8 / LCL5和CCA1昼夜节律功能的机制似乎有所不同:虽然CCA1通过促进组蛋白H3的低乙酰化状态抑制 TOC1 表达,但RVE8 / LCL5有助于 TOC1 位点促进H3乙酰化来表达i>。尽管CCA1在该调节中起主要作用,但我们的结果显示RVE8 / LCL5的相反功能提出了有趣的问题,涉及转录调节子和染色质重塑活动的复杂网络,这些网络需要以协同和拮抗的方式整合以产生昼夜节律。

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