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首页> 外文期刊>Molecular and Cellular Biology >Histone Deacetylases RPD3 and HOS2 Regulate the Transcriptional Activation of DNA Damage-Inducible Genes
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Histone Deacetylases RPD3 and HOS2 Regulate the Transcriptional Activation of DNA Damage-Inducible Genes

机译：组蛋白脱乙酰基酶RPD3和HOS2调节DNA损伤诱导基因的转录激活。

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DNA microarray and genetic studies of Saccharomyces cerevisiae have demonstrated that histone deacetylases (HDACs) are required for transcriptional activation and repression, but the mechanism by which they activate transcription remains poorly understood. We show that two HDACs, RPD3 and HOS2, are required for the activation of DNA damage-inducible genes RNR3 and HUG1. Using mutants specific for the Rpd3L complex, we show that the complex is responsible for regulating RNR3. Furthermore, unlike what was described for the GAL genes, Rpd3L regulates the activation of RNR3 by deacetylating nucleosomes at the promoter, not at the open reading frame. Rpd3 is recruited to the upstream repression sequence of RNR3, which surprisingly does not require Tup1 or Crt1. Chromatin remodeling and TFIID recruitment are largely unaffected in the Δrpd3/Δhos2 mutant, but the recruitment of RNA polymerase II is strongly reduced, arguing that Rpd3 and Hos2 regulate later stages in the assembly of the preinitiation complex or facilitate multiple rounds of polymerase recruitment. Furthermore, the histone H4 acetyltransferase Esa1 is required for the activation of RNR3 and HUG1. Thus, reduced or unregulated constitutive histone H4 acetylation is detrimental to promoter activity, suggesting that HDAC-dependent mechanisms are in place to reset promoters to allow high levels of transcription.
机译：DNA芯片和酿酒酵母的遗传研究表明，组蛋白脱乙酰基酶（HDACs）是转录激活和抑制所必需的，但它们激活转录的机制仍知之甚少。我们发现，激活DNA损伤诱导基因 RNR3 和 HUG1 需要两个HDAC， RPD3 和 HOS2 。 em>。使用特定于Rpd3L复合体的突变体，我们表明该复合体负责调节 RNR3 。此外，与GAL基因所描述的不同，Rpd3L通过在启动子而非开放阅读框使核小体脱乙酰基来调节 RNR3 的激活。 Rpd3被募集到 RNR3 的上游阻遏序列，这令人惊讶地不需要Tup1或Crt1。染色质重塑和TFIID募集在Δ rpd3 / Δ hos2 突变体中基本不受影响，但RNA聚合酶II的募集被大大降低，理由是Rpd3和Hos2调控后期。组装预启动复合物或促进多轮聚合酶募集。此外，组蛋白H4乙酰转移酶Esa1是激活 RNR3 和 HUG1 所必需的。因此，减少或不受调节的组成性组蛋白H4乙酰化不利于启动子活性，表明存在HDAC依赖性机制来重置启动子以允许高水平的转录。

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