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The Saccharomyces cerevisiae Cdk8 Mediator Represses AQY1 Transcription by Inhibiting Set1p-Dependent Histone Methylation

机译:酿酒酵母Cdk8介体通过抑制Set1p依赖性组蛋白甲基化抑制AQY1转录。

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摘要

In the budding yeast Saccharomyces cerevisiae, nutrient depletion induces massive transcriptional reprogramming that relies upon communication between transcription factors, post-translational histone modifications, and the RNA polymerase II holoenzyme complex. Histone H3Lys4 methylation (H3Lys4 me), regulated by the -containing COMPASS methyltransferase complex and demethylase, is one of the most well-studied histone modifications. We previously demonstrated that the RNA polymerase II mediator components - inhibit locus-specific H3Lys4 3me independently of . Here, we identify loci subject to - and -dependent histone H3Lys4 3me inhibition using chromatin immunoprecipitation (ChIP)-seq. We further characterized the independent and combined roles of and in controlling H3Lys4 3me and transcription in response to fermentable and nonfermentable carbon at multiple loci. These experiments suggest that H3Lys4 3me alone is insufficient to induce transcription. Interestingly, we identified an unexpected role for - in repressing transcription, an aquaporin whose expression is normally induced during nutrient deprivation. These experiments, combined with previous work in other labs, support a two-step model in which - mediate transcriptional repression by stimulating transcription factor proteolysis and preventing recruitment to the href="http://www.yeastgenome.org/locus/S000006396/overview" data-ga-action="click_feat_suppl" ref="reftype=extlink&article-id=5345701&issue-id=289139&journal-id=1684&FROM=Article%7CFront%20Matter&TO=External%7CLink%7CURI" target="_blank">AQY1 locus.
机译:在出芽的酿酒酵母中,营养物质的消耗会导致大量的转录重编程,这依赖于转录因子,翻译后组蛋白修饰和RNA聚合酶II全酶复合物之间的通讯。组蛋白H3Lys4甲基化(H3Lys4 me)受含COMPASS甲基转移酶复合物和脱甲基酶的调节,是研究最深入的组蛋白修饰之一。我们先前证明了RNA聚合酶II介体成分-独立于基因座抑制H3Lys4 3me。在这里,我们使用染色质免疫沉淀(ChIP)-seq识别受-和-依赖性组蛋白H3Lys4 3me抑制的基因座。我们进一步表征了在多个位点响应可发酵和不可发酵碳而控制H3Lys4 3me和转录的独立和组合作用。这些实验表明,单独的H3Lys4 3me不足以诱导转录。有趣的是,我们确定了-在抑制转录中水通道蛋白的意外作用,该水通道蛋白的表达通常在营养剥夺期间被诱导。这些实验与其他实验室的先前工作相结合,支持两步模型,其中-通过刺激转录因子蛋白水解并防止募集到href =“ http://www.yeastgenome.org/locus/ S000006396 / overview“ data-ga-action =” click_feat_suppl“ ref =” reftype = extlink&article-id = 5345701&issue-id = 289139&journal-id = 1684&FROM = Article%7CFront%20Matter&TO = External%7CLink%7CURI“ target =” _ blank“> AQY1 位置。

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