首页> 美国卫生研究院文献>Eukaryotic Cell >The Paf1 Complex Represses SER3 Transcription in Saccharomyces cerevisiae by Facilitating Intergenic Transcription-Dependent Nucleosome Occupancy of the SER3 Promoter
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The Paf1 Complex Represses SER3 Transcription in Saccharomyces cerevisiae by Facilitating Intergenic Transcription-Dependent Nucleosome Occupancy of the SER3 Promoter

机译:Paf1复合体通过促进SER3启动子的基因间转录依赖性核小体占据抑制酿酒酵母中的SER3转录。

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摘要

Previous studies have shown that repression of the Saccharomyces cerevisiae SER3 gene is dependent on transcription of SRG1 from noncoding DNA initiating within the intergenic region 5′ of SER3 and extending across the SER3 promoter region. By a mechanism dependent on the activities of the Swi/Snf chromatin remodeling factor, the HMG-like factor Spt2, and the Spt6 and Spt16 histone chaperones, SRG1 transcription deposits nucleosomes over the SER3 promoter to prevent transcription factors from binding and activating SER3. In this study, we uncover a role for the Paf1 transcription elongation complex in SER3 repression. We find that SER3 repression is primarily dependent on the Paf1 and Ctr9 subunits of this complex, with minor contributions by the Rtf1, Cdc73, and Leo1 subunits. We show that the Paf1 complex localizes to the SRG1 transcribed region under conditions that repress SER3, consistent with it having a direct role in mediating SRG1 transcription-dependent SER3 repression. Importantly, we show that the defect in SER3 repression in strains lacking Paf1 subunits is not a result of reduced SRG1 transcription or reduced levels of known Paf1 complex-dependent histone modifications. Rather, we find that strains lacking subunits of the Paf1 complex exhibit reduced nucleosome occupancy and reduced recruitment of Spt16 and, to a lesser extent, Spt6 at the SER3 promoter. Taken together, our results suggest that Paf1 and Ctr9 repress SER3 by maintaining SRG1 transcription-dependent nucleosome occupancy.
机译:以前的研究表明,酿酒酵母SER3基因的抑制依赖于SRG1从非编码DNA的转录,该非编码DNA在SER3的基因间区域5'内起始并延伸到SER3启动子区域。通过依赖于Swi / Snf染色质重塑因子,HMG样因子Spt2以及Spt6和Spt16组蛋白伴侣的活性的机制,SRG1转录在SER3启动子上沉积核小体,以防止转录因子结合和激活SER3。在这项研究中,我们发现了Paf1转录延伸复合体在SER3抑制中的作用。我们发现,SER3抑制主要取决于此复合体的Paf1和Ctr9亚基,而Rtf1,Cdc73和Leo1亚基的贡献较小。我们显示,Paf1复合体在抑制SER3的条件下位于SRG1转录区域,这与其在介导SRG1转录依赖性SER3抑制中具有直接作用一致。重要的是,我们表明缺乏Paf1亚基的菌株中SER3抑制的缺陷不是SRG1转录降低或已知Paf1复合物依赖性组蛋白修饰水平降低的结果。相反,我们发现缺少Paf1复合体亚基的菌株在 SER3 启动子上减少了核小体的占有,减少了Spt16的募集,并减少了Spt6的募集。两者合计,我们的结果表明Paf1和Ctr9通过维持 SRG1 转录依赖性核小体的占有来抑制 SER3

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