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Gcn5 facilitates Pol II progression rather than recruitment to nucleosome-depleted stress promoters in Schizosaccharomyces pombe

机译:Gcn5促进粟酒裂殖酵母中的Pol II进程而不是募集到耗尽核小体的应激启动子

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摘要

In the fission yeast, the MAP kinase Sty1 and the transcription factor Atf1 regulate up to 400 genes in response to environmental signals, and both proteins have been shown to bind to their promoters in a stress-dependent manner. In a genetic search, we have isolated the histone H3 acetyltransferase Gcn5, a component of the SAGA complex, as being essential for oxidative stress survival and activation of those genes. Upon stress, Gcn5 is recruited to promoters and coding sequences of stress genes in a Sty1- and Atf1-dependent manner, causing both an enhanced acetylation of histone H3 and nucleosome eviction. Unexpectedly, recruitment of RNA polymerase II (Pol II) is not impaired in Δgcn5 cells. We show here that stress genes display a 400-bp long nucleosome depleted region upstream of the transcription start site even prior to activation. Stress treatment does not alter promoter nucleosome architecture, but induces eviction of the downstream nucleosomes at stress genes, which is not observed in Δgcn5 cells. We conclude that, while Pol II is recruited to nucleosome-free stress promoters in a transcription factor dependent manner, Gcn5 mediates eviction of nucleosomes positioned downstream of promoters, allowing efficient Pol II progression along the genes.
机译:在裂变酵母中,MAP激酶Sty1和转录因子Atf1响应环境信号调节多达400个基因,并且两种蛋白质都已显示出以应激依赖的方式与其启动子结合。在遗传搜索中,我们分离出了组蛋白H3乙酰转移酶Gcn5(SAGA复合物的一个组成部分),对于氧化应激的存活和这些基因的激活至关重要。应激后,Gcn5以Sty1和Atf1依赖的方式募集到应激基因的启动子和编码序列,从而导致组蛋白H3的乙酰化增强和核小体驱逐。出乎意料的是,Δgcn5细胞中RNA聚合酶II(Pol II)的募集并没有受到损害。我们在这里显示,应力基因甚至在激活之前在转录起始位点上游显示一个400 bp长的核小体耗尽区域。应激处理不会改变启动子核小体的结构,但会诱导应激基因下游核小体的逐出,这在Δgcn5细胞中未观察到。我们得出的结论是,虽然Pol II以转录因子依赖性方式被募集到无核小体的应激启动子,但Gcn5介导了位于启动子下游的核小体的逐出,从而使Pol II沿着基因有效地发展。

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