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RSC调节II型基因处的核小体定位以及III型基因处的密度。

RSC regulates nucleosome positioning at Pol II genes and density at Pol III genes.

作者信息

Parnell Timothy J, Huff Jason T, Cairns Bradley R

机构信息

Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.

出版信息

EMBO J. 2008 Jan 9;27(1):100-10. doi: 10.1038/sj.emboj.7601946. Epub 2007 Dec 6.

Abstract

Nucleosomes can restrict the access of transcription factors to chromatin. RSC is a SWI/SNF-family chromatin-remodeling complex from yeast that repositions and ejects nucleosomes in vitro. Here, we examined these activities and their importance in vivo. We utilized array-based methods to examine nucleosome occupancy and positioning at more than 200 locations in the genome following the controlled destruction of the catalytic subunit of RSC, Sth1. Loss of RSC function caused pronounced and general reductions in new transcription from Pol I, II, and III genes. At Pol III genes, Sth1 loss conferred a general reduction in RNA Pol III occupancy and a gain in nucleosome density. Notably at the one Pol III gene examined, histone restoration was partly replication-dependent. In contrast, at Pol II promoters we observed primarily single nucleosome changes, including movement. Importantly, alterations near the transcription start site were more common at RSC-occupied promoters than at non-occupied promoters. Thus, RSC action affects both nucleosome density and positioning in vivo, but applies these remodeling modes differently at Pol II and Pol III genes.

摘要

核小体能够限制转录因子与染色质的结合。RSC是一种来自酵母的SWI/SNF家族染色质重塑复合体,它能在体外重新定位并移除核小体。在此,我们研究了这些活性及其在体内的重要性。我们利用基于芯片的方法,在可控地破坏RSC的催化亚基Sth1后,检测了基因组中200多个位点的核小体占有率和定位情况。RSC功能的丧失导致RNA聚合酶I、II和III基因的新转录普遍显著减少。在RNA聚合酶III基因处,Sth1的缺失导致RNA聚合酶III占有率普遍降低,核小体密度增加。值得注意的是,在所检测的一个RNA聚合酶III基因处,组蛋白的恢复部分依赖于复制。相比之下,在RNA聚合酶II启动子处,我们主要观察到单个核小体的变化,包括移动。重要的是,在转录起始位点附近的改变在RSC占据的启动子处比在未占据的启动子处更常见。因此,RSC的作用在体内影响核小体密度和定位,但在RNA聚合酶II和III基因处应用这些重塑模式的方式不同。

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