Department of Biological Sciences, Oakland University, Rochester, MI 48309, USA.
Genetics. 2021 Apr 15;217(4). doi: 10.1093/genetics/iyab021.
RSC (Remodels the Structure of Chromatin) is a conserved ATP-dependent chromatin remodeling complex that regulates many biological processes, including transcription by RNA polymerase II (Pol II). We report that RSC contributes in generating accessible nucleosomes in transcribed coding sequences (CDSs). RSC MNase ChIP-seq data revealed that RSC-bound nucleosome fragments were very heterogenous (∼80 bp to 180 bp) compared to a sharper profile displayed by the MNase inputs (140 bp to 160 bp), supporting the idea that RSC promotes accessibility of nucleosomal DNA. Notably, RSC binding to +1 nucleosomes and CDSs, but not with -1 nucleosomes, strongly correlated with Pol II occupancies, suggesting that RSC enrichment in CDSs is linked to transcription. We also observed that Pol II associates with nucleosomes throughout transcribed CDSs, and similar to RSC, Pol II-protected fragments were highly heterogenous, consistent with the idea that Pol II interacts with remodeled nucleosomes in CDSs. This idea is supported by the observation that the genes harboring high-levels of Pol II in their CDSs were the most strongly affected by ablating RSC function. Additionally, rapid nuclear depletion of Sth1 decreases nucleosome accessibility and results in accumulation of Pol II in highly transcribed CDSs. This is consistent with a slower clearance of elongating Pol II in cells with reduced RSC function, and is distinct from the effect of RSC depletion on PIC assembly. Altogether, our data provide evidence in support of the role of RSC in promoting Pol II elongation, in addition to its role in regulating transcription initiation.
RSC(重塑染色质结构)是一种保守的 ATP 依赖性染色质重塑复合物,调节许多生物学过程,包括 RNA 聚合酶 II(Pol II)转录。我们报告称,RSC 有助于生成转录编码序列(CDS)中可及的核小体。RSC MNase ChIP-seq 数据显示,与 MNase 输入显示的更锐利轮廓(140bp 至 160bp)相比,RSC 结合的核小体片段非常异质(~80bp 至 180bp),支持 RSC 促进核小体 DNA 可及性的观点。值得注意的是,RSC 与+1 核小体和 CDS 的结合,但不与-1 核小体结合,与 Pol II 占有率强烈相关,表明 RSC 在 CDS 中的富集与转录有关。我们还观察到 Pol II 与整个转录 CDS 中的核小体结合,并且与 RSC 相似,Pol II 保护的片段高度异质,这与 Pol II 在 CDS 中与重塑核小体相互作用的观点一致。这一观点得到了以下观察结果的支持:在其 CDS 中含有高水平 Pol II 的基因受到 RSC 功能缺失的影响最大。此外,Sth1 的快速核耗竭降低核小体可及性,并导致高度转录的 CDS 中 Pol II 的积累。这与在 RSC 功能降低的细胞中延长的 Pol II 清除速度较慢一致,与 RSC 耗竭对 PIC 组装的影响不同。总之,我们的数据提供了证据支持 RSC 在促进 Pol II 延伸中的作用,除了其在调节转录起始中的作用。