Ganguli Dwaipayan, Chereji Răzvan V, Iben James R, Cole Hope A, Clark David J
Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute for Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Program in Genomics of Differentiation, Eunice Kennedy Shriver National Institute for Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA
Genome Res. 2014 Oct;24(10):1637-49. doi: 10.1101/gr.177014.114. Epub 2014 Jul 11.
RSC and SWI/SNF are related ATP-dependent chromatin remodeling machines that move nucleosomes, regulating access to DNA. We addressed their roles in nucleosome phasing relative to transcription start sites in yeast. SWI/SNF has no effect on phasing at the global level. In contrast, RSC depletion results in global nucleosome repositioning: Both upstream and downstream nucleosomal arrays shift toward the nucleosome-depleted region (NDR), with no change in spacing, resulting in a narrower and partly filled NDR. The global picture of RSC-depleted chromatin represents the average of a range of chromatin structures, with most genes showing a shift of the +1 or the -1 nucleosome into the NDR. Using RSC ChIP data reported by others, we show that RSC occupancy is highest on the coding regions of heavily transcribed genes, though not at their NDRs. We propose that RSC has a role in restoring chromatin structure after transcription. Analysis of gene pairs in different orientations demonstrates that phasing patterns reflect competition between phasing signals emanating from neighboring NDRs. These signals may be in phase, resulting in constructive interference and a regular array, or out of phase, resulting in destructive interference and fuzzy positioning. We propose a modified barrier model, in which a stable complex located at the NDR acts as a bidirectional phasing barrier. In RSC-depleted cells, this barrier has a smaller footprint, resulting in narrower NDRs. Thus, RSC plays a critical role in organizing yeast chromatin.
RSC和SWI/SNF是相关的依赖ATP的染色质重塑机器，它们移动核小体，调节对DNA的访问。我们研究了它们在酵母中相对于转录起始位点的核小体相位中的作用。SWI/SNF在全局水平上对相位没有影响。相比之下，RSC的缺失导致全局核小体重新定位：上游和下游的核小体阵列都向核小体缺失区域（NDR）移动，间距不变，导致NDR变窄且部分填充。RSC缺失的染色质的全局图景代表了一系列染色质结构的平均值，大多数基因显示+1或-1核小体向NDR移动。利用其他人报道的RSC ChIP数据，我们表明RSC在高转录基因的编码区域上占据率最高，尽管在其NDR处不是这样。我们提出RSC在转录后恢复染色质结构中起作用。对不同方向的基因对的分析表明，相位模式反映了来自相邻NDR的相位信号之间的竞争。这些信号可能同相，导致相长干涉和规则排列，也可能异相，导致相消干涉和模糊定位。我们提出了一个改进的屏障模型，其中位于NDR的稳定复合物作为双向相位屏障。在RSC缺失的细胞中，这个屏障的足迹较小，导致NDR变窄。因此，RSC在组织酵母染色质中起关键作用。
