A complex interplay between chromatin and topological machineries is critical for genome architecture and function. However, little is known about these reciprocal interactions, even for cohesin, despite its multiple roles in DNA metabolism. We have used genome-wide analyses to address how cohesins and chromatin structure impact each other in yeast. Cohesin inactivation in scc1-73 mutants during the S and G2 phases causes specific changes in chromatin structure that preferentially take place at promoters; these changes include a significant increase in the occupancy of the − 1 and + 1 nucleosomes. In addition, cohesins play a major role in transcription regulation that is associated with specific promoter chromatin architecture. In scc1-73 cells, downregulated genes are enriched in promoters with short or no nucleosome-free region (NFR) and a fragile “nucleosome − 1/RSC complex” particle. These results, together with a preferential increase in the occupancy of nucleosome − 1 of these genes, suggest that cohesins promote transcription activation by helping RSC to form the NFR. In sharp contrast, the scc1-73 upregulated genes are enriched in promoters with an “open” chromatin structure and are mostly at cohesin-enriched regions, suggesting that a local accumulation of cohesins might help to inhibit transcription. On the other hand, a dramatic loss of chromatin integrity by histone depletion during DNA replication has a moderate effect on the accumulation and distribution of cohesin peaks along the genome. Our analyses of the interplay between chromatin integrity and cohesin activity suggest that cohesins play a major role in transcription regulation, which is associated with specific chromatin architecture and cohesin-mediated nucleosome alterations of the regulated promoters. In contrast, chromatin integrity plays only a minor role in the binding and distribution of cohesins.

中文翻译：

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染色质结构，黏附素活性和转录之间的串扰。

染色质和拓扑结构之间复杂的相互作用对于基因组结构和功能至关重要。然而，尽管它们在DNA代谢中起多种作用，但即使对于粘着蛋白，对这些相互的相互作用知之甚少。我们已经使用全基因组分析来解决粘蛋白和染色质结构如何在酵母中相互影响。在S和G2阶段，scc1-73突变体中的黏附素失活会导致染色质结构发生特定变化，这种变化优先发生在启动子上。这些变化包括− 1和+ 1核小体的占有率显着增加。另外，粘着蛋白在与特定启动子染色质结构相关的转录调节中起主要作用。在scc1-73细胞中 下调的基因富含具有短或无无核小体区域（NFR）和易碎的“核小体-1 / RSC复合体”粒子的启动子。这些结果，以及这些基因中核小体-1占有率的优先增加，表明粘着蛋白通过帮助RSC形成NFR来促进转录激活。与之形成鲜明对比的是，scc1-73上调的基因富含具有“开放”染色质结构的启动子，并且大多位于粘着蛋白富集的区域，这表明粘着蛋白的局部积累可能有助于抑制转录。另一方面，DNA复制过程中由于组蛋白消耗而导致的染色质完整性急剧下降，对沿基因组的凝聚素峰的积累和分布有中等程度的影响。我们对染色质完整性和黏附素活性之间相互作用的分析表明，黏附素在转录调控中起主要作用，这与特定的染色质结构和黏附素介导的调控启动子的核小体改变有关。相反，染色质完整性在黏着蛋白的结合和分布中仅起次要作用。