Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, Utah, United States of America.
Bioinformatics Shared Resource, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
PLoS Genet. 2020 Dec 31;16(12):e1009133. doi: 10.1371/journal.pgen.1009133. eCollection 2020 Dec.
Transcriptional regulation of the Saccharomyces cerevisiae HO gene is highly complex, requiring a balance of multiple activating and repressing factors to ensure that only a few transcripts are produced in mother cells within a narrow window of the cell cycle. Here, we show that the Ash1 repressor associates with two DNA sequences that are usually concealed within nucleosomes in the HO promoter and recruits the Tup1 corepressor and the Rpd3 histone deacetylase, both of which are required for full repression in daughters. Genome-wide ChIP identified greater than 200 additional sites of co-localization of these factors, primarily within large, intergenic regions from which they could regulate adjacent genes. Most Ash1 binding sites are in nucleosome depleted regions (NDRs), while a small number overlap nucleosomes, similar to HO. We demonstrate that Ash1 binding to the HO promoter does not occur in the absence of the Swi5 transcription factor, which recruits coactivators that evict nucleosomes, including the nucleosomes obscuring the Ash1 binding sites. In the absence of Swi5, artificial nucleosome depletion allowed Ash1 to bind, demonstrating that nucleosomes are inhibitory to Ash1 binding. The location of binding sites within nucleosomes may therefore be a mechanism for limiting repressive activity to periods of nucleosome eviction that are otherwise associated with activation of the promoter. Our results illustrate that activation and repression can be intricately connected, and events set in motion by an activator may also ensure the appropriate level of repression and reset the promoter for the next activation cycle.
酿酒酵母 HO 基因的转录调控非常复杂,需要多种激活和抑制因子的平衡,以确保在细胞周期的狭窄窗口内,母细胞中只有少数转录本产生。在这里,我们表明 Ash1 阻遏物与 HO 启动子内通常隐藏在核小体中的两个 DNA 序列结合,并招募 Tup1 核心抑制物和 Rpd3 组蛋白去乙酰化酶,这两者对于在子细胞中进行完全抑制都是必需的。全基因组 ChIP 鉴定了这些因子的 200 多个额外的共定位位点,主要位于从这些位点可以调节相邻基因的大型基因间区域内。大多数 Ash1 结合位点位于核小体缺失区域(NDR)中,而一小部分与核小体重叠,类似于 HO。我们证明,在没有 Swi5 转录因子的情况下,Ash1 不会结合到 HO 启动子上,Swi5 招募了驱逐核小体的共激活因子,包括掩盖 Ash1 结合位点的核小体。在没有 Swi5 的情况下,人工核小体耗竭允许 Ash1 结合,表明核小体对 Ash1 结合具有抑制作用。核小体内部结合位点的位置因此可能是一种将抑制活性限制在核小体驱逐期的机制,否则核小体驱逐期与启动子的激活相关。我们的结果表明,激活和抑制可以紧密相连,激活剂引发的事件也可以确保适当水平的抑制,并为下一个激活周期重置启动子。