Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065 Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065.
Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065 Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065 Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10065
Genetics. 2015 Oct;201(2):525-42. doi: 10.1534/genetics.115.178293. Epub 2015 Aug 5.
Meiotic recombination initiates with DNA double-strand breaks (DSBs) made by Spo11. In Saccharomyces cerevisiae, many DSBs occur in "hotspots" coinciding with nucleosome-depleted gene promoters. Transcription factors (TFs) stimulate DSB formation in some hotspots, but TF roles are complex and variable between locations. Until now, available data for TF effects on global DSB patterns were of low spatial resolution and confined to a single TF. Here, we examine at high resolution the contributions of two TFs to genome-wide DSB distributions: Bas1, which was known to regulate DSB activity at some loci, and Ino4, for which some binding sites were known to be within strong DSB hotspots. We examined fine-scale DSB distributions in TF mutant strains by deep sequencing oligonucleotides that remain covalently bound to Spo11 as a byproduct of DSB formation, mapped Bas1 and Ino4 binding sites in meiotic cells, evaluated chromatin structure around DSB hotspots, and measured changes in global messenger RNA levels. Our findings show that binding of these TFs has essentially no predictive power for DSB hotspot activity and definitively support the hypothesis that TF control of DSB numbers is context dependent and frequently indirect. TFs often affected the fine-scale distributions of DSBs within hotspots, and when seen, these effects paralleled effects on local chromatin structure. In contrast, changes in DSB frequencies in hotspots did not correlate with quantitative measures of chromatin accessibility, histone H3 lysine 4 trimethylation, or transcript levels. We also ruled out hotspot competition as a major source of indirect TF effects on DSB distributions. Thus, counter to prevailing models, roles of these TFs on DSB hotspot strength cannot be simply explained via chromatin "openness," histone modification, or compensatory interactions between adjacent hotspots.
减数分裂重组由 Spo11 产生的 DNA 双链断裂 (DSB) 引发。在酿酒酵母中,许多 DSB 出现在与核小体缺失的基因启动子重合的“热点”中。转录因子 (TF) 在某些热点中刺激 DSB 的形成,但 TF 的作用在不同位置是复杂且多变的。到目前为止,关于 TF 对全局 DSB 模式影响的可用数据空间分辨率较低,并且仅限于单个 TF。在这里,我们以高分辨率检查了两个 TF 对全基因组 DSB 分布的贡献:Bas1,已知它调节一些基因座上的 DSB 活性,而 Ino4,已知其一些结合位点位于强 DSB 热点内。我们通过深度测序寡核苷酸来检查 TF 突变株中精细的 DSB 分布,这些寡核苷酸作为 DSB 形成的副产物与 Spo11 共价结合,在减数分裂细胞中绘制 Bas1 和 Ino4 结合位点,评估 DSB 热点周围的染色质结构,并测量全局信使 RNA 水平的变化。我们的研究结果表明,这些 TF 的结合对 DSB 热点活性几乎没有预测能力,并明确支持这样一种假设,即 TF 对 DSB 数量的控制是上下文相关的,并且经常是间接的。TF 通常会影响热点内 DSB 的精细分布,当观察到这些影响时,这些影响与局部染色质结构的影响平行。相比之下,热点中 DSB 频率的变化与染色质可及性的定量测量、组蛋白 H3 赖氨酸 4 三甲基化或转录本水平没有相关性。我们还排除了热点竞争作为 TF 对 DSB 分布间接影响的主要来源。因此,与流行模型相反,这些 TF 在 DSB 热点强度上的作用不能简单地通过染色质“开放性”、组蛋白修饰或相邻热点之间的补偿相互作用来解释。