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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >The Double-Bromodomain Proteins Bdf1 and Bdf2 Modulate Chromatin Structure to Regulate S-Phase Stress Response in Schizosaccharomyces pombe
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The Double-Bromodomain Proteins Bdf1 and Bdf2 Modulate Chromatin Structure to Regulate S-Phase Stress Response in Schizosaccharomyces pombe

机译：双Bromodomain蛋白Bdf1和Bdf2调节染色质结构，以调节粟酒裂殖酵母的S期应激反应。

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Bromodomain proteins bind acetylated histones to regulate transcription. Emerging evidence suggests that histone acetylation plays an important role in DNA replication and repair, although its precise mechanisms are not well understood. Here we report studies of two double bromodomain-containing proteins, Bdf1 and Bdf2, in fission yeast. Loss of Bdf1 or Bdf2 led to a reduction in the level of histone H4 acetylation. Both bdf1 Delta and bdf2 Delta cells showed sensitivity to DNA damaging agents, including camptothecin, that cause replication fork breakage. Consistently, Bdf1 and Bdf2 were important for recovery of broken replication forks and suppression of DNA damage. Surprisingly, deletion of bdf1 or bdf2 partially suppressed sensitivity of various checkpoint mutants including swi1 Delta, mrc1 Delta, cds1 Delta, crb2 Delta, chk1 Delta, and rad3 Delta, to hydroxyurea, a compound that stalls replication forks and activates the Cds1-dependent S-phase checkpoint. This suppression was not due to reactivation of Cds1. Instead, we found that bdf2 deletion alleviates DNA damage accumulation caused by defects in the DNA replication checkpoint. We also show that hydroxyurea sensitivity of mrc1 Delta and swi1 Delta was suppressed by mutations in histone H4 acetyltransferase subunits or histone H4. These results suggest that the double bromodomain-containing proteins modulate chromatin structure to coordinate DNA replication and S-phase stress response.
机译：溴结构域蛋白结合乙酰化的组蛋白来调节转录。新兴证据表明，组蛋白乙酰化在DNA复制和修复中起着重要作用，尽管其确切机制尚不清楚。在这里，我们报告裂变酵母中的两个双含溴结构域的蛋白质，Bdf1和Bdf2的研究。 Bdf1或Bdf2的丢失导致组蛋白H4乙酰化水平的降低。 bdf1 Delta和bdf2 Delta细胞均显示出对DNA破坏剂（包括喜树碱）的敏感性，这会导致复制叉断裂。一致地，Bdf1和Bdf2对于恢复断裂的复制叉和抑制DNA损伤很重要。令人惊讶的是，bdf1或bdf2的缺失部分抑制了各种检查点突变体（包括swi1 Delta，mrc1 Delta，cds1 Delta，crb2 Delta，chk1 Delta和rad3 Delta）对羟基脲的敏感性，羟基脲使复制叉停滞并激活了Cds1依赖性S相检查点。这种抑制不是由于Cds1的重新激活引起的。相反，我们发现bdf2缺失减轻了DNA复制检查点中的缺陷引起的DNA损伤积累。我们还表明，mrc1 Delta和swi1 Delta的羟基脲敏感性受到组蛋白H4乙酰转移酶亚基或组蛋白H4突变的抑制。这些结果表明，含双溴结构域的蛋白质可调节染色质结构，以协调DNA复制和S期应激反应。

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