Histone H3 Lysine 4 Hypermethylation Prevents Aberrant Nucleosome Remodeling at the PHO5 Promoter

Histone H3 Lysine 4 Hypermethylation Prevents Aberrant Nucleosome Remodeling at the PHO5 Promoter
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组蛋白 H3 赖氨酸 4 高甲基化可防止 PHO5 启动子处的异常核小体重塑

DOI:
10.1128/mcb.05017-11
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发表时间:
2011-06
影响因子:
5.3
通讯作者:
Zhou, Jin-Qiu
Zhou, Jin-Qiu
中科院分区:
生物学2区
文献类型:
--
作者:
Wang, Shan-Shan;Zhou, Bo O.;Zhou, Jin-Qiu

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摘要近年来的研究表明,酿酒酵母中存在组蛋白H3 K4甲基化(H3 K4 me)依赖的转录抑制,但其机制尚不清楚。在这里,我们报告说,H3 K4 me抑制基础PHO 5转录在高磷酸盐条件下,通过抑制核小体解体的启动子。我们发现,通过SET 1缺失的PHO 5启动子的去阻遏导致不稳定的染色质结构,允许更多的RNA聚合酶II(Pol II)的结合,但不是反式激活因子Pho 2和Pho 4。我们进一步表明,Pho 23和Cti 6,两个植物同源结构域(PHD)的蛋白质,合作锚定的大Rpd 3(Rpd 3L)复合物的H3 K4-甲基化PHO 5启动子。Rpd 3对组蛋白H3的脱乙酰化活性是Set 1在PHO 5启动子处发挥功能所必需的。两者合计,我们的数据表明,Set 1介导的H3 K4 me抑制核小体重塑PHO 5启动子,从而减少基础转录PHO 5抑制条件下。我们认为,限制异常核小体重塑有助于严格控制基因转录的反式激活因子。
ABSTRACT Recent studies have highlighted the histone H3K4 methylation (H3K4me)-dependent transcriptional repression in Saccharomyces cerevisiae; however, the underlying mechanism remains inexplicit. Here, we report that H3K4me inhibits the basal PHO5 transcription under high-phosphate conditions by suppressing nucleosome disassembly at the promoter. We found that derepression of the PHO5 promoter by SET1 deletion resulted in a labile chromatin structure, allowing more binding of RNA polymerase II (Pol II) but not the transactivators Pho2 and Pho4. We further showed that Pho23 and Cti6, two plant homeodomain (PHD)-containing proteins, cooperatively anchored the large Rpd3 (Rpd3L) complex to the H3K4-methylated PHO5 promoter. The deacetylation activity of Rpd3 on histone H3 was required for the function of Set1 at the PHO5 promoter. Taken together, our data suggest that Set1-mediated H3K4me suppresses nucleosome remodeling at the PHO5 promoter so as to reduce basal transcription of PHO5 under repressive conditions. We propose that the restriction of aberrant nucleosome remodeling contributes to strict control of gene transcription by the transactivators.
组蛋白脱乙酰酶 Rpd3 拮抗 Sir2 依赖性沉默染色质增殖。
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发表时间: 1991-02
期刊: The EMBO Journal
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发表时间: 1989-12
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