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首页> 外文期刊>Nature >Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin
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Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin

机译：Aurora B的组蛋白H3丝氨酸10磷酸化导致HP1从异染色质解离

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摘要

Histones are subject to numerous post-translational modifications. Some of these 'epigenetic' marks recruit proteins that modulate chromatin structure. For example, heterochromatin protein 1 (HP1) binds to histone H3 when its Iysine 9 residue has been tri-methylated by the methyltransferase Suv39h (refs 2-6). During mitosis, H3 is also phosphorylated by the kinase Aurora B. Although H3 phosphorylation is a hallmark of mitosis, its function remains mysterious. It has been proposed that histone phosphorylation controls the binding of proteins to chromatin, but any such mechanisms are unknown. Here we show that antibodies against mitotic chromosomal antigens that are associated with human autoimmune diseases specifically recognize H3 molecules that are modified by both tri-methylation of lysine 9 and phosphorylation of serine 10 (H3K9me3S10ph). The generation of H3K9me3S10ph depends on Suv39h and Aurora B, and occurs at pericentric heterochromatin during mitosis in different eukaryotes. Most HP1 typically dissociates from chromosomes during mitosis, but if phosphorylation of H3 serine 10 is inhibited, HP1 remains chromosome-bound throughout mitosis. H3 phosphorylation by Aurora B is therefore part of a 'methyl/ phos switch' mechanism that displaces HP1 and perhaps other proteins from mitotic heterochromatin.
机译：组蛋白会经历许多翻译后修饰。这些“表观遗传”标记中的一些募集了可调节染色质结构的蛋白质。例如，异染色质蛋白1（HP1）当其赖氨酸9残基已被甲基转移酶Suv39h三甲基化时与组蛋白H3结合（参考文献2-6）。在有丝分裂期间，H3也会被Aurora B激酶磷酸化。尽管H3磷酸化是有丝分裂的标志，但其功能仍然神秘。已经提出，组蛋白磷酸化控制蛋白质与染色质的结合，但是任何这样的机制都是未知的。在这里，我们显示针对与人类自身免疫性疾病相关的有丝分裂染色体抗原的抗体，特异性识别由赖氨酸9的三甲基化和丝氨酸10的磷酸化（H3K9me3S10ph）修饰的H3分子。 H3K9me3S10ph的生成取决于Suv39h和Aurora B，并在不同真核生物的有丝分裂过程中发生在周缘异染色质上。大多数HP1通常在有丝分裂期间从染色体上解离，但是如果H3丝氨酸10的磷酸化被抑制，则HP1在整个有丝分裂中仍保持染色体结合状态。因此，极光B的H3磷酸化是“甲基/磷转换”机制的一部分，该机制取代了有丝分裂异染色质中的HP1和其他蛋白质。

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  • 来源
    《Nature》 |2005年第7071期|p.1176-1180|共5页
  • 作者

    Toru Hirota; Jesse J. Lipp; Ban-Hock Toh; Jan-Michael Peters;

  • 作者单位

    Department of Experimental Pathology, Cancer Institute, Japanese Foundation for Cancer Research, 3-10-6 Ariake, Koto-ku, Tokyo 135-8550, Japan;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 自然科学总论;
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