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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Heterochromatin protein 1 homologue Swi6 acts in concert with Ers1 to regulate RNAi-directed heterochromatin assembly
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Heterochromatin protein 1 homologue Swi6 acts in concert with Ers1 to regulate RNAi-directed heterochromatin assembly

机译：异染色质蛋白1同源物Swi6与Ers1协同调节RNAi定向的异染色质组装

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摘要

In fission yeast, the RNAi pathway is required for centromeric heterochromatin assembly. siRNAs derived from centromeric transcripts are incorporated into the RNA-induced transcriptional silencing (RITS) complex and direct it to nascent homologous transcripts. The RNA-induced transcriptional silencing-bound nascent transcripts further recruit the RNA-directed RNA polymerase complex (RDRC) to promote dsRNA synthesis and siRNA production. Heterochromatin coated with Swi6/Heterochromain Protein 1 is then formed following recruitment of chromatin modification machinery. Swi6 is also required for the upstream production of siRNA, although the mechanism for this has remained obscure. Here, we demonstrate that Swi6 recruits RDRC to heterochromatin through Ers1, an RNAi factor intermediate. An ers1+ mutant allele (ers1-C62) was identified in a genetic screen for mutants that alleviate centromeric silencing, and this phenotype was suppressed by overexpres-sion of either the Hrr1 RDRC subunit or Clr4 histone H3-K9 methyltransferase. Ers1 physically interacts with Hrr1, and loss of Ers1 impairs RDRC centromeric localization. Although Ers1 failed to bind Clr4, a direct interaction with Swi6 was detected, and centromeric localization of Swi6 was enhanced by Clr4 overexpression in ers1-C62 cells. Consistent with this, deletion of swi6+ reduced centromeric localization of Ers1 and RDRC. Moreover, tethering of Ers1 or Hrr1 to centromeric heterochromatin partially bypassed Swi6 function. These findings demonstrate an alternative mechanism for RDRC recruitment and explain the essential role of Swi6/Heter-ochromain Protein 1 in RNAi-directed heterochromatin assembly.
机译：在裂变酵母中，着丝粒异染色质组装需要RNAi途径。将源自着丝粒转录本的siRNA整合到RNA诱导的转录沉默（RITS）复合物中，并将其引导至新生的同源转录本。 RNA诱导的转录沉默结合的新生转录本进一步募集了RNA定向的RNA聚合酶复合物（RDRC），以促进dsRNA的合成和siRNA的产生。然后，在募集染色质修饰机制后，形成涂有Swi6 / Heterochromain蛋白1的异染色质。 siRNA的上游生产也需要Swi6，尽管其机制仍然不清楚。在这里，我们证明Swi6通过RNAi因子中间体Ers1将RDRC募集到异染色质。一个ers1 +突变体等位基因（ers1-C62）在减轻中心粒沉默的突变体的遗传筛选中被鉴定出来，并且该表型被Hrr1 RDRC亚基或Clr4组蛋白H3-K9甲基转移酶的过度表达所抑制。 Ers1在物理上与Hrr1相互作用，而Ers1的缺失会损害RDRC着丝粒定位。尽管Ers1未能结合Clr4，但检测到与Swi6的直接相互作用，并且在ers1-C62细胞中Clr4过表达增强了Swi6的着丝粒定位。与此一致，swi6 +的缺失降低了Ers1和RDRC着丝粒的定位。此外，Ers1或Hrr1绑定到着丝粒异染色质部分绕过Swi6功能。这些发现证明了RDRC募集的替代机制，并解释了Swi6 / Heter-ochromain蛋白1在RNAi定向异染色质组装中的重要作用。

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    Aki Hayashi; Mayumi lshida; Rika Kawaguchi; Takeshi Urano; Yota Murakami; Jun-ichi Nakayama;

  • 作者单位

    Laboratory for Chromatin Dynamics, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan;

    Laboratory for Chromatin Dynamics, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan,Department of Bioscience, Graduate School of Science and Technology, Kwansei-Gakuin University, Sanda, Hyogo 669-1337, Japan;

    Laboratory for Chromatin Dynamics, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan;

    Department of Biochemistry, Shimane University School of Medicine,Izumo 693-8501, Japan;

    Laboratory of Bioorganic Chemistry, Department of Chemistry, Faculty of Science, Hokkaido University, Kita-ku, Sapporo 060-0810, Japan;

    Laboratory for Chromatin Dynamics, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan,Department of Bioscience, Graduate School of Science and Technology, Kwansei-Gakuin University, Sanda, Hyogo 669-1337, Japan;

  • 收录信息 美国《科学引文索引》(SCI);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
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  • 关键词

    rna interference; histone h3-lysine 9 methylation;

    机译：RNA干扰组蛋白h3-赖氨酸9甲基化;

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