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Caracterisation de la fonction des complexes histone deacetylases Rpd3S et Set3C.

机译：组蛋白脱乙酰基酶复合物Rpd3S和Set3C的功能表征。

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摘要

Chromatin is essential for the maintenance of genomic integrity but, ironically, is also the main barrier to gene transcription. Many mechanisms, such as histone acetylation, have evolved to overcome this problem. Histone acetylation, catalyzed by histone acetyltransferases (HATs), weakens the internucleosomal and nucleosome-DNA interactions, thus permitting the transcriptional machinery access to its template. However, this permissive chromatin state also allows for opportunistic DNA binding events. Histone deacetylases (HDACs) help restore a compact chromatin structure by catalyzing the removal of acetyl moieties from histones.;This thesis focuses on the characterization of the function and of the recruitment mechanism of HDAC complexes Rpd3S and Set3C. The Rpd3S complex is recruited to actively transcribed coding regions through interactions with the hyperphosphorylated C-terminal domain of Rpb1, a subunit of RNA polymerase II, with the DSIF elongation factor playing a role in limiting this recruitment. However, the HDAC activity of Rpd3S depends on H3K36 methylation, which is catalyzed by the Set2 histone methyltransferase.;The Set3C complex' function is still not clearly defined. It is recruited to most of its targets through the interaction between the Set3 PHD domain and di- or trimethylated H3K4. However, Set3C recruitment to genes displaying high RNA polymerase II occupancy is independent of H3K4 methylation. The mechanism by which Set3C is recruited to this gene subset is under investigation.;These results have mostly been obtained through chromatin immunoprecipitation coupled to tiling microarrays (ChIP-chip). The protocol and experimental design challenges inherent to this technique will also be discussed in depth.;Keywords : Chromatin immunoprecipitation; ChIP-chip; microarrays; histone acetyltransferase (HAT); histone deacetylase (HDAC); histone methyltransferase (HMT);
机译：染色质对于维持基因组完整性至关重要，但具有讽刺意味的是，它也是基因转录的主要障碍。为了克服这个问题，已经发展了许多机制，例如组蛋白乙酰化。组蛋白乙酰基转移酶（HATs）催化的组蛋白乙酰化作用减弱了核小体间和核小体与DNA的相互作用，从而使转录机制可接近其模板。但是，这种允许的染色质状态也允许机会性的DNA结合事件。组蛋白脱乙酰基酶（HDACs）通过催化从组蛋白中去除乙酰基部分，帮助恢复致密的染色质结构。本论文着重研究了HDAC复合物Rpd3S和Set3C的功能和募集机制。 Rpd3S复合物通过与RNA聚合酶II的亚基Rpb1的超磷酸化C末端结构域相互作用而被募集，以主动转录编码区，而DSIF延伸因子在限制这种募集中起作用。然而，Rpd3S的HDAC活性取决于H3K36甲基化，这是由Set2组蛋白甲基转移酶催化的。Set3C配合物的功能仍不清楚。通过Set3 PHD域与二甲基或三甲基化的H3K4之间的相互作用，将其招募到大多数目标。但是，Set3C募集到显示高RNA聚合酶II占用率的基因与H3K4甲基化无关。正在研究将Set3C募集到该基因子集的机制。这些结果主要是通过染色质免疫沉淀与平铺微阵列（ChIP-chip）结合获得的。该技术固有的方案和实验设计挑战也将进行深入讨论。芯片微阵列组蛋白乙酰转移酶（HAT）;组蛋白脱乙酰基酶（HDAC）;组蛋白甲基转移酶（HMT）;

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  • 作者

    Drouin, Simon.;

  • 作者单位

    Universite de Montreal (Canada).;

  • 授予单位 Universite de Montreal (Canada).;
  • 学科 Biology Molecular.
  • 学位 Ph.D.
  • 年度 2011
  • 页码 185 p.
  • 总页数 185
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

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