Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo (Retracted article. See vol. 81, pg. 5112, 2021)
Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo (Retracted article. See vol. 81, pg. 5112, 2021)
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DOI：
10.1016/j.molcel.2006.06.029
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发表时间：
2006-08-18
期刊：
影响因子：
16
通讯作者：
Mullenders, Leon H. F.
中科院分区：
文献类型：
--
作者：
Fousteri, Maria;Vermeulen, Wim;Mullenders, Leon H. F.
紫外线抑制转录的恢复需要通过转录偶联修复(TCR)去除转录阻断的DNA损伤。在哺乳动物中，TCR依赖于CsA和CSB蛋白；然而，它们的功能在很大程度上是未知的。在这里，我们分析了来自人类细胞的紫外线停滞转录延伸复合体的组成。我们发现CSB和CsA在TCR特异性因子的招募中显示出不同的作用，并且TCR的组装不会中断UV停滞的RNA聚合酶11(RNAPIIo)。CSB作为一个关键的偶联因子，吸引了组蛋白乙酰转移酶p300、核苷酸切除修复(NER)蛋白和CsA-DDB1 E3-泛素连接酶与COP9信号体的复合体。CsA对于NER蛋白与病变停滞的RNAPIIo的吸引是必不可少的，但在与CSB的合作中，需要招募XAB2、核小体结合蛋白HMGN1和TFIIS。这些结果深入了解了在染色体DNA背景下TCR期间发生的分子事件的性质和顺序。
Restoration of UV-inhibited transcription requires removal of transcription-blocking DNA lesions by transcription-coupled repair (TCR). In mammals, TCR is dependent on CSA and CSB proteins; however, their functions are largely unknown. Here, we analyzed the composition of UV-stalled transcription elongation complexes from human cells. We show that CSB and CSA display differential roles in recruitment of TCR-specific factors and that assembly for TCR occurs without disruption of the UV-stalled RNA polymerase 11 (RNAPIIo). CSB fulfills a key role as a coupling factor to attract histone acetyltransferase p300, nucleotide excision repair (NER) proteins, and CSA-DDB1 E3-ubiquitin ligase complex with the COP9 signalosome. CSA is dispensable for attraction of NER proteins to lesion-stalled RNAPIIo, yet in cooperation with CSB is required to recruit XAB2, the nucleosomal binding protein HMGN1, and TFIIS. These results give insight into the nature and order of molecular events that take place during TCR in the context of chromosomal DNA.