Modulation of DNA repair by mutations flanking the DNA channel through RNA polymerase
Modulation of DNA repair by mutations flanking the DNA channel through RNA polymerase
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DOI：
10.1093/emboj/cdf654
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发表时间：
2002-12-16
期刊：
影响因子：
11.4
通讯作者：
Lloyd, RG
中科院分区：
文献类型：
--
作者：
Trautinger, BW;Lloyd, RG
RuvABC和RecBCD蛋白促进拯救大肠杆菌中停滞或断裂的DNA复制叉。缺乏这些蛋白质的菌株科普DNA损伤的能力很差，并且在染色体分离和细胞分裂方面存在问题。我们展示了如何克服这些困难，在不同程度上由一个子类的RNA聚合酶突变选择其严格的表型。对35个突变进行了测序。除了一个以外，所有RpoB或RpoC中位于DNA通过酶所采取的路径上或附近的单个氨基酸都发生了变化，表明它们可能影响转录复合物的稳定性。四个突变酶显示，形成不稳定的开放式复合物在dacro启动子。至少一个也可以释放停滞的复合物或限制它们的形成，因为它减少了对GreA或GreB重新激活转录的需要，以及对Mfd的UV损伤的转录偶联DNA修复的需要。这些结果揭示了DNA复制和转录之间的相互作用，并提出了避免或解决这两个重要细胞过程之间冲突的方法。
The RuvABC and RecBCD proteins promote rescue of stalled or broken DNA replication forks in Escherichia coli. Strains lacking these proteins cope poorly with DNA damage and have problems with chromosome segregation and cell division. We show how these difficulties are overcome to varying degrees by a sub-class of RNA polymerase mutations selected for their stringent phenotype. Thirty-five mutations were sequenced. All but one change single amino acids in RpoB or RpoC that lie on or near the path taken by DNA through the enzyme, indicating they may affect the stability of transcription complexes. Four mutant enzymes are shown to form unstable open complexes at the lambdacro promoter. At least one may also release stalled complexes or limit their formation, as it re duces the need for reactivation of transcription by GreA or GreB, and for transcription-coupled DNA repair of UV damage by Mfd. The results shed light on the interplay between DNA replication and transcription and suggest ways in which conflicts between these two vital cellular processes are avoided or resolved.