Adebali Ogun, Sancar Aziz, Selby Christopher P
From the Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7260.
From the Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7260
J Biol Chem. 2017 Nov 10;292(45):18386-18391. doi: 10.1074/jbc.C117.818807. Epub 2017 Oct 6.
Nucleotide excision repair in is stimulated by transcription, specifically in the transcribed strand. Previously, it was shown that this transcription-coupled repair (TCR) is mediated by the Mfd translocase. Recently, it was proposed that in fact the majority of TCR in is catalyzed by a second pathway ("backtracking-mediated TCR") that is dependent on the UvrD helicase and the guanosine pentaphosphate (ppGpp) alarmone/stringent response regulator. Recently, we reported that as measured by the excision repair-sequencing (XR-seq), UvrD plays no role in TCR genome-wide. Here, we tested the role of ppGpp and UvrD in TCR genome-wide and in the operon using the XR-seq method, which directly measures repair. We found that the mutation abolishes TCR genome-wide and in the operon. In contrast, the mutant deficient in ppGpp synthesis carries out normal TCR. We conclude that UvrD and ppGpp play no role in TCR in .
转录可刺激大肠杆菌中的核苷酸切除修复，特别是在转录链中。此前研究表明，这种转录偶联修复（TCR）由Mfd转位酶介导。最近，有人提出实际上大肠杆菌中大部分的TCR是由第二条途径（“回溯介导的TCR”）催化的，该途径依赖于UvrD解旋酶和鸟苷五磷酸（ppGpp）警报素/严格反应调节因子。最近，我们报道通过切除修复测序（XR-seq）测量发现，UvrD在全基因组范围的TCR中不起作用。在此，我们使用可直接测量修复的XR-seq方法，测试了ppGpp和UvrD在全基因组范围的TCR以及在乳糖操纵子中的作用。我们发现Δmfd突变消除了全基因组范围以及乳糖操纵子中的TCR。相反，缺乏ppGpp合成能力的relA突变体可进行正常的TCR。我们得出结论，UvrD和ppGpp在大肠杆菌的TCR中不起作用。
