Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli
Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli
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DOI：
10.1074/jbc.c117.818807
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发表时间：
2017-11-10
影响因子：
4.8
通讯作者：
Selby, Christopher P.
中科院分区：
文献类型：
--
作者：
Adebali, Ogun;Sancar, Aziz;Selby, Christopher P.
大肠杆菌中的核苷酸切除修复受转录刺激，特别是在转录链中。以前，它表明，这种转录偶联修复（TCR）是由Mfd易位酶介导的。最近有人提出，事实上，大肠杆菌TCR的大部分是在大肠杆菌中。大肠杆菌由第二条途径（回溯介导的TCR）催化，该途径依赖于UvrD解旋酶和五磷酸鸟苷（ppGpp）警报素/严格反应调节因子。最近，我们报道了通过切除修复测序（XR-seq）测量，UvrD在TCR全基因组中不起作用。在这里，我们使用直接测量修复的XR-seq方法测试了ppGpp和UvrD在TCR全基因组和lacZ操纵子中的作用。我们发现，mfd突变废除TCR全基因组和lacZ操纵子。相反，在ppGpp合成中缺陷的relA（-）spoT（-）突变体进行正常的TCR。结论UvrD和ppGpp在大肠杆菌TCR中不起作用。杆菌
Nucleotide excision repair in Escherichia coli 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 E. coli 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 lacZ operon using the XR-seq method, which directly measures repair. We found that the mfd mutation abolishes TCR genome-wide and in the lacZ operon. In contrast, the relA(-)spoT(-) mutant deficient in ppGpp synthesis carries out normal TCR. We conclude that UvrD and ppGpp play no role in TCR in E. coli.