| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3399047 | Current Opinion in Microbiology | 2015 | 6 Pages |
•UvrD is the first transcription factor that forces RNA polymerase to backtrack.•Elongation factor NusA assists UvrD in stimulating backtracking.•UvrD/NusA-mediated transcription coupled DNA repair (TCR) is Mfd-independent.•RNAP may serve as a global scanner for DNA lesions due to ubiquitous transcription.
Nucleotide excision repair (NER) is an evolutionarily conserved, multistep process that can detect a wide variety of DNA lesions. Transcription coupled repair (TCR) is a subpathway of NER that repairs the transcribed DNA strand faster than the rest of the genome. RNA polymerase (RNAP) stalled at DNA lesions mediates the recruitment of NER enzymes to the damage site. In this review we focus on a newly identified bacterial TCR pathway in which the NER enzyme UvrD, in conjunction with NusA, plays a major role in initiating the repair process. We discuss the tradeoff between the new and conventional models of TCR, how and when each pathway operates to repair DNA damage, and the necessity of pervasive transcription in maintaining genome integrity.
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