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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Arch Toxicol. 2016 Aug 22;90(11):2583–2594. doi: 10.1007/s00204-016-1820-x

Fig. 1. NER in E. coli.

Fig. 1

A DNA lesion that does not block transcription may be detected by the combined action of the UvrAB complex. If transcription arrest occurs, two alternative modes of displacing the RNAP can operate: the Mfd-mediated forward movement that implies transcription termination or bypass of the lesion, and the UvrD/NusA-mediated backtracking that allows resumption of transcription once the lesion is repaired. Both Mfd and UvrD/NusA can recruit the UvrAB complex, which binds to the DNA and recognizes and verifies the damage to be repaired. Repair then proceeds through a common series of steps. UvrA dissociates from the preincision complex leaving 1 or 2 molecules of UvrB bound to the DNA. UvrC interacts with UvrB and catalyzes two nicks in the DNA, one on either side of the lesion. The combined action of UvrD (helicase I) and DNA polymerase I removes the oligonucleotide containing the lesion, as well as UvrB and UvrC, from the DNA and results in the synthesis of a patch using the undamaged complementary strand as a template. DNA ligase I seals the patch to the contiguous DNA strand, thus restoring the DNA to its original form