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Recruitment of UvrBC complexes to UV-induced damage in the absence of UvrA increases cell survival.

ABSTRACT: Nucleotide excision repair (NER) is the primary mechanism for removal of ultraviolet light (UV)-induced DNA photoproducts and is mechanistically conserved across all kingdoms of life. Bacterial NER involves damage recognition by UvrA2 and UvrB, followed by UvrC-mediated incision either side of the lesion. Here, using a combination of in vitro and in vivo single-molecule studies we show that a UvrBC complex is capable of lesion identification in the absence of UvrA. Single-molecule analysis of eGFP-labelled UvrB and UvrC in living cells showed that UV damage caused these proteins to switch from cytoplasmic diffusion to stable complexes on DNA. Surprisingly, ectopic expression of UvrC in a uvrA deleted strain increased UV survival. These data provide evidence for a previously unrealized mechanism of survival that can occur through direct lesion recognition by a UvrBC complex.

SUBMITTER: Springall L 

PROVIDER: S-EPMC5814901 | biostudies-other | 2018 Feb

REPOSITORIES: biostudies-other

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Recruitment of UvrBC complexes to UV-induced damage in the absence of UvrA increases cell survival.

Springall Luke L   Hughes Craig D CD   Simons Michelle M   Azinas Stavros S   Van Houten Bennett B   Kad Neil M NM  

Nucleic acids research 20180201 3

Nucleotide excision repair (NER) is the primary mechanism for removal of ultraviolet light (UV)-induced DNA photoproducts and is mechanistically conserved across all kingdoms of life. Bacterial NER involves damage recognition by UvrA2 and UvrB, followed by UvrC-mediated incision either side of the lesion. Here, using a combination of in vitro and in vivo single-molecule studies we show that a UvrBC complex is capable of lesion identification in the absence of UvrA. Single-molecule analysis of eG  ...[more]