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

Springall, Luke, Hughes, Craig D., Simons, Michelle, Azinas, Stavros, Van Houten, Bennett, Kad, Neil M (2018) Recruitment of UvrBC complexes to UV-induced damage in the absence of UvrA increases cell survival. Nucleic Acids Research, 46 (3). pp. 1256-1265. ISSN 0305-1048. E-ISSN 1362-4962. (doi:10.1093/nar/gkx1244)

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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.

Item Type: Article
DOI/Identification number: 10.1093/nar/gkx1244
Uncontrolled keywords: DNA repair, fluorescence, single molecule
Subjects: Q Science
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: N. Kad
Date Deposited: 12 Dec 2017 16:32 UTC
Last Modified: 29 May 2019 20:04 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/65331 (The current URI for this page, for reference purposes)
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