期刊
NUCLEIC ACIDS RESEARCH
卷 46, 期 3, 页码 1256-1265出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkx1244
关键词
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资金
- Biotechnology and Biological Sciences Research Council (BBSRC) [BB/P00847X/1, BB/M019144/1, BB/I003460/1]
- National Institutes of Health [5R01ES019566]
- Hillman Cancer Center [2P30CA047904]
- [BBSRC BB/P00847X/1]
- BBSRC [BB/P00847X/1, BB/I003460/1, BB/M019144/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/P00847X/1, BB/M019144/1, BB/I003460/1] Funding Source: researchfish
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 UvrA(2) 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.
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