Repair of DNA-protein crosslink damage: Coordinated actions of nucleotide excision repair and homologous recombination

Abstract DNA-protein crosslinks (DPCs) are extremely bulky DNA lesions, and steric hindrance imposed by covalently trapped proteins would hamper the transaction of DNA such as replication, transcription, and repair. However, it has been largely elusive how cells mitigate the genotoxic effect of DPCs...

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Bibliographic Details
Published inNucleic Acids Symposium Series Vol. 52; no. 1; pp. 57 - 58
Main Authors Ide, Hiroshi, Nakano, Toshiaki, Salem, Amir M.H., Terato, Hiroaki, Pack, Seung Pil, Makino, Keisuke
Format Journal Article
LanguageEnglish
Published Oxford University Press 01.09.2008
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Summary:Abstract DNA-protein crosslinks (DPCs) are extremely bulky DNA lesions, and steric hindrance imposed by covalently trapped proteins would hamper the transaction of DNA such as replication, transcription, and repair. However, it has been largely elusive how cells mitigate the genotoxic effect of DPCs. We have recently shown that nucleotide excision repair (NER) and homologous recombination (HR) differentially contribute to the repair of DPCs in E. coli cells. Several lines of genetic and biochemical evidence indicate that NER repairs DPCs with crosslinked proteins (CLPs) of sizes less than 12-14 kDa, whereas DPCs with oversized CLPs are processed exclusively by RecBCD-dependent HR. The present result shows that cells use the coordinated actions of NER and HR to deal with unusually bulky DNA lesions like DPCs.
ISSN:0261-3166
1746-8272
DOI:10.1093/nass/nrn029