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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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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Abstract 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.
AbstractList 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.
Author Ide, Hiroshi
Pack, Seung Pil
Nakano, Toshiaki
Terato, Hiroaki
Salem, Amir M.H.
Makino, Keisuke
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  givenname: Keisuke
  surname: Makino
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  organization: 1 Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima 739-8526, Japan and 2Institute of Advanced Energy, Kyoto University, Gokasho, Uji 611-0011, Japan
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Snippet Abstract DNA-protein crosslinks (DPCs) are extremely bulky DNA lesions, and steric hindrance imposed by covalently trapped proteins would hamper the...
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Title Repair of DNA-protein crosslink damage: Coordinated actions of nucleotide excision repair and homologous recombination
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