Repair of DNA-protein crosslink damage: coordinated actions of nucleotide excision repair and homologous recombination.
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.
Ide
Hiroshi
H
Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima 739-8526, Japan. ideh@hiroshima-u.ac.jp
Nakano
Toshiaki
T
Salem
Amir M H
AM
Terato
Hiroaki
H
Pack
Seung Pil
SP
Makino
Keisuke
K
D004247:DNA / Q000737:chemistry*; D004249:DNA Damage; D004260:DNA Repair / Q000235:genetics; D004268:DNA-Binding Proteins / Q000737:chemistry*; D004926:Escherichia coli / Q000235:genetics; D011684:Purine Nucleosides / Q000737:chemistry; D011995:Recombination, Genetic
D004268:DNA-Binding Proteins; D011684:Purine Nucleosides; C468766:oxanine; D004247:DNA