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.
| Original language | English |
|---|---|
| Pages (from-to) | 57-58 |
| Number of pages | 2 |
| Journal | Nucleic acids symposium series (2004) |
| Issue number | 52 |
| Publication status | Published - Dec 1 2008 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
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Repair of DNA-protein crosslink damage : coordinated actions of nucleotide excision repair and homologous recombination. / Ide, Hiroshi; Nakano, Toshiaki; Salem, Amir M.H.; Terato, Hiroaki; Pack, Seung Pil; Makino, Keisuke.
In: Nucleic acids symposium series (2004), No. 52, 01.12.2008, p. 57-58.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Repair of DNA-protein crosslink damage
T2 - coordinated actions of nucleotide excision repair and homologous recombination.
AU - Ide, Hiroshi
AU - Nakano, Toshiaki
AU - Salem, Amir M.H.
AU - Terato, Hiroaki
AU - Pack, Seung Pil
AU - Makino, Keisuke
PY - 2008/12/1
Y1 - 2008/12/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=78649433704&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78649433704&partnerID=8YFLogxK
M3 - Article
C2 - 18776251
AN - SCOPUS:78649433704
SP - 57
EP - 58
JO - Nucleic acids symposium series (2004)
JF - Nucleic acids symposium series (2004)
SN - 1746-8272
IS - 52
ER -