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Nucleotide excision repair and homologous recombination systems commit differentially to the repair of DNA-protein crosslinks.
- Source :
-
Molecular cell [Mol Cell] 2007 Oct 12; Vol. 28 (1), pp. 147-58. - Publication Year :
- 2007
-
Abstract
- DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.
- Subjects :
- Animals
Azacitidine metabolism
Chromosomes genetics
Cross-Linking Reagents metabolism
DNA genetics
DNA Helicases genetics
DNA Helicases metabolism
Endodeoxyribonucleases metabolism
Escherichia coli metabolism
Escherichia coli Proteins genetics
Escherichia coli Proteins metabolism
Exodeoxyribonuclease V genetics
Exodeoxyribonuclease V metabolism
Formaldehyde metabolism
Humans
Plasmids genetics
Plasmids metabolism
DNA metabolism
DNA Damage
DNA Repair
DNA Replication
Recombination, Genetic
Subjects
Details
- Language :
- English
- ISSN :
- 1097-2765
- Volume :
- 28
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Molecular cell
- Publication Type :
- Academic Journal
- Accession number :
- 17936711
- Full Text :
- https://doi.org/10.1016/j.molcel.2007.07.029