Nucleic Acids Research · 2009 · 92 citations · 54 references
Life SciencesGeneticsMolecular BiologyDna RepairDna ReplicationRecombinationDna Damage SignalingDna Double-strand Break RepairDna Strand BreaksDouble-strand Break RepairHomologous RecombinationNucleotide Excision RepairDna Damage Repair PathwaysDna Double-strand BreaksDouble-strand Break Repair PathwaysDouble-strand Dna BreaksHomologous Recombination At Stalled ForksHomologous Recombination RepairMitomycin C TreatmentRepair Of Replication-associated Breaks
Both the ERCC1-XPF complex and the proteins involved in homoIogous recombination (HR) have critical roles in inter-strand cross-link (ICL) repair. Here, we report that mitomycin C-induced lesions inhibit replication fork elongation. Furthermore, mitomycin C-induced DNA double-strand breaks (DSBs) are the result of the collapse of ICL-stalled replication forks. These are not formed through replication run off, as we show that mitomycin C or cisplatin-induced DNA lesions are not incised by global genome nucleotide excision repair (GGR). We also suggest that ICL-lesion repair is initiated either by replication or transcription, as the GGR does not incise ICL-lesions. Furthermore, we report that RAD51 foci are induced by cisplatin or mitomycin C independently of ERCC1, but that mitomycin C-induced HR measured in a reporter construct is impaired in ERCC1-defective cells. These data suggest that ERCC1-XPF plays a role in completion of HR in ICL repair. We also find no additional sensitivity to cisplatin by siRNA co-depletion of XRCC3 and ERCC1, showing that the two proteins act on the same pathway to promote survival.
54
Sequential Assembly of the Nucleotide Excision Repair Factors In Vivo
Marcel Volker, Martijn J. Moné, Parimal Karmakar et al. · Molecular Cell · 2001 · 775 citations · Full text
Thomas Haaf, Efim I. Golub, G. N. Manjunatha Reddy et al. · Proceedings of the National Academy of Sciences · 1995 · 552 citations