PARP-1 ensures regulation of replication fork progression by homologous recombination on damaged DNA.
作者： Kazuto Sugimura , Shin-ichiro Takebayashi , Hiroshi Taguchi , Shunichi Takeda , Katsuzumi Okumura
关键词: DNA repair 、 Postreplication repair 、 DNA Replication Fork 、 Molecular biology 、 S phase 、 Biology 、 Replication protein A 、 Topoisomerase-I Inhibitor 、 DNA damage 、 DNA repair protein XRCC4
摘要: Poly-ADP ribose polymerase 1 (PARP-1) is activated by DNA damage and has been implicated in the repair of single-strand breaks (SSBs). Involvement PARP-1 other responses remains controversial. In this study, we show that required for replication fork slowing on damaged DNA. Fork progression PARP-1−/− DT40 cells not slowed down even presence induced topoisomerase I inhibitor camptothecin (CPT). Mammalian treated with a PARP or PARP-1–specific small interfering RNAs similar results. The expression human restores cells. affects SSB repair, homologous recombination (HR), nonhomologous end joining; therefore, analyzed effect CPT clones deficient these pathways. We find correlated proficiency HR-mediated repair. Our data support novel checkpoint pathway which initiation HR but delays progression.
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