| Abstract
| - In mammalian cells, damaged bases in DNA are corrected by the base excision repair pathwaywhich is divided into two distinct pathways depending on the length of the resynthesized patch, replacementof one nucleotide for short-patch repair, and resynthesis of several nucleotides for long-patch repair. Theinvolvement of poly(ADP-ribose) polymerase-1 (PARP-1) in both pathways has been investigated byusing PARP-1-deficient cell extracts to repair single abasic sites derived from uracil or 8-oxoguaninelocated in a double-stranded circular plasmid. For both lesions, PARP-1-deficient cell extracts were abouthalf as efficient as wild-type cells at the polymerization step of the short-patch repair synthesis, but werehighly inefficient at the long-patch repair. We provided evidence that PARP-1 constitutively interactswith DNA polymerase β. Using cell-free extracts from mouse embryonic cells deficient in DNA polymeraseβ, we demonstrated that DNA polymerase β is involved in the repair of uracil-derived AP sites via boththe short and the long-patch repair pathways. When both PARP-1 and DNA polymerase β were absent,the two repair pathways were dramatically affected, indicating that base excision repair was highlyinefficient. These results show that PARP-1 is an active player in DNA base excision repair.
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