The DNA helicases acting in nucleotide excision repair, XPD, CSB and XPB, are not required for PCNA-dependent repair of abasic sites

DNA repair of abasic sites is accomplished in mammalian cells by two distin ct base excision repair (BER) pathways: a single nucleotide insertion pathw ay and a proliferating cell nuclear antigen (PCNA)-dependent pathway involv ing a resynthesis patch of 2-10 nucleotides 3' to the lesion. The latter pa thway shares some enzymatic components with the nucleotide excision repair (NER) pathway acting on damage induced by ultraviolet light: both pathways are strictly dependent on PCNA and several observations suggest that the po lymerization and ligation phases may be carried out by common enzymatic act ivities (DNA polymerase delta/epsilon and DNA ligase I). Furthermore, it ha s been postulated that the transcription-NER coupling factor Cockayne syndr ome B has a role in BER. We have investigated whether three NER proteins en dowed with DNA helicase activities (the xeroderma pigmentosum D and B gene products and the Cockayne syndrome B gene product) may also be involved in repair of natural abasic sites, by using the Chinese hamster ovary mutant c ell lines UV5, UV61 and 27-1. No defect of either the PCNA-dependent or the single nucleotide insertion pathways could be observed in UV5, UV61 or 27- 1 mutant cell extracts, thus showing that the partial enzymatic overlap bet ween PCNA-dependent BER and NER does not extend to DNA helicase activities.