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

Enrico Cappelli, Fabio Carrozzino, Angelo Abbondandolo, Guido Frosina

Research output: Contribution to journalArticlepeer-review

Abstract

DNA repair of abasic sites is accomplished in mammalian cells by two distinct base excision repair (BER) pathways: a single nucleotide insertion pathway and a proliferating cell nuclear antigen (PCNA)-dependent pathway involving a resynthesis patch of 2-10 nucleotides 3' to the lesion. The latter pathway 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 polymerization and ligation phases may be carried out by common enzymatic activities (DNA polymerase δ/ε and DNA ligase I). Furthermore, it has been postulated that the transcription-NER coupling factor Cockayne syndrome B has a role in BER. We have investigated whether three NER proteins endowed 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 cell 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 between PCNA- dependent BER and NER does not extend to DNA helicase activities.

Original languageEnglish
Pages (from-to)325-330
Number of pages6
JournalEuropean Journal of Biochemistry
Volume259
Issue number1-2
DOIs
Publication statusPublished - Jan 15 1999

Keywords

  • Abasic sites, DNA helicases, xeroderma pigmentosum
  • Base excision repair
  • Cockayne's syndrome

ASJC Scopus subject areas

  • Biochemistry

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