Yeast base excision repair: interconnections and networks.

Published

Journal Article (Review)

The removal of oxidative base damage from the genome of Saccharomyces cerevisiae is thought to occur primarily via the base excision repair (BER) pathway in a process initiated by several DNA N-glycosylase/AP lyases. We have found that yeast strains containing simultaneous multiple disruptions of BER genes are not hypersensitive to killing by oxidizing agents, but exhibit a spontaneous hyperrecombinogenic (hyper-rec) and mutator phenotype. The hyper-rec and mutator phenotypes are further enhanced by elimination of the nucleotide excision repair (NER) pathway. Furthermore, elimination of either the lesion bypass (REV3-dependent) or recombination (RAD52-dependent) pathway results in a further, specific enhancement of the hyper-rec or mutator phenotypes, respectively. Sensitivity (cell killing) to oxidizing agents is not observed unless multiple pathways are eliminated simultaneously. These data suggest that the BER, NER, recombination, and lesion bypass pathways have overlapping specificities in the removal of, or tolerance to, exogenous or spontaneous oxidative DNA damage in S. cerevisiae. Our results also suggest a physiological role for the AP lyase activity of certain BER N-glycosylases in vivo.

Full Text

Duke Authors

Cited Authors

  • Doetsch, PW; Morey, NJ; Swanson, RL; Jinks-Robertson, S

Published Date

  • 2001

Published In

Volume / Issue

  • 68 /

Start / End Page

  • 29 - 39

PubMed ID

  • 11554305

Pubmed Central ID

  • 11554305

International Standard Serial Number (ISSN)

  • 0079-6603

Language

  • eng

Conference Location

  • United States