The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 genes are required for tolerating irreparable, ultraviolet-induced DNA damage

A. G. Paulovich, C. D. Armour, Leland Hartwell

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

In wild-type Saccharomyces cerevisiae, a checkpoint slows the rate of progression of an ongoing S phase in response to exposure to a DNA-alkylating agent. Mutations that eliminate S phase regulation also confer sensitivity to alkylating agents, leading us to suggest that, by regulating the S phase rate, cells are either better able to repair or better able to replicate damaged DNA. In this study, we determine the effects of mutations that impair S phase regulation on the ability of excision repair-defective cells to replicate irreparably UV-damaged DNA. We assay survival after UV irradiation, as well as the genetic consequences of replicating a damaged template, namely mutation and sister chromatid exchange induction. We find that RAD9, RAD17, RAD24, and MEC3 are required for UV-induced (although not spontaneous) mutagenesis, and that RAD9 and RAD17 (but not REV3, RAD24, and MEC3) are required for maximal induction of replication-dependent sister chromatid exchange. Therefore, checkpoint genes not only control cell cycle progression in response to damage, but also play a role in accommodating DNA damage during replication.

Original languageEnglish (US)
Pages (from-to)75-93
Number of pages19
JournalGenetics
Volume150
Issue number1
StatePublished - Sep 1998
Externally publishedYes

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S Phase
DNA Damage
Saccharomyces cerevisiae
Sister Chromatid Exchange
Alkylating Agents
Mutation
Genes
DNA
Cell Cycle Checkpoints
Mutagenesis
DNA Repair

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

Cite this

The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 genes are required for tolerating irreparable, ultraviolet-induced DNA damage. / Paulovich, A. G.; Armour, C. D.; Hartwell, Leland.

In: Genetics, Vol. 150, No. 1, 09.1998, p. 75-93.

Research output: Contribution to journalArticle

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