Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S- phase but arrest permanently in G2 after cisplatin treatment

Kenneth F. Grossmann, Alex M. Ward, Robb E. Moses

Research output: Contribution to journalArticle

35 Scopus citations


The role of Snm1, Rev3 and Rad51 in S-phase after cisplatin (CDDP) DNA treatment has been examined. When isogenic deletion mutants snm1Δ, rev3Δ and rad51Δ were arrested in G1 and treated with doses of CDDP causing significant lethality (< 20% survival in the mutant strains), they progressed through S-phase with normal kinetics. The mutants arrested in G2 like wild- type cells, however they did not exit the arrest and reenter the cell cycle. This finding demonstrates that these genes are not required to allow DNA replication in the presence of damage. Therefore, Snm1, Rev3 and Rad51 may act after S to allow repair. At high levels of damage (< 40% survival in wild-type cells) S-phase was slowed in a MEC1-dependent fashion. The cross- link incision kinetics of snm1Δ and rev3Δ mutants were also examined; both showed no deficiencies in incision of cross-linked DNA. (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)1-13
Number of pages13
JournalMutation Research - DNA Repair
Issue number1
StatePublished - Sep 15 2000



  • 8-MOP - 8-methoxypsoralen
  • CDDP - cisplatin
  • Cell cycle checkpoint
  • DNA cross-link repair
  • Yeast Saccharomyces cerevisiae

ASJC Scopus subject areas

  • Molecular Biology
  • Toxicology
  • Genetics

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