Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage

Eris Duro, Jessica A. Vaisica, Grant W. Brown, John Rouse*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors. (c) 2008 Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)811-818
Number of pages8
JournalDNA Repair
Volume7
Issue number5
DOIs
Publication statusPublished - 3 May 2008

Keywords

  • GENES
  • HISTONE-H3
  • REPAIR
  • NATURAL PAUSE SITES
  • DNA-DAMAGE
  • MMS22
  • DAMAGED REPLICATION FORKS
  • genotoxin
  • DNA damage
  • MMS1
  • CHECKPOINT
  • SENSITIVE MUTANTS
  • INTEGRITY
  • homologous recombination
  • SACCHAROMYCES-CEREVISIAE
  • MMS

Fingerprint

Dive into the research topics of 'Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage'. Together they form a unique fingerprint.

Cite this