Activation of a novel pathway involving Mms1 and Rad59 in sgs1 cells

Ayako Ui, Masayuki Seki, Hideaki Ogiwara, Mong Sing Lai, Kazuo Yamamoto, Shusuke Tada, Takemi Enomoto

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Unequal sister chromatid recombination (uSCR) is elevated in budding yeast sgs1 mutants, which lack a homolog of the human BLM gene that causes Bloom syndrome. Examination of the mechanism responsible for elevated uSCR in sgs1 mutants showed that mutation of RAD51 also resulted in hyper-uSCR. Data from this study show that defects in the Rad51-Sgs1-dependent and Sgs1-dependent lesion-bypass pathways activate Rad59-Rad1- and Rad59-dependent pathways, respectively, resulting in uSCR. Moreover, the elevation of uSCR in sgs1 and rad51 mutants was dependent on MMS1, which encodes one of the components of the Mms22 module. Lastly, a putative role of Mms1 in the elevation of uSCR and a possible mechanism by which uSCR is elevated as a result of defective Sgs1 and Rad51 are discussed.

Original languageEnglish
Pages (from-to)1031-1037
Number of pages7
JournalBiochemical and biophysical research communications
Volume356
Issue number4
DOIs
Publication statusPublished - 2007 May 18

Keywords

  • Bloom syndrome
  • Mms1
  • Mms22
  • Rad51
  • RecQ
  • Recombination
  • Rtt101
  • Rtt107
  • Rtt109
  • Template switch

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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