Molecular and General Genetics MGG

, Volume 262, Issue 6, pp 1132–1146

Characterization of a Saccharomyces cerevisiae homologue of Schizosaccharomyces pombe Chk1 involved in DNA-damage-induced M-phase arrest

Authors

  • Y. Liu
    • Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA E-mail: wsiede@emory.edu Tel.: +1-404-7782170; Fax: +1-404-7785016
  • G. Vidanes
    • Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA E-mail: wsiede@emory.edu Tel.: +1-404-7782170; Fax: +1-404-7785016
  • Y. -C. Lin
    • Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA E-mail: wsiede@emory.edu Tel.: +1-404-7782170; Fax: +1-404-7785016
  • S. Mori
    • Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA E-mail: wsiede@emory.edu Tel.: +1-404-7782170; Fax: +1-404-7785016
  • W. Siede
    • Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA E-mail: wsiede@emory.edu Tel.: +1-404-7782170; Fax: +1-404-7785016
ORIGINAL PAPER

DOI: 10.1007/PL00008656

Cite this article as:
Liu, Y., Vidanes, G., Lin, Y. et al. Mol Gen Genet (2000) 262: 1132. doi:10.1007/PL00008656
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Abstract

Chk1 is an evolutionarily conserved protein kinase that plays an essential role in mediating G2 arrest in response to DNA damage in Schizosaccharomyces pombe and human cells. It functions by maintaining the inhibition (by phosphorylation of a specific tyrosine residue) of the cyclin-dependent kinase Cdc2 that initiates the G2/M transition. Here, we characterize a structural homologue of Chk1 in the budding yeast Saccharomyces cerevisiae. In this organism, G2/M arrest following DNA damage is considered to be independent of tyrosine phosphorylation of the Cdc2 homologue Cdc28. Nevertheless, a partial defect in G2/M-phase arrest following treatment with ionizing radiation, but not UV radiation, is associated with deletion of CHK1. The fact that such an effect remains detectable in cells synchronized with the microtubule inhibitor nocodazole prior to γ irradiation implies the existence of a CHK1-dependent checkpoint in M phase. We conclude from epistasis analysis that Chk1 participates in the Pds1-dependent subpathway of M-phase arrest. In spite of the partial checkpoint defect of the chk1 mutant, the survival of colony-forming cells is not notably decreased following UV and γ irradiation. In two-hybrid screens, we identified a heme-binding stress protein (encoded by the yeast ORF YNL234W), a protein involved in genomic silencing (Sas3) and Chk1 itself as interacting partners of Chk1.

Key words YeastCell CycleCheckpointsDNA damage
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© Springer-Verlag Berlin Heidelberg 2000