Molecular and General Genetics MGG

, Volume 253, Issue 1, pp 138–148

Cdc20, a β-transducin homologue, links RAD9-mediated G2/M checkpoint control to mitosis in Saccharomyces cerevisiae

  • H. H. Lim
  • U. Surana
ORIGINAL PAPER

DOI: 10.1007/s004380050306

Cite this article as:
Lim, H. & Surana, U. Mol Gen Genet (1996) 253: 138. doi:10.1007/s004380050306

Abstract

 In the budding yeast Saccharomyces cerevisiae, the DNA damage-induced G2 arrest requires the checkpoint control genes RAD9, RAD17, RAD24, MEC1, MEC2 and MEC3. These genes also prevent entry into mitosis of a temperature-sensitive mutant, cdc13, that accumulates chromosome damage at 37° C. Here we show that a cdc13 mutant overexpressing Cdc20, a β-transducin homologue, no longer arrests in G2 at the restrictive temperature but instead undergoes nuclear division, exits mitosis and enters a subsequent division cycle, which suggests that the DNA damage-induced G2/M checkpoint control is not functional in these cells. This is consistent with our observation that overexpression of CDC20 in wild-type cells results in increased sensitivity to UV irradiation. Overproduction of Cdc20 does not influence the arrest phenotype of the cdc mutants whose cell cycle block is independent of RAD9-mediated checkpoint control. Therefore, we suggest that the DNA damage-induced checkpoint controls prevent mitosis by inhibiting the nuclear division pathway requiring CDC20 function.

Key words Checkpoint controlCDC20Yeast cell cycle

Copyright information

© Springer-Verlag Berlin Heidelberg 1996

Authors and Affiliations

  • H. H. Lim
    • 1
  • U. Surana
    • 1
  1. 1.Institute of Molecular and Cell Biology, National University of Singapore, 10, Kent Ridge Crescent, Singapore 119260SG