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

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 degrees C. Here we show that a cdc13 mutant overexpressing Cdc20, a beta-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.

Pubmed ID: 9003297

Authors

  • Lim HH
  • Surana U

Journal

Molecular & general genetics : MGG

Publication Data

November 27, 1996

Associated Grants

None

Mesh Terms

  • Cdc20 Proteins
  • Cell Cycle Proteins
  • Culture Media
  • DNA Damage
  • DNA, Fungal
  • Fungal Proteins
  • G2 Phase
  • Genes, Fungal
  • Mitosis
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Temperature
  • Ultraviolet Rays