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.
Mesh Terms:
Cell Cycle Proteins, Culture Media, DNA Damage, DNA, Fungal, Fungal Proteins, G2 Phase, Genes, Fungal, Mitosis, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Temperature, Ultraviolet Rays
Cell Cycle Proteins, Culture Media, DNA Damage, DNA, Fungal, Fungal Proteins, G2 Phase, Genes, Fungal, Mitosis, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Temperature, Ultraviolet Rays
Mol. Gen. Genet.
Date: Nov. 27, 1996
PubMed ID: 9003297
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