CDC20, A S-TRANSDUCIN HOMOLOG, 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, ME C1, MEC2 and MEC3. These genes also prevent entry into mitosis of a te mperature-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 restrict ive temperature but instead undergoes nuclear division, exits mitosis and enters a subsequent division cycle, which suggests that the DNA da mage-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 th e cde mutants whose cell cycle block is independent of RAD9-mediated c heckpoint control. Therefore, we suggest that the DNA damage-induced c heckpoint controls prevent mitosis by inhibiting the nuclear division pathway requiring CDC20 function.