CELL-CYCLE ARREST IN CDC20 MUTANTS OF SACCHAROMYCES-CEREVISIAE IS INDEPENDENT OF NDC10P AND KINETOCHORE FUNCTION BUT REQUIRES A SUBSET OF SPINDLE CHECKPOINT GENES

The spindle checkpoint ensures accurate chromosome segregation by inhi biting anaphase onset in response to altered microtubule function and impaired kinetochore function. In this study, we report that the abili ty of the anti-microtubule drug nocodazole to inhibit cell cycle progr ession in Saccharomyces cerevisiae depends on the function of the kine tochore protein encoded by NDC10. We examined the role of the spindle checkpoint in the arrest in cdc20 mutants that arrest prior to anaphas e with an aberrant spindle. The arrest in cdc20 defective cells is dep endent on the BUB2 checkpoint and independent of the BUB1, BUB3, and M AD spindle checkpoint genes. We show that the lesion recognized by Bub 2p is not excess microtubules, and the cdc20 arrest is independent of kinetochore function. We show that Cdc20p is not required for cyclin p roteolysis at two points in the cell cycle, suggesting that CDC20 is d istinct from genes encoding integral proteins of the anaphase promotin g complex.