Modeling the Budding Yeast Cell Cycle

Checkpoint proteins

Wild type cells arrest in mitosis in response to spindle damage (Taylor, 1999; Hoyt, 2000) when treated with nocodazole or benomyl. The genes involved in the surveillance mechanism are: MAD1-3 (Li & Murray, 1991) and BUB1-3 (Hoyt et al., 1991). ("MAD" stands for "Mitotic Arrest Deficient" and "BUB" for "Budding Uninhibited by Benomyl" respectively, which describe mutant phenotypes when the genes are not functional.) These genes are non-essential; deletions of MAD2 and BUB2 behave like wild-type (Fraschini et al., 1999; Alexandru et al., 1999, Fig. 4). In the model Mad2 controls Cdc20 activation (Alexandru et al., 1999), and Bub2 regulates Cdh1 activation (Tavormina & Burke, 1998; Alexandru et al., 1999).

Function and level: Mad2 and Bub2 are involved in spindle assembly checkpoint but respond to spindle damage via two different, interacting pathways (Alexandru et al., 1999; Li, 1999; Fraschini et al., 1999; Gardner & Burke, 2000).