THE SWI5 TRANSCRIPTION FACTOR OF SACCHAROMYCES-CEREVISIAE HAS A ROLE IN EXIT FROM MITOSIS THROUGH INDUCTION OF THE CDK-INHIBITOR SIC1 IN TELOPHASE

Deactivation of the B cyclin kinase (Cdc28/Clb) drives the telophase t o G1 cell cycle transition. Here we investigate one of the control pat hways that contributes to kinase deactivation, involving the cell cycl e-regulated production of the cdk inhibitor Sic1. We show that the cel l cycle timing of SIC1 expression depends on the transcription factor Swi5, and that Swi5-dependent SIC1 expression begins during telophase. In contrast to Swi5, the related transcription factor Ace2, which can also induce SIC1 expression, is not active during telophase. The func tional consequence of Swi5-regulated SIC1 expression in vivo is that b oth sic1 Delta and swi5 Delta strains have identical mitotic exit-rela ted phenotypes. First, both are synthetically lethal with dbf2 Delta, resulting in cell cycle arrest in telophase. Second, both are hypersen sitive to overexpression of the B cyclin CLB2. Thus, Swi5-dependent ac tivation of the SIC1 gene contributes to the deactivation of the B cyc lin kinase, and hence exit from mitosis.