Genetics, Vol 145, 85-96, Copyright © 1997

INVESTIGATIONS

The Swi5 Transcription Factor of Saccharomyces cerevisiae Has a Role in Exit From Mitosis Through Induction of the cdk-Inhibitor Sic1 in Telophase

J. H. Toyn, A. L. Johnson, J. D. Donovan, W. M. Toone and L. H. Johnston
Division of Yeast Genetics, National Institute for Medical Research, London NW7 1AA, United Kingdom

Deactivation of the B cyclin kinase (Cdc28/Clb) drives the telophase to G1 cell cycle transition. Here we investigate one of the control pathways that contributes to kinase deactivation, involving the cell cycle-regulated production of the cdk inhibitor Sic1. We show that the cell 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 functional consequence of Swi5-regulated SIC1 expression in vivo is that both sic1{Delta} and swi5{Delta} strains have identical mitotic exit-related phenotypes. First, both are synthetically lethal with dbf2{Delta}, resulting in cell cycle arrest in telophase. Second, both are hypersensitive to overexpression of the B cyclin CLB2. Thus, Swi5-dependent activation of the SIC1 gene contributes to the deactivation of the B cyclin kinase, and hence exit from mitosis.

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