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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 to G1 cell cycle transition. Here we investigate one of the control pathways than contributes to kinase deactivation, involving the cell cycle-regulated production of the cdk inhibition 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 dbj2 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.

Pubmed ID: 9017392


  • Toyn JH
  • Johnson AL
  • Donovan JD
  • Toone WM
  • Johnston LH



Publication Data

January 8, 1997

Associated Grants


Mesh Terms

  • CDC28 Protein Kinase, S cerevisiae
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor Proteins
  • DNA-Binding Proteins
  • Enzyme Inhibitors
  • Fungal Proteins
  • G1 Phase
  • GTP-Binding Proteins
  • Gene Expression Regulation, Fungal
  • Mitosis
  • Phenotype
  • Protein Kinases
  • Protein-Serine-Threonine Kinases
  • RNA, Messenger
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Telophase
  • Transcription Factors