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Linkage of replication to start by the Cdk inhibitor Sic1

B L Schneider1, Q H Yang, A B Futcher

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

Science (New York, N.Y.)
|April 26, 1996
PubMed

Insights

The study reveals that Sic1 inactivation is the key role of G1 cyclins (Clns) in yeast cell division. Phosphorylation and degradation of Sic1 by Clns regulate DNA replication commitment at the Start transition.

Area of Science:

  • Cell biology
  • Molecular biology
  • Yeast genetics

Background:

  • Three G1 cyclins (Clns) regulate the Start event in Saccharomyces cerevisiae, committing cells to division.
  • Sic1 is a known inhibitor of C1b-Cdc28 kinases, crucial for cell cycle progression.

Purpose of the Study:

  • To elucidate the essential function of G1 cyclins (Clns) in yeast cell division.
  • To investigate the role of Sic1 phosphorylation and degradation in the Start transition.

Main Methods:

  • Analysis of Saccharomyces cerevisiae mutants lacking specific cyclins and Sic1.
  • Investigating the phosphorylation and degradation of Sic1 in relation to Cln activity.

Main Results:

  • Sic1 phosphorylation at Start is dependent on Cln activity.
  • Sic1 degradation requires Clns and the ubiquitin-conjugating enzyme Cdc34.
  • Sic1 inactivation is the sole nonredundant essential function of Clns, as sic1 deletion rescues cln1 cln2 cln3 triple mutants.
  • sic1 mutants exhibit uncoupled DNA replication and budding.

Conclusions:

  • Sic1 is a likely substrate of Cln-Cdc28 complexes.
  • Phosphorylation and subsequent proteolysis of Sic1 by Clns are critical for regulating commitment to DNA replication at the Start transition.

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