Abstract
In Saccharomyces cerevisiae , three G 1 cyclins (Clns) are important for Start, the event committing cells to division. Sic1, an inhibitor of Clb-Cdc28 kinases, became phosphorylated at Start, and this phosphorylation depended on the activity of Clns. Sic1 was subsequently lost, which depended on the activity of Clns and the ubiquitin-conjugating enzyme Cdc34. Inactivation of Sic1 was the only nonredundant essential function of Clns, because a sic1 deletion rescued the inviability of the cln1 cln2 cln3 triple mutant. In sic1 mutants, DNA replication became uncoupled from budding. Thus, Sic1 may be a substrate of Cln-Cdc28 complexes, and phosphorylation and proteolysis of Sic1 may regulate commitment to replication at Start.
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Dates
Type | When |
---|---|
Created | 18 years, 9 months ago (Oct. 27, 2006, 2:30 p.m.) |
Deposited | 1 year, 7 months ago (Jan. 12, 2024, 4:57 p.m.) |
Indexed | 1 year ago (Aug. 7, 2024, 8:35 a.m.) |
Issued | 29 years, 3 months ago (April 26, 1996) |
Published | 29 years, 3 months ago (April 26, 1996) |
Published Print | 29 years, 3 months ago (April 26, 1996) |
@article{Schneider_1996, title={Linkage of Replication to Start by the Cdk Inhibitor Sic1}, volume={272}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.272.5261.560}, DOI={10.1126/science.272.5261.560}, number={5261}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Schneider, B. L. and Yang, Q.-H. and Futcher, A. B.}, year={1996}, month=apr, pages={560–562} }