Phosphorylation of the Sic1 inhibitor of B-type cyclins in Saccharomyces cerevisiae is not essential but contributes to cell cycle robustness.

摘要: In budding yeast, B-type cyclin (Clb)-dependent kinase activity is essential for S phase and mitosis. newborn G1 cells, Clb accumulation blocked, in part because of the Sic1 stoichiometric inhibitor. Previous results strongly suggested that cyclin-dependent phosphorylation, its consequent degradation, phase. However, cells containing a precise endogenous gene replacement SIC1 with SIC1-0P (all nine phosphorylation sites mutated) were fully viable. Unphosphorylatable was abundant nuclear throughout cell cycle effectively inhibited vitro. had lengthened increased transcriptional activation variable delays budded cycle. lethal when combined deletion CLB2, CLB3, or CLB5, major cyclins. provides sharp link between activation, but failure proteolysis imposes delay extreme sensitivity to dosage, rather than block.