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All events of the fission yeast cell cycle can be orchestrated by fluctuations of a single cyclin-dependent protein kinase, the Cdc13/Cdc2 heterodimer. The G1/S transition is controlled by interactions of Cdc13/Cdc2 and its stoichiometric inhibitor, Rum1. The G2/M transition is regulated by a kinase-phosphatase pair, Wee1 and Cdc25, which determine the phosphorylation state of the Tyr-15 residue of Cdc2. The meta/anaphase transition is controlled by interactions between Cdc13/Cdc2 and the anaphase promoting complex, which labels Cdc13 subunits for proteolysis. We construct a mathematical model of fission yeast growth and division that encompasses all three crucial checkpoint controls. By numerical simulations we show that the model is consistent with a broad selection of cell cycle mutants, and we predict the phenotypes of several multiple-mutant strains that have not yet been constructed.

Type

Journal article

Journal

Biophys Chem

Publication Date

1998

Volume

72

Pages

185 - 200

Keywords

Anaphase/physiology Cell Cycle/*physiology Cyclins/physiology Fungal Proteins/physiology G1 Phase/physiology G2 Phase/physiology Mathematical Computing Metaphase/physiology Mitosis/physiology *Models, Biological S Phase/physiology Schizosaccharomyces/*cytology *Schizosaccharomyces pombe Proteins