Novak B, Csikasz-Nagy A, Gyorffy B, Chen K, Tyson J J
Department of Agricultural Chemical Technology, Technical University of Budapest, Hungary.
Biophys Chem. 1998 May 5;72(1-2):185-200. doi: 10.1016/s0301-4622(98)00133-1.
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.
裂殖酵母细胞周期的所有事件都可由单一的细胞周期蛋白依赖性蛋白激酶Cdc13/Cdc2异二聚体的波动来协调。G1/S期转换由Cdc13/Cdc2及其化学计量抑制剂Rum1的相互作用控制。G2/M期转换由激酶-磷酸酶对Wee1和Cdc25调节,它们决定Cdc2的Tyr-15残基的磷酸化状态。中期/后期转换由Cdc13/Cdc2与后期促进复合物之间的相互作用控制,后期促进复合物标记Cdc13亚基进行蛋白水解。我们构建了一个涵盖所有三个关键检查点控制的裂殖酵母生长和分裂的数学模型。通过数值模拟,我们表明该模型与广泛选择的细胞周期突变体一致,并且我们预测了几种尚未构建的多重突变菌株的表型。