Novak, Pataki, Ciliberto, Tyson, 2001

Model Status

This CellML version of the model has been checked in COR and PCEnv and the model runs to replicate the results in the original published paper. The units have been checked and are consistent.

Model Structure

ABSTRACT: Much is known about the genes and proteins controlling the cell cycle of fission yeast. Can these molecular components be spun together into a consistent mechanism that accounts for the observed behavior of growth and division in fission yeast cells? To answer this question, we propose a mechanism for the control system, convert it into a set of 14 differential and algebraic equations, study these equations by numerical simulation and bifurcation theory, and compare our results to the physiology of wild-type and mutant cells. In wild-type cells, progress through the cell cycle (G1-->S-->G2-->M) is related to cyclic progression around a hysteresis loop, driven by cell growth and chromosome alignment on the metaphase plate. However, the control system operates much differently in double-mutant cells, wee1(-) cdc25Delta, which are defective in progress through the latter half of the cell cycle (G2 and M phases). These cells exhibit "quantized" cycles (interdivision times clustering around 90, 160, and 230 min). We show that these quantized cycles are associated with a supercritical Hopf bifurcation in the mechanism, when the wee1 and cdc25 genes are disabled. (c) 2001 American Institute of Physics.

The original paper reference is cited below:

Mathematical model of the cell division cycle of fission yeast, Bela Novak, and Zsuzsa Pataki, 2001, CHAOS, 11, 277-286. PubMed ID: 12779461

Diagram of the fission-yeast cell cycle. In the middle of the diagram is Cdc2/Cdc13 (MPF), which is regulated by proteolysis of the Cdc13 component, phosphorylation of the Cdc2 component, and stoichiometric inhibition of the complex.
Derived from workspace Novak, Pataki, Ciliberto, Tyson, 2001 at changeset 8dce5c2f9133.
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