The eukaryotic cell cycle is driven by a biochemical oscillator

The hypothesis that a biochemical oscillator of the limit cycle type controls the onset of mitosis has been proposed for long (Sel kov, 1970 Gilbert, 1974,1978 Winfree, 1980,1984 for an earlier discussion of cell division in terms of a chemical oscillatory process, see Rashevsky, 1948) and was put forward, in particular detail, on the basis of experiments performed on the slime mould Physarum (Kauffman, 1974 Kauffman 

An alternative view holds that cell division is brought about by the accumulation of a mitogenic factor that, above some threshold, triggers mitosis the latter, discontinuous event brings this factor back to a low value and a new cycle starts as the accumulation of the mitogenic factor resumes. Models of such a discontinuous nature (Fantes et al, 1975) differ in several respects from the continuous biochemical oscillatory mechanism for a comparative discussion of the two classes of mechanism, see Tyson Sachsenmaier (1978) and Winfree (1980,1984). 

These results have opened the way to the construction of more realistic models for the mitotic oscillator. The purpose of this chapter is briefly to present these models and to classify them according to the type of regulation responsible for oscillatory behaviour. The way sustained oscillations are generated is examined in detail in a minimal model based on the cascade of phosphorylation-dephosphorylation cycles that controls the onset of mitosis in embryonic cells. Extensions of the cascade model taking into account additional, recently uncovered phosphorylation-dephosphorylation cycles are considered. Ways of arresting the cell division cycle in that model and the control of the mitotic oscillator by growth factors are also discussed. 

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