In this paper we showed, using numerical analysis, that a purely deterministic cell cycle model for the interplay of cell growth and the kinetics of MPF, UBE and nuclear SPF, can give rise to size distributions qualitatively similar to those found in experiments. Due to this interplay cells do not all pass START at the same minimal size (i.e. there is a size distribution at START), but they all do pass START with the same concentration of active G1-transcription factor.
Unfortunately the size distributions resulting from the current model are not as wide as observed. This indicates that the cells are not yet as variable in length as they should be. We could allow for additional stochastic processes making the distribution wider, e.g. randomizing the size separation at division, adding a probability for passing START at some state in G1, or adding a microhetrogeneity in growth rate. But considering the strict regulation of cell division, we would like to continue our search for variation based on the molecular control mechanisms. For example, activation of the SBF switch (2) may be a more complicated function (rather than a simple monotonous function) of mass. Such kinetics then leads to a broader range of time spend in G1, and therefore to a broader range in cell size. At this moment we are searching for experimental evidence supporting this idea. In one experiment (Kron et al. 1994) in which cells grow in filamentous pseudohyphal forms instead of single cells, cell cycle variations seem to be less. Unfortunately molecular mechanisms explaining this loss of variability were not indicated.