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Organisms across all domains of life regulate the size of their cells.However, the means by which this is done is poorly understood. We study twoabstracted "molecular" models for size regulation: inhibitor dilution andinitiator accumulation. We apply the models to two settings: bacteria likeEscherichia coli, that grow fully before they set a division plane and divideinto two equally sized cells, and cells that form a bud early in the celldivision cycle, confine new growth to that bud, and divide at the connectionbetween that bud and the mother cell, like the budding yeast Saccharomycescerevisiae. In budding cells, delaying cell division until buds reach the samesize as their mother leads to very weak size control, with average cell sizeand standard deviation of cell size increasing over time and saturating up to100-fold higher than those values for cells that divide when the bud is stillsubstantially smaller than its mother. In budding yeast, both inhibitordilution or initiator accumulation models are consistent with the observationthat the daughters of diploid cells add a constant volume before they divide.This adder behavior has also been observed in bacteria. We find that inbacteria an inhibitor dilution model produces adder correlations that are notrobust to noise in the timing of DNA replication initiation or in the timingfrom initiation of DNA replication to cell division (the C + D period). Incontrast, in bacteria an initiator accumulation model yields robust addercorrelations in the regime where noise in the timing of DNA replicationinitiation is much greater than noise in the C + D period, as reportedpreviously [1]. In bacteria, division into two equally sized cells does notbroaden the size distribution.

Details Matter: noise and model structure set the relationship between cell size and cell cycle timing