Size homeostasis can be intrinsic to growing cell populations and explained without size sensing or signalling



M. Krantz and E. Klipp, Theoretical Biophysics, Humboldt-Universität zu Berlin, Invalidenstr. 42, 10115 Berlin, Germany

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The cell division cycle orchestrates cellular growth and division. The machinery underpinning the cell division cycle is well characterized, but the actual cue(s) driving the cell division cycle remains unknown. In rapidly growing and dividing yeast cells, this cue has been proposed to be cell size. Presumably, a mechanism communicating cell size acts as gatekeeper for the cell division cycle via the G1 network, which triggers G1 exit only when a critical size has been reached. Here, we evaluate this hypothesis with a minimal core model linking metabolism, growth and the cell division cycle. Using this model, we (a) present support for coordinated regulation of G1/S and G2/M transition in Saccharomyces cerevisiae in response to altered growth conditions, (b) illustrate the intrinsic antagonism between G1 progression and cell size and (c) provide evidence that the coupling of growth and division is sufficient to allow for size homeostasis without directly communicating or measuring cell size. We show that even with a rudimentary version of the G1 network consisting of a single unregulated cyclin, size homeostasis is maintained in populations during autocatalytic growth when the geometric constraint on nutrient supply is considered. Taken together, our results support the notion that cell size is a consequence rather than a regulator of growth and division.