Relevant parameters in models of cell division control

Abstract

A recent burst of dynamic single-cell growth-division data makes it possible to characterize the stochastic dynamics of cell division control in bacteria. Different modeling frameworks were used to infer specific mechanisms from such data, but the links between frameworks are poorly explored, with relevant consequences for how well any particular mechanism can be supported by the data. Here, we describe a simple and generic framework in which two common formalisms can be used interchangeably: (i) a continuous-time division process described by a hazard function and (ii) a discrete-time equation describing cell size across generations (where the unit of time is a cell cycle). In our framework, this second process is a discrete-time Langevin equation with a simple physical analogue. By perturbative expansion around the mean initial size (or inter-division time), we show explicitly how this framework describes a wide range of division control mechanisms, including combinations of time and size control, as well as the constant added size mechanism recently found to capture several aspects of the cell division behavior of different bacteria. As we show by analytical estimates and numerical simulation, the available data are characterized with great precision by the first-order approximation of this expansion. Hence, a single dimensionless parameter defines the strength and the action of the division control. However, this parameter may emerge from several mechanisms, which are distinguished only by higher-order terms in our perturbative expansion. An analytical estimate of the sample size needed to distinguish between second-order effects shows that this is larger than what is available in the current datasets. These results provide a unified framework for future studies and clarify the relevant parameters at play in the control of cell division.

15 pages, 5 figures

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• Master equation approach to the stochastic accumulation dynamics of bacterial cell cycle
• Modeling cell size regulation: From single-cell level statistics to molecular mechanisms and population level effects