Abstract
Bacteria are able to maintain a narrow distribution of cell sizes by regulating the timing of cell divisions. In rich nutrient conditions, cells divide much faster than their chromosomes replicate. This implies that cells maintain multiple rounds of chromosome replication per cell division by regulating the timing of chromosome replications. Here, we show that both cell size and chromosome replication may be simultaneously regulated by the long-standing initiator accumulation strategy. The strategy proposes that initiators are produced in proportion to the volume increase and is accumulated at each origin of replication, and chromosome replication is initiated when a critical amount per origin has accumulated. We show that this model maps to the incremental model of size control, which was previously shown to reproduce experimentally observed correlations between various events in the cell cycle and explains the exponential dependence of cell size on the growth rate of the cell. Furthermore, we show that this model also leads to the efficient regulation of the timing of initiation and the number of origins consistent with existing experimental results.
Highlights
Bacterial cells are extremely proficient in regulating and coordinating the different processes of the cell cycle
Multiple Origins Accumulation Robustly and Efficiently Regulates the Number of Origins of Replication An important measurable consequence of the tight coupling between replication initiation and cell division is the average number of origins of replication per cell
If the initiators are expressed as in the autorepressor model, this strategy corresponds to Equation (1), which in turn reduces to the incremental model of size control, which predicts distributions, correlations, and scalings consistent with existing measurements
Summary
Bacterial cells are extremely proficient in regulating and coordinating the different processes of the cell cycle. The Cooper-Helmstetter model proposes a molecular mechanism that couples two such processes, the replication of the chromosome and the division of the cell (Cooper and Helmstetter, 1968). Cell division occurs a constant duration after the initiation of chromosome replication. The model implies a tight coordination between replication initiation and cell division such that in cells able to double faster than their chromosomes can replicate, multiple rounds of replications proceed simultaneously (Yoshikawa et al, 1964; Cooper and Helmstetter, 1968). Since the conception of the above model, many experiments and models have attempted to capture the molecular mechanisms responsible for the initiation of multiple rounds of replication. No model has been completely satisfactory (Donachie and Blakely, 2003)
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