Abstract
Understanding the classic problem of how single E.coli cells coordinate cell division with genome replication would open the way to addressing cell-cycle progression at the single-cell level. Recent studies produced new data, but the contrast in their conclusions and proposed mechanisms makes the emerging picture fragmented and unclear. Here, we re-evaluate available data and models, including generalizations based on the same assumptions. We show that although they provide useful insights, none of the proposed models captures all correlation patterns observed in data. We conclude that the assumption that replication is the bottleneck process for cell division is too restrictive. Instead, we propose that two concurrent cycles responsible for division and initiation of DNA replication set the time of cell division. This framework allows us to select a nearly constant added size per origin between subsequent initiations as the most likely mechanism setting initiation of replication.
Highlights
Each cell needs two copies of the genome to divide
Determining how cell division is coordinated with genome replication in E. coli is still an open problem
Review of Current Models of the E. coli Cell Cycle We start by reviewing available models and the key differences in their predictions (Figure 1) that need to be reconciled
Summary
Each cell needs two copies of the genome to divide. The notion that this simple principle must be central for the cell cycle was already clear in early studies (Meselson and Stahl, 1958; Nurse et al, 1998). For the model organism E. coli, a wealth of information was gathered starting from the late 1950s (Cooper and Helmstetter, 1968; Donachie, 1968; Schaechter et al, 1958, 1962), leading to important insights about cell-cycle progression. The reason is that our knowledge is still based mostly on population averages, which mask the behavior of single cells (Osella et al, 2017). We do not know for sure whether replication initiation is triggered at a critical size in single cells (Ho and Amir, 2015; Osella et al, 2017; Wallden et al, 2016), whether there are licensing constraints inhibiting initiations (Bates and Kleckner, 2005; Osella et al, 2017), and whether the rate-limiting checkpoint for the decision to divide is typically independent from replication initiation (Harris and Theriot, 2016)
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