期刊
CELL REPORTS
卷 25, 期 3, 页码 761-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.09.061
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资金
- International Human Frontier Science Program Organization grant [HFSP RGY0070/2014]
- Departments of Excellence 2018-2022'' grant - Italian Ministry of Education, University and Research (MIUR) [L. 2018-2022]
- Omidyar Postdoctoral Fellowship at the Santa Fe Institute
- Swiss National Science Foundation [31003A_169978]
- Swiss National Science Foundation (SNF) [31003A_169978] Funding Source: Swiss National Science Foundation (SNF)
Understanding the classic problem of how single E. coli cells coordinate cell division with genome replication would open the way to addressing cellcycle 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.
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