Dissecting the Control Mechanisms for DNA Replication and Cell Division in E. coli.
| Autor: | Micali G; Department of Environmental Microbiology, Eawag, Dübendorf, Switzerland; Department of Environmental Systems Science, ETH Zürich, Zürich, Switzerland., Grilli J; Santa Fe Institute, 1399 Hyde Park Road, Santa Fe, NM 87501, USA; The Abdus Salam International Centre for Theoretical Physics (ICTP), Strada Costiera 11, 34014 Trieste, Italy., Marchi J; Laboratoire de Physique Théorique, Département de Physique, École Normale Supérieure, PSL, Sorbonne Universités, UPMC Université Paris 06, CNRS, 75005 Paris, France., Osella M; Physics Department, University of Turin, Via Giuria 16, Torino, Italy; I.N.F.N., Torino, Italy., Cosentino Lagomarsino M; Sorbonne Universités, UPMC Univ. Paris 06, Paris, France; CNRS, UMR 7238, Paris, France; IFOM, FIRC Institute of Molecular Oncology, Milan, Italy. Electronic address: marco.cosentino-lagomarsino@ifom.eu. |
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| Jazyk: | angličtina |
| Zdroj: | Cell reports [Cell Rep] 2018 Oct 16; Vol. 25 (3), pp. 761-771.e4. |
| DOI: | 10.1016/j.celrep.2018.09.061 |
| Abstrakt: | 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. (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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