A simple molecular mechanism explains multiple patterns of cell-size regulation

• Type of Material: Article
• Authors: Morgan Delarue, University of California Berkeley; Daniel Weissman, Emory University; Oskar Hallatschek, University of California Berkeley
• Language: English
• Date: 2017-08-16
• Publisher: Public Library of Science
• Publication Version: Final Published Version
• Copyright Statement: © 2017 Delarue et al
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1371/journal.pone.0182633
• Title of Journal or Parent Work: PLoS ONE
• ISSN: 1932-6203
• Volume: 12
• Issue: 8
• Start Page: e0182633
• End Page: e0182633
• Grant/Funding Information: This study was supported by the National Institute of General Medical Sciences (grant no. R01GM115851) and the Simons Foundation to OH.
• Keywords: Chaperone proteins; Schizosaccharomyces pombe; G1 phase; Cell division; Cell cycle; Cell membranes; Cell division analysis; Cell cycle inhibitors
• Research Categories: Biology, Cell; Biology, Genetics; Biophysics, Medical

Abstract

Increasingly accurate and massive data have recently shed light on the fundamental question of how cells maintain a stable size trajectory as they progress through the cell cycle. Microbes seem to use strategies ranging from a pure sizer, where the end of a given phase is triggered when the cell reaches a critical size, to pure adder, where the cell adds a constant size during a phase. Yet the biological origins of the observed spectrum of behavior remain elusive. We analyze a molecular size-control mechanism, based on experimental data from the yeast S. cerevisiae, that gives rise to behaviors smoothly interpolating between adder and sizer. The size-control is obtained from the accumulation of an activator protein that titrates an inhibitor protein. Strikingly, the size-control is composed of two different regimes: for small initial cell size, the size-control is a sizer, whereas for larger initial cell size, it is an imperfect adder, in agreement with recent experiments. Our model thus indicates that the adder and critical size behaviors may just be different dynamical regimes of a single simple biophysical mechanism.