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Curr Biol. 2015 Feb 2;25(3):385-391. doi: 10.1016/j.cub.2014.12.009. Epub 2014 Dec 24.

Cell-size control and homeostasis in bacteria.

Author information

1
Department of Physics, University of California San Diego, La Jolla, CA 92093.
2
Initiative for the Theoretical Sciences, The Graduate Center, City University of New York, 365 Fifth Ave., New York, NY 10016.
3
Department of Molecular & Cell Biology, University of California, Berkeley, CA 94720.
4
Department of Biology, Washington University, Saint Louis, MO 63130.
5
Department of Systems Biology, Harvard Medical School, Longwood, MA 02115.
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Contributed equally

Abstract

How cells control their size and maintain size homeostasis is a fundamental open question. Cell-size homeostasis has been discussed in the context of two major paradigms: "sizer," in which the cell actively monitors its size and triggers the cell cycle once it reaches a critical size, and "timer," in which the cell attempts to grow for a specific amount of time before division. These paradigms, in conjunction with the "growth law" [1] and the quantitative bacterial cell-cycle model [2], inspired numerous theoretical models [3-9] and experimental investigations, from growth [10, 11] to cell cycle and size control [12-15]. However, experimental evidence involved difficult-to-verify assumptions or population-averaged data, which allowed different interpretations [1-5, 16-20] or limited conclusions [4-9]. In particular, population-averaged data and correlations are inconclusive as the averaging process masks causal effects at the cellular level. In this work, we extended a microfluidic "mother machine" [21] and monitored hundreds of thousands of Gram-negative Escherichia coli and Gram-positive Bacillus subtilis cells under a wide range of steady-state growth conditions. Our combined experimental results and quantitative analysis demonstrate that cells add a constant volume each generation, irrespective of their newborn sizes, conclusively supporting the so-called constant Δ model. This model was introduced for E. coli [6, 7] and recently revisited [9], but experimental evidence was limited to correlations. This "adder" principle quantitatively explains experimental data at both the population and single-cell levels, including the origin and the hierarchy of variability in the size-control mechanisms and how cells maintain size homeostasis.

PMID:
25544609
PMCID:
PMC4323405
DOI:
10.1016/j.cub.2014.12.009
[Indexed for MEDLINE]
Free PMC Article

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