Bulletin of the American Physical Society
APS March Meeting 2015
Volume 60, Number 1
Monday–Friday, March 2–6, 2015; San Antonio, Texas
Session T46: Invited Session: From Bacteria to Eukaryotes: Shape Organization in Living Matter |
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Sponsoring Units: DBIO Chair: Shiladitya Banerjee, University of Chicago Room: 217A |
Thursday, March 5, 2015 11:15AM - 11:51AM |
T46.00001: Cell size control in microorganisms Invited Speaker: Ariel Amir Organisms in all kingdoms of life face a challenge of regulating the size of their cells, control of which is essential for their viability. How do cells decide when to divide? For decades, a popular hypothesis has been that cells can measure their absolute size, and that reaching a critical size triggers the division process. This would imply that a cell that was born smaller than average will not be smaller than average when it divides - in contrast to experiments showing that such correlations exist, and that size is partly inherited. I will present a biophysical model that sheds new light on this problem, showing that a cell does not need to know its absolute size to regulate size robustly, quantitatively explaining the experimentally measured correlations in both E. coli and budding yeast, and predicting that average cell size should depend exponentially on the growth rate. [Preview Abstract] |
Thursday, March 5, 2015 11:51AM - 12:27PM |
T46.00002: Determinants of Bacterial Cell Shape Invited Speaker: Aaron Dinner We determine intergenerational shape dynamics of single Caulobacter crescentus cells. We use imaging techniques that enable us to study >100 cells across >4000 total generations to achieve high statistical precision. Our data show that constriction initiates early in the cell cycle and that its dynamics is controlled by the time scale of exponential longitudinal growth. Furthermore, we find that the division plane location is inherited from the previous generation. Based on our observations, we develop a minimal mechanical model that quantitatively accounts for the cell shape dynamics and suggests that the asymmetric location of the division plane reflects the distinct mechanical properties of the stalked and swarmer poles. Generalization of the model can provide a common framework for understanding bacterial cell shape. [Preview Abstract] |
Thursday, March 5, 2015 12:27PM - 1:03PM |
T46.00003: How do bacteria couple growth to division? Invited Speaker: Manuel Campos Cell size control is an intrinsic feature of the cell cycle. In bacteria, cell growth and division are thought to be coupled through a cell size threshold. Here, we provide direct experimental evidence disproving the critical size paradigm. Instead, we show through single-cell microscopy and modeling that the evolutionarily distant bacteria Escherichia coli and Caulobacter crescentus achieve cell size homeostasis by growing on average the same amount between divisions, irrespective of cell length at birth. This simple mechanism provides a remarkably robust cell size control without the need of being precise, abating size deviations exponentially within a few generations. This size homeostasis mechanism is broadly applicable for symmetric and asymmetric divisions as well as for different growth rates. Furthermore, our data suggest that constant size extension is implemented at or close to division, implying that the initiation of DNA replication or the formation of the FtsZ cytokinetic ring are unlikely to dictate the timing of division. Altogether, our findings provide fundamentally distinct governing principles for cell size and cell cycle control in bacteria. [Preview Abstract] |
Thursday, March 5, 2015 1:03PM - 1:39PM |
T46.00004: ABSTRACT WITHDRAWN |
Thursday, March 5, 2015 1:39PM - 2:15PM |
T46.00005: The physics of cytokinesis in animal cells Invited Speaker: Herve Turlier Cytokinesis is the process of physical cleavage during cell division. It proceeds by the ingression of an actin-myosin-enriched furrow at the equator of the cell. We identify the contractile actomyosin cortex as the main source of mechanical dissipation and active tension controlling cell shape dynamics. We derive a viscous active non-linear membrane theory of the cortex that explicitly includes the turnover of actin and where myosin activity is controlled in time and space by the cell. A Lagrangian implementation of this model allows us to calculate the full deformation of an initially spherical cell, when it is subject to a band of overactivity at the cell equator that mimics the RhoA signaling pattern. Our simulations reproduce the formation and ingression the actomyosin ring, with cell shapes and dynamics mirroring thoroughly the ones observed experimentally. This model predicts cytokinesis completion above a well-defined threshold of equatorial contractility excess, and simple scaling arguments unveil the key mechanism for this first-order transition: cytoplasmic incompressibility results in a competition between the furrow line tension and the cell poles surface tension. Our theory explains how cytokinesis duration may be independent on cell size in embryos and predicts a critical role for actin turnover on the rate and success of furrow constriction. We extend our theoretical approach to explore cell shape dynamics in other essential cellular processes, such as cell polarization or cell-cell adhesion.\\[4pt] In collaboration with Basile Audoly, Universite Pierre et Marie Curie; Jacques Prost, Institut Curie; and Jean-Francois Joanny, Institut Curie, ESPCI. [Preview Abstract] |
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