Abstract
Cytokinesis occurs through the coordinated action of several biochemically-mediated stresses acting on the cytoskeleton. Here, we develop a computational model of cellular mechanics, and using a large number of experimentally measured biophysical parameters, we simulate cell division under a number of different scenarios. We demonstrate that traction-mediated protrusive forces or contractile forces due to myosin II are sufficient to initiate furrow ingression. Furthermore, we show that passive forces due to the cell's cortical tension and surface curvature allow the furrow to complete ingression. We compare quantitatively the furrow thinning trajectories obtained from simulation with those observed experimentally in both wild-type and myosin II null Dictyostelium cells. Our simulations highlight the relative contributions of different biomechanical subsystems to cell shape progression during cell division.
Highlights
Cytokinesis, the separation of a mother cell into two daughter cells, is a highly stereotypical cell shape change
Though there is ample evidence in many systems that myosin II provides some of this force, it is well known that some cell types can divide in the absence of myosin II
To elucidate the mechanisms by which cells control furrow ingression, we developed a computational model of cellular dynamics during cytokinesis in the social amoeba, Dictyostelium discoideum
Summary
Cytokinesis, the separation of a mother cell into two daughter cells, is a highly stereotypical cell shape change. The core process can be altered to produce asymmetric cell division events in which the daughter cells differ dramatically in size and/or cell differentiation fate [3,4,5]. Myosin II works on the actin network to alter the cell’s mechanical properties in complex ways. By pulling on the filaments, myosin II can slide the polymers. Myosin II pulls on anchored actin filaments, leading to an effective tension due to the stalling of the myosin II motor in the isometric state [8,9]. Myosin II is not rate-limiting for furrow ingression, and previous analyses have indicated that the furrow ingresses some 30–50-fold more slowly than predicted from the myosin II unloaded actin filament sliding velocity [10]
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