Abstract
The process by which actin polymerization generates pulling forces in cellular processes such as endocytosis is less well understood than pushing-force generation. To clarify the basic mechanisms of pulling-force generation, we perform stochastic polymerization simulations for a square array of polymerizing semiflexible actin filaments, having different interactions with the membrane. The filaments near the array center have a strong attractive component. Filament bending and actin-network elasticity are treated explicitly. We find that the outer filaments push on the membrane and the inner filaments pull, with a net balance of forces. The total calculated pulling force is maximized when the central filaments have a very deep potential well, and the outer filaments have no well. The steady-state force is unaffected by the gel rigidity, but equilibration takes longer for softer gels. The force distributions are flat over the pulling and pushing regions. Actin polymerization is enhanced by softening the gel or reducing the filament binding to the membrane. Filament-membrane detachment can occur for softer gels, even if the total binding energy of the filaments to the membrane is 100 or more. It propagates via a stress-concentration mechanism similar to that of a brittle crack in a solid, and the breaking stress is determined by a criterion similar to that of the ‘Griffith’ theory of crack propagation.
Highlights
In many cellular processes that require large forces to generate membrane curvature, such as formation of protrusions, endocytosis, and phagocytosis, actin is an essential factor [1]
We evaluate the total magnitude of the pulling force, its spatial distribution, the dynamics of the force buildup, and the conditions that lead to detachment of the pulling actin filaments from the membrane
We evaluate the dependence of the time scale of force generation rate on the gel stiffness
Summary
In many cellular processes that require large forces to generate membrane curvature, such as formation of protrusions, endocytosis, and phagocytosis, actin is an essential factor [1]. We find that strengthening the filament-obstacle binding by choosing deeper potential wells for the central filaments decreases the growth rate of the actin network in this region This increases the total pulling force up to a maximum that becomes the sum of the stall forces of the surrounding pushing filaments when the central filaments do not polymerize at all. Diffusive motion of bases describes elastic deformation of the actin gel induced by the forces from the filaments In treating this effect, crosslinks between bases of adjacent filaments are modeled as springs that constrain the relative motion of filaments in the direction perpendicular to the obstacle. The obstacle moves stochastically in response to forces from the filaments, via biased Brownian motion
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