Abstract
The forces that arise from the actin cortex play a crucial role in determining the membrane deformation. These include protrusive forces due to actin polymerization, pulling forces due to transient attachment of actin filaments to the membrane, retrograde flow powered by contraction of actomyosin network, and adhesion to the extracellular matrix. Here we present a theoretical model for membrane deformation resulting from the feedback between the membrane shape and the forces acting on the membrane. We model the membrane as a series of beads connected by springs and determine the final steady-state shape of the membrane arising from the interplay between pushing/pulling forces of the actin network and the resisting membrane tension. We specifically investigate the effect of the gel dynamics on the spatio-temporal deformation of the membrane until a stable lamellipodium is formed. We show that the retrograde flow and the cross-linking velocity play an essential role in the final elongation of the membrane. Interestingly, in the simulations where motor-induced contractility is switched off, reduced retrograde flow results in an increase in the rate and amplitude of membrane protrusion. These simulations are consistent with experimental observations that report an enhancement in protrusion efficiency as myosin II molecular motors are inhibited.
Highlights
Cell motility is essential for many biological processes including development, immune response, wound healing, phagocytosis and tumor metastasis
Our aim is to investigate membrane dynamics as a function of various control parameters such as cross-linking velocity, retrograde flow driven by molecular motors and membrane tension
The model we present here is the combination of series of events that are happening at the leading edge of the lamellipodium, and are influenced by the presence of plasma membrane
Summary
Cell motility is essential for many biological processes including development, immune response, wound healing, phagocytosis and tumor metastasis. Many cells form a wide flat membrane protrusion, known as the lamellipodium, in the direction of movement. The main driving mechanism for lamellipodium formation is the force generated by treadmilling actin network underneath the membrane [1]. Actin treadmilling is a nonequilibrium process, requires the consumption of ATP [2] and is regulated by several proteins [3]. In this process, the barbed ends of actin filaments polymerize and push against the membrane, whereas their pointed ends are anchored in the gel bulk formed by strongly entangled and highly cross-linked actin filaments.
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