Motility is an essential component for cellular life with implications for wound repair and immune response. Although it is well established that actin-based polymerization forces are the primary driver of cell motility, recapitulating this process in engineered systems has proven elusive, mainly due to the difficulty in incorporating the integrin-like mechanism typical of mammalian cells in these synthetic systems. Recently, using a method to optically control actin polymerization within giant unilamellar vesicles, we showed that actin network reorganization triggered outward membrane protrusions, as well as directional motility, in the absence of external actin anchorage. However, an open question that remains is the mechanism by which actin filaments push on and deform the membrane in the absence of external actin anchorage. To address this, we employ agent-based simulations to study how actin filaments and actin-binding proteins work together to deform synthetic vesicles. We develop a simulation framework that integrates cytosim with our recently developed model for simulating membrane deformations. We systematically vary the compositions of actin-binding proteins, filament growth rate, and inter-filament interactions and examine how the interplay between actin network architecture, network growth rate, and membrane mechanical properties impacts vesicle deformation. We find that a faster network growth rate leads to increased membrane deformation. We also observe that, for the same filament growth rate, increasing the inter-filament interactions induced larger deformations in the membrane. This work improves our understanding of actin-driven motility and provides insights into governing biophysical principles of actin-membrane deformations.
Akenuwa et al. (Sun,) studied this question.