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We investigate how an encapsulated active particle deforms a lipid vesicle using a lipid-resolved coarse-grained model, revealing that membrane deformation and rupture are non-monotonically dependent on particle activity, peaking at intermediate levels. The study quantifies these effects via asphericity and excess bending energy, demonstrating that membrane surface tension critically regulates the dynamics of activity-induced deformation. High activity leads to premature membrane rupture, limiting large-scale remodeling.
Encapsulated active particles drive vesicle deformation and rupture in a non-monotonic manner with activity, with rupture occurring before significant remodeling at high energy inputs.
Biological membranes are highly deformable structures that undergo shape transformations during numerous cellular processes. These transformations are often driven by active agents, including molecular motors, cytoskeletal machinery, and motile microorganisms, which consume energy and maintain biological systems far from equilibrium. Here, we investigate how a single active particle confined within a lipid vesicle drives membrane deformation. Using a lipid-resolved coarse-grained model, we examine how the activity and shape of an encapsulated self-propelled particle influence vesicle dynamics and morphology. Active particles generate persistent propulsion that exerts mechanical stresses on the enclosing membrane, thereby driving its deformation. Using particles of different shapes but identical surface area, we systematically investigate membrane morphologies as functions of activity and bending rigidity. We quantify membrane deformation through asphericity and excess bending energy relative to the equilibrium spherical state. Both measures exhibit a non-monotonic dependence on activity, peaking at intermediate activity. At sufficiently high activity, membrane rupture occurs before significant large-scale deformation can develop, limiting further remodeling. We further demonstrate that membrane surface tension plays a significant role in regulating activity-induced deformation dynamics.