Actin assembly alone can drive inward and outward membrane deformations

The cell membrane is able to deform inward, as during the initiation of endocytosis, or outward, as during the formation of filopodia. Interestingly, both deformations are generated by the same branched, Arp2/3-based, polymerizing actin network. How an inward or an outward deformation can be obtained in the same network structure? What are the physical parameters that will trigger the direction of membrane deformation? To address these questions, we use a reconstituted membrane system of liposomes and purified actin. We investigate the conditions under which the actin cytoskeleton induces inward or outward membrane deformations. We reveal that actin dynamics are the essential player of membrane deformations by photo-damaging the actin structure that relaxes membrane shape. Lowering membrane tension is key to produce filopodia-like structures. Oppositely, endocytic-like structures are robust features that only weakly depend on membrane tension. A pulse-chase two color actin experiment and the labeling of the proteins associated to actin reveal the details of network growth during inward or outward membrane deformation. Our results, supported by theoretical models, explain how such deformations depend on a mechanical balance between the membrane and the actin network.