Amoeboid cell migration and shape dynamics driven by actin polymerization
Cell migration is fundamental to development, tissue organization, immune response, and disease progression. Amoeboid motility is distinguished by rapid motion and strongly fluctuating cell shapes, reflecting the intrinsically nonlinear nature of active living matter far from equilibrium. Here we introduce a minimal active-shell model of an amoeboid cell that couples actin polymerization, cortical flows, and membrane deformation through nonlocal mechanical interactions. The model gives rise to a rich spectrum of emergent behaviors. A symmetric non-motile state can spontaneously break symmetry and transition toward persistent directed migration driven solely by polymerization-induced retrograde flow, even in the absence of shape deformation. Increasing activity further triggers a cascade of dynamical states, including circular trajectories, oscillatory zigzag motion, and irregular chaotic-like migration with fluctuating protrusions and multi-lobed morphologies. Although these migratory modes are observed experimentally in distinct cellular contexts, our results show that they can emerge from the same underlying physical mechanism, providing a unified framework for amoeboid dynamics. Notably, contractile stresses induced by molecular motors are not required to generate spontaneous motility, polarity, or complex migration patterns. Our findings highlight how collective active processes at the cellular scale can self-organize into complex dynamical states, revealing generic principles of nonlinear behavior in living systems.