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Cell movement is required in many physiological and pathological processes such as the immune system response and cancer metastasis. Two of a broad spectrum of migratory mechanisms are amoeboid migration, characterized by repetitive cycles of fast shape changes, and pressure-driven migration, where intracellular fluid flows are important for locomotion. Here, I present (1) a simple model to mechanistically explain the emergence of periodic changes in length and spatiotemporal coordination observed in amoeboid motility and (2) a model for simulating a porous viscoelastic cytoplasm and how its material properties affect locomotion driven by fluid dynamics. The first model focuses on cell-surface interaction and in contrast to the biochemical mechanisms that have been implicated in the coordination of some cellular processes, we show that many features of amoeboid locomotion emerge from a simple mechanochemical model. In the second model, we present a novel, simple description of viscoelasticity on a moving structure, and an application of the modeling framework is provided: cell moving in a microfluidic channel.

Reception to follow the talk.