Cell deformations generated by dynamic cortical actin waves drive in vivo swimming migration

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Amoeboid cell migration drives many important developmental and disease-related processes including immune responses and cancer metastasis. Swimming cell migration is a subtype of amoeboid migration observed in cells in suspension ex vivo. However, the mechanism underlying swimming migration in vivo under physiological conditions is unknown. Using Drosophila fat body cells (FBCs) as a model, we show that FBCs actively swim to patrol the pupa. Their stop-and-go random walk is powered through the generation of oscillatory actomyosin waves, rather than persistent actin flows used by cells swimming in vitro. These actomyosin waves exert peristaltic compressive forces as they move to the cell rear. This causes cell elongation towards the front to propel the cell forward. In addition, we demonstrate that, unlike in other types of amoeboid migration, all three RhoGTPases, RhoA, Cdc42 and Rac1, are required for FBC migration. They control actin wave formation by regulating actin polymerisation through the formin Dia. Furthermore, RhoA at the cell rear induces actomyosin contractions via Rho kinase and myosin II to generate cell deformations. Importantly, our work reveals that swimming migration is a novel in vivo migration mode for rapid and long-range cell dispersal, potentially also used by other cells such as immune cells and cancer cells when encountering an aqueous environment.

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