bioRxiv · 10.1101/433631
Membrane-cytoskeleton mechanical feedback mediated by myosin-I controls phagocytic efficiency
Abstract
Phagocytosis of invading pathogens or cellular debris requires a dramatic change in cell shape driven by actin polymerization. For antibody-covered targets, phagocytosis is thought to proceed through the sequential engagement of Fc-receptors on the phagocyte with antibodies on the target surface, leading to the extension and closure of the phagocytic cup around the target. We have found that two actin-dependent molecular motors, class 1 myosins myosin 1e and myosin 1f, are specifically localized to Fc-receptor adhesions and required for efficient phagocytosis of antibody-opsonized targets. Using primary macrophages lacking both myosin 1e and myosin 1f, we found that without the actin-membrane linkage mediated by these myosins, the organization of individual adhesions is compromised, leading to excessive actin polymerization, slower adhesion turnover, and deficient phagocytic internalization. This work identifies a novel role for class 1 myosins in coordinated adhesion turnover during phagocytosis and supports a model for a membrane-tension based feedback mechanism for phagocytic cup closure.\n\nO_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY
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Barger, S. R., Reilly, N. S., Shutova, M. S., Li, Q., Maiuri, P., Mooseker, M. S., Flavell, R. A., Svitkina, T., Oakes, P. W., Krendel, M., Gauthier, N.. 2018-10-02. Membrane-cytoskeleton mechanical feedback mediated by myosin-I controls phagocytic efficiency. https://doi.org/10.1101/433631
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