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Nat Commun. 2019 Mar 19;10(1):1249. doi: 10.1038/s41467-019-09104-1.

Membrane-cytoskeletal crosstalk mediated by myosin-I regulates adhesion turnover during phagocytosis.

Author information

1
Cell and Developmental Biology Department, State University of New York Upstate Medical University, Syracuse, 13210, NY, USA.
2
Department of Physics, University of Rochester, Rochester, 14627, NY, USA.
3
Department of Biology, University of Pennsylvania, Philadelphia, 19104, PA, USA.
4
IFOM, FIRC Institute of Molecular Oncology, Milan, 20139, Italy.
5
Advanced Imaging Center, Howard Hughes Medical Institute Janelia Research Campus, Ashburn, 20147, VA, USA.
6
Molecular, Cellular and Developmental Biology, Yale University, New Haven, 06520, CT, USA.
7
Department of Immunobiology, Yale University School of Medicine, New Haven, 06519, CT, USA.
8
Howard Hughes Medical Institute, Yale University, New Haven, 06519, CT, USA.
9
Department of Biology, University of Rochester, Rochester, 14627, NY, USA.
10
Cell and Developmental Biology Department, State University of New York Upstate Medical University, Syracuse, 13210, NY, USA. krendelm@upstate.edu.
11
IFOM, FIRC Institute of Molecular Oncology, Milan, 20139, Italy. nils.gauthier@ifom.eu.

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 find 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 find 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 role for class 1 myosins in coordinated adhesion turnover during phagocytosis and supports a mechanism involving membrane-cytoskeletal crosstalk for phagocytic cup closure.

PMID:
30890704
PMCID:
PMC6425032
DOI:
10.1038/s41467-019-09104-1
[Indexed for MEDLINE]
Free PMC Article

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