ArticleScience advances2024
Myosin-I synergizes with Arp2/3 complex to enhance the pushing forces of branched actin networks.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mechanisms of actin-binding proteins in glycolysis-cytoskeleton coupling.Journal of translational medicine · 2026Review
- Role of eCIRP in Mediating Post-ischemia Microglial Phagocytosis via TREM-2 Receptor: Insights from Porcine and Mouse Cellular Models.Molecular neurobiology · 2026Article
- Coordinated regulation of Capping Protein by CARMIL and V-1/myotrophin.The Journal of biological chemistry · 2026Review
- Coordinated Arp2/3-mediated actin branching and myosin-dependent force generation in membrane-cytoskeleton remodeling.Frontiers in physiology · 2026Review
- Myosins 1e/f at the podosome base regulate podosome dynamics and promote macrophage migration.European journal of cell biology · 2025Article
- Force-insensitive myosin-I enhances endocytosis robustness through actin network-scale collective ratcheting.Molecular biology of the cell · 2025Article
- Reconstituted systems for studying the architecture and dynamics of actin networks.The Biochemical journal · 2025Review
- Article
- Coupling between the lever arm and active site via an N-terminal extension tunes force sensitivity in the myosin-1 family.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fumonisin B1 Exerts Immunosuppressive Effects Through Cytoskeleton Remodeling and Function Attenuation of Mature Dendritic Cells.International journal of molecular sciences · 2025Article
- High-resolution structures of Myosin-IC reveal a unique actin-binding orientation, ADP release pathway, and power stroke trajectory.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- High resolution structures of Myosin-IC reveal a unique actin-binding orientation, ADP release pathway, and power stroke trajectory.bioRxiv : the preprint server for biology · 2025Article
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8 authors.
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Abstract
Class I myosins (myosin-Is) colocalize with Arp2/3 complex-nucleated actin networks at sites of membrane protrusion and invagination, but the mechanisms by which myosin-I motor activity coordinates with branched actin assembly to generate force are unknown. We mimicked the interplay of these proteins using the "comet tail" bead motility assay, where branched actin networks are nucleated by the Arp2/3 complex on the surface of beads coated with myosin-I and nucleation-promoting factor. We observed that myosin-I increased bead movement efficiency by thinning actin networks without affecting growth rates. Myosin-I triggered symmetry breaking and comet tail formation in dense networks resistant to spontaneous fracturing. Even with arrested actin assembly, myosin-I alone could break the network. Computational modeling recapitulated these observations, suggesting myosin-I acts as a repulsive force shaping the network's architecture and boosting its force-generating capacity. We propose that myosin-I leverages its power stroke to amplify the forces generated by Arp2/3 complex-nucleated actin networks.
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