ArticleLife science alliance2025
Vinculin-Arp2/3 interaction inhibits branched actin assembly to control migration and proliferation.
Article in Life science alliance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Molecular insights into profilin 1-dependent regulation of cellular phosphatidylinositol (4,5)-bisphosphate.Journal of cell science · 2026Article
- Identification of PKN2 and MOB4 as Coordinators of Collective Cell Migration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Actomyosin-dependent assembly of the mechanosensitive machinery from adherens junctions triggers actin polymerization and organization.Science advances · 2026Article
- Molecular insights into Profilin1-dependent regulation of cellular phosphatidylinositol-(4,5)-bisphosphate.bioRxiv : the preprint server for biology · 2025Article
- Paths to stability - actin regulation of adherens junction mechanics.Journal of cell science · 2025Review
- Integrins from extracellular vesicles as players in tumor microenvironment and metastasis.Cancer metastasis reviews · 2025Review
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Authors and funding
10 authors.
Funding
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Abstract
Vinculin is a mechanotransducer that reinforces links between cell adhesions and linear arrays of actin filaments upon myosin-mediated contractility. Both adhesions to the substratum and neighboring cells, however, are initiated within membrane protrusions that originate from Arp2/3-nucleated branched actin networks. Vinculin has been reported to interact with the Arp2/3 complex, but the role of this interaction remains poorly understood. Here, we compared the phenotypes of vinculin knock-out (KO) cells with those of knock-in (KI-P878A) cells, where the point mutation P878A that impairs the Arp2/3 interaction is introduced in the two vinculin alleles of MCF10A mammary epithelial cells. The interaction of vinculin with Arp2/3 inhibits actin polymerization at membrane protrusions and decreases migration persistence of single cells. In cell monolayers, vinculin recruits Arp2/3 and the vinculin-Arp2/3 interaction participates in cell-cell junction plasticity. Through this interaction, vinculin controls the decision to enter a new cell cycle as a function of cell density.
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