ArticleMolecular biology of the cell2022
α-Catenin-dependent vinculin recruitment to adherens junctions is antagonistic to focal adhesions.
Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Moderately Reduced Contractility Decreases Epithelial Cell-Cell Contact Rupture Under Large External Stretch.bioRxiv : the preprint server for biology · 2026Article
- Stiffening of soft silicone upon deep UV treatment as characterized using nanoindentation.PloS one · 2026Article
- Regulation of mechanical intercellular junctions and components of the mitochondrial electron transport chain and the TCA cycle in the hypertrophic heart by pyridostigmine or trandolapril.Frontiers in molecular biosciences · 2026Article
- A conformational change in α-catenin's actin-binding domain governs adherens junction maturation.Communications biology · 2025Article
- E-Cadherin: A conductor of cellular signaling.Current opinion in cell biology · 2025Review
- Mechano-gradients drive morphogen-noise correction to ensure robust patterning.Science advances · 2024Article
- Leader cells mechanically respond to aligned collagen architecture to direct collective migration.PloS one · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Vinculin is a protein found in both focal adhesions (FAs) and adherens junctions (AJs) which regulates actin connectivity to these structures. Many studies have demonstrated that mechanical perturbations of cells result in enhanced recruitment of vinculin to FAs and/or AJs. Likewise, many other studies have shown "cross-talk" between FAs and AJs. Vinculin itself has been suggested to be a probable regulator of this adhesion cross-talk. In this study we used MDCK as a model system of epithelia, developing cell lines in which vinculin recruitment was reduced or enhanced at AJs. Careful analysis of these cells revealed that perturbing vinculin recruitment to AJs resulted in a reduction of detectable FAs. Interestingly the cross-talk between these two structures was not due to a limited pool of vinculin, as increasing expression of vinculin did not rescue FA formation. Instead, we demonstrate that vinculin translocation between AJs and FAs is necessary for actin cytoskeleton rearrangements that occur during cell migration, which is necessary for large, well-formed FAs. Last, we show using a wound assay that collective cell migration is similarly hindered when vinculin recruitment is reduced or enhanced at AJs, highlighting that vinculin translocation between each compartment is necessary for efficient collective migration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.