ArticleBMC cell biology2011
Myosin II activity dependent and independent vinculin recruitment to the sites of E-cadherin-mediated cell-cell adhesion.
Article in BMC cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Coupling during collective cell migration is controlled by a vinculin mechanochemical switch.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Vinculin is essential for sustaining normal levels of endogenous forces at cell-cell contacts.Biophysical journal · 2023Article
- α-Catenin-dependent vinculin recruitment to adherens junctions is antagonistic to focal adhesions.Molecular biology of the cell · 2022Article
- Local contractions regulate E-cadherin rigidity sensing.Science advances · 2022Article
- An asymmetric junctional mechanoresponse coordinates mitotic rounding with epithelial integrity.The Journal of cell biology · 2021Article
- Article
- Mechanical Stabilization of the Glandular Acinus by Linker of Nucleoskeleton and Cytoskeleton Complex.Current biology : CB · 2019Article
- Nonmuscle myosin IIA is involved in recruitment of apical junction components through activation of α-catenin.Biology open · 2018Article
- The expression of VE-cadherin in breast cancer cells modulates cell dynamics as a function of tumor differentiation and promotes tumor-endothelial cell interactions.Histochemistry and cell biology · 2018Article
- Nanoscale architecture of cadherin-based cell adhesions.Nature cell biology · 2017Article
- Cell adhesion in epidermal development and barrier formation.Current topics in developmental biology · 2015Review
- Force dependent biotinylation of myosin IIA by α-catenin tagged with a promiscuous biotin ligase.PloS one · 2015Article
- In vivo collective cell migration requires an LPAR2-dependent increase in tissue fluidity.The Journal of cell biology · 2014Article
- Vinculin phosphorylation differentially regulates mechanotransduction at cell-cell and cell-matrix adhesions.The Journal of cell biology · 2014Article
- A helping hand: How vinculin contributes to cell-matrix and cell-cell force transfer.Cell adhesion & migration · 2014Article
- Self-contact elimination by membrane fusion.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Cadherin mechanotransduction in tissue remodeling.Cellular and molecular life sciences : CMLS · 2013Review
- Regulation of Stem Cell Fate in a Three-Dimensional Micropatterned Dual-Crosslinked Hydrogel System.Advanced functional materials · 2013Article
- α-Catenin and vinculin cooperate to promote high E-cadherin-based adhesion strength.The Journal of biological chemistry · 2013Article
- E-cadherin is under constitutive actomyosin-generated tension that is increased at cell-cell contacts upon externally applied stretch.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMaintaining proper adhesion between neighboring cells depends on the ability of cells to mechanically respond to tension at cell-cell junctions through the actin cytoskeleton. Thus, identifying the molecules involved in responding to cell tension would provide insight into the maintenance, regulation, and breakdown of cell-cell junctions during various biological processes. Vinculin, an actin-binding protein that associates with the cadherin complex, is recruited to cell-cell contacts under increased tension in a myosin II-dependent manner. However, the precise role of vinculin at force-bearing cell-cell junctions and how myosin II activity alters the recruitment of vinculin at quiescent cell-cell contacts have not been demonstrated.
resultsWe generated vinculin knockdown cells using shRNA specific to vinculin and MDCK epithelial cells. These vinculin-deficient MDCK cells form smaller cell clusters in a suspension than wild-type cells. In wound healing assays, GFP-vinculin accumulated at cell-cell junctions along the wound edge while vinculin-deficient cells displayed a slower wound closure rate compared to vinculin-expressing cells. In the presence of blebbistatin (myosin II inhibitor), vinculin localization at quiescent cell-cell contacts was unaffected while in the presence of jasplakinolide (F-actin stabilizer), vinculin recruitment increased in mature MDCK cell monolayers.
conclusionThese results demonstrate that vinculin plays an active role at adherens junctions under increased tension at cell-cell contacts where vinculin recruitment occurs in a myosin II activity-dependent manner, whereas vinculin recruitment to the quiescent cell-cell junctions depends on F-actin stabilization.
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