Vinculin potentiates E-cadherin mechanosensing and is recruited to actin-anchored sites within adherens junctions in a myosin II–dependent manner

Duc, Quint le; Shi, Quanming; Blonk, Iris; Sonnenberg, Arnoud; Wang, Ning; Leckband, Deborah; Rooij, Johan de

doi:10.1083/jcb.20100114920101020c

Cited by 160 publications

(283 citation statements)

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“…This nonuniform distribution of force may explain the enhanced localization of E-cadherin observed as plaques at the contact edges of epithelial cell pairs as cadherin localization is known to be force dependent (8,9). This also suggests that cadherins at the contact edges sustain greater forces and may be specialized zones of enhanced localized signaling in response to enhanced mechanical cues.…”

Section: Discussionmentioning

confidence: 78%

“…The forces exerted at these bonafide cell-cell contacts are not only substantial but also comparable in magnitude to traction forces measured at focal adhesions. Considering recent evidence that suggests that cadherin-based adhesions are sites of mechanosensation (8,9), this implies that biochemical cues arising from mechanotransduction at cell-cell and cell-ECM contacts will both play significant roles in regulating cell physiology.…”

Section: Discussionmentioning

confidence: 99%

“…Here, morphological changes are driven by the forces generated and sustained at both cell-cell and cell-ECM adhesions. Although it is known that cadherin-mediated adhesions to neighboring cells share similar characteristics of forcedependent growth and signaling observed at focal adhesions (3,8,9) and have the potential to sustain large tensile loads (9,10), little is known about the magnitude of tension sustained at endogenous cell-cell contacts.…”

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confidence: 99%

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Cell-ECM traction force modulates endogenous tension at cell–cell contacts

Maruthamuthu

Sabass²,

Schwarz³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

477

451

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Cells in tissues are mechanically coupled both to the ECM and neighboring cells, but the coordination and interdependency of forces sustained at cell-ECM and cell-cell adhesions are unknown. In this paper, we demonstrate that the endogenous force sustained at the cell-cell contact between a pair of epithelial cells is approximately 100 nN, directed perpendicular to the cell-cell interface and concentrated at the contact edges. This force is stably maintained over time despite significant fluctuations in cell-cell contact length and cell morphology. A direct relationship between the total cellular traction force on the ECM and the endogenous cell-cell force exists, indicating that the cell-cell tension is a constant fraction of the cell-ECM traction. Thus, modulation of ECM properties that impact cell-ECM traction alters cell-cell tension. Finally, we show in a minimal model of a tissue that all cells experience similar forces from the surrounding microenvironment, despite differences in the extent of cell-ECM and cell-cell adhesion. This interdependence of cell-cell and cell-ECM forces has significant implications for the maintenance of the mechanical integrity of tissues, mechanotransduction, and tumor mechanobiology.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Cell-ECM traction force modulates endogenous tension at cell–cell contacts

Maruthamuthu

Sabass²,

Schwarz³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

477

451

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show abstract

“…3). NM-IIdependent recruitment of vinculin to AJs revealed a mechanosensing role for E-cadherin (le Duc et al 2010). Yonemura and colleagues showed an NM-II-dependent mechanism for stabilization of AJs that involves a forcedependent interaction between vinculin and a-catenin (Miyake et al 2006;Yonemura et al 2010).…”

Section: Ajs As Mechanosensorsmentioning

confidence: 99%

Phosphoinositides in Cell Architecture

Shewan

Eastburn²,

Mostov

2011

Cold Spring Harbor Perspectives in Biology

173

159

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Inositol phospholipids have been implicated in almost all aspects of cellular physiology including spatiotemporal regulation of cellular signaling, acquisition of cellular polarity, specification of membrane identity, cytoskeletal dynamics, and regulation of cellular adhesion, motility, and cytokinesis. In this review, we examine the critical role phosphoinositides play in these processes to execute the establishment and maintenance of cellular architecture. Epithelial tissues perform essential barrier and transport functions in almost all major organs. Key to their development and function is the establishment of epithelial cell polarity. We place a special emphasis on highlighting recent studies demonstrating phosphoinositide regulation of epithelial cell polarity and how individual cells use phosphoinositides to further organize into epithelial tissues.P hosphoinositides (PIs) are essential components of cellular membranes in eukaryotes. Though these specialized lipids comprise less than 1% of the cellular lipid cohort, they play key roles in many fundamental biological processes (Di Paolo and De Camilli 2006;Saarikangas et al. 2010). PIs possess such far ranging roles by serving as specialized membrane docking sites for effectors of numerous cellular signal transduction cascades. PIs also serve as precursors of lipid second messengers. They are concentrated on the cytosolic face of cellular membranes (Fig. 1A) and rapidly diffuse within the plane of the membrane. Reversible phosphorylation of the myo-inositol head group of phosphatidylinositol (PtdIns) at positions 3, 4, and 5 (Fig. 1B) gives rise to the seven PI isoforms identified in eukaryotic cells. PtdIns(4)P and PtdIns(4,5)P 2 are constitutively present in membranes and comprise the largest pool of cellular PIs, whereas PtdIns(3,4,5)P 3 is essentially undetectable in most types of unstimulated cells (Lemmon and Ferguson 2000;Saarikangas et al. 2010).The spatiotemporally regulated production and turnover of phosphoinositides is crucial for localized PI signaling and function. Numerous phosphatidylinositol kinases and phosphatases are involved in regulating the metabolism of the various PI isoforms (Fig. 1)

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“…[30][31][32] Vinculin, a mechanical linker protein known to participate in the transduction of mechanical signals through cell-ECM interactions, co-localizes with E-cadherin in response to a shear force. 33 This co-localization depends upon the activity of myosin II. hESCs cultured on polyacrylamide coated with an E-cadherin substrate exert higher traction stresses than hESCs treated with blebbistatin, an inhibitor of NMMIIA, suggesting that mechanical signals are indeed transduced through E-cadherin and NMMIIA in hESCs.…”

Section: Mechanical Properties Of Hpscsmentioning

confidence: 99%

Mechanobiology of Human Pluripotent Stem Cells

Earls

Jin

2013

Tissue Engineering Part B: Reviews

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Human pluripotent stem cells (hPSCs) are self-renewing and have the potential to differentiate into any cell type in the body, making them attractive cell sources for applications in tissue engineering and regenerative medicine. However, in order for hPSCs to find use in the clinic, the mechanisms underlying their self-renewal and lineage commitment must be better understood. Many technologies that have been developed for the maintenance and directed differentiation of hPSCs involve the use of soluble growth factors, but recent studies suggest that other elements of the hPSC microenvironment also influence the growth and differentiation of hPSCs. This includes the influences of cell-cell interactions, substrate mechanics, cellular interactions with extracellular matrix, as well as the nanotopography of the substrate and physical forces such as shear stress, cyclic mechanical strain, and compression. In this review, we highlight the recent progress of this area of research and discuss ways in which the mechanical cues may be incorporated into hPSC culture regimes to improve methods for expanding and differentiating hPSCs.

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Vinculin potentiates E-cadherin mechanosensing and is recruited to actin-anchored sites within adherens junctions in a myosin II–dependent manner

Cited by 160 publications

References 0 publications

Cell-ECM traction force modulates endogenous tension at cell–cell contacts

Cell-ECM traction force modulates endogenous tension at cell–cell contacts

Phosphoinositides in Cell Architecture

Mechanobiology of Human Pluripotent Stem Cells

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