αE-catenin regulates actin dynamics independently of cadherin-mediated cell–cell adhesion

Benjamin, Jacqueline M.; Kwiatkowski, Adam V.; Yang, Chao; Korobova, Farida; Pokutta, Sabine; Svitkina, Tatyana; Weis, William I.; Nelson, W. James

doi:10.1083/jcb.200910041

Cited by 142 publications

(179 citation statements)

References 50 publications

(90 reference statements)

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“…S2). To assess further the importance of cell-cell adhesion for coordinated collective migration, we analyzed the migration of MDCK cells in which α-catenin has been stably knocked down and hence cannot form stable intercellular contacts (36). These cells migrated in a highly uncoordinated and random fashion leading to significantly lower migration velocity (approximately 13 μm∕h across fibronectin strips of all widths) of the overall cell front compared to normal MDCK cells (Movie S6).…”

Section: Contrast Images (Movie S2mentioning

confidence: 99%

“…Because cellcell interactions appeared to play a key role in the observed modes of migration, we examined the role of intercellular adhesion proteins. Cell-cell junction proteins such as E-cadherins and their linkage to actin cytoskeleton through various cytoplasmic adaptor molecules (e.g., α-catenin) are crucial to maintain the cohesiveness and physical integrity of epithelial cell sheets (36).…”

Section: Contrast Images (Movie S2mentioning

confidence: 99%

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Emerging modes of collective cell migration induced by geometrical constraints

Vedula

Leong

Lai

et al. 2012

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

415

480

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The role of geometrical confinement on collective cell migration has been recognized but has not been elucidated yet. Here, we show that the geometrical properties of the environment regulate the formation of collective cell migration patterns through cell-cell interactions. Using microfabrication techniques to allow epithelial cell sheets to migrate into strips whose width was varied from one up to several cell diameters, we identified the modes of collective migration in response to geometrical constraints. We observed that a decrease in the width of the strips is accompanied by an overall increase in the speed of the migrating cell sheet. Moreover, largescale vortices over tens of cell lengths appeared in the wide strips whereas a contraction-elongation type of motion is observed in the narrow strips. Velocity fields and traction force signatures within the cellular population revealed migration modes with alternative pulling and/or pushing mechanisms that depend on extrinsic constraints. Force transmission through intercellular contacts plays a key role in this process because the disruption of cell-cell junctions abolishes directed collective migration and passive cell-cell adhesions tend to move the cells uniformly together independent of the geometry. Altogether, these findings not only demonstrate the existence of patterns of collective cell migration depending on external constraints but also provide a mechanical explanation for how large-scale interactions through cell-cell junctions can feed back to regulate the organization of migrating tissues.cell traction forces | collective dynamics | madin darby canine kidney epithelial cells | particle image velocimetry C ollective behavior is a fundamental phenomenon exhibited by a wide variety of systems such as flows in granular matter (1), collective movements of animals (2), self-organization of bacteria (3), and morphogenesis of biological tissues (4). Although collective behaviors have been observed across diverse physical and biological systems, it is increasingly clear that there are broad unifying and common parameters that govern the emergence of this phenomenon such as the density of the constituent particles, the boundary conditions within which the movements occur, and the nature of coupling between the individual particles. In this context, collective behavior in migrating cells is of particular interest as a highly out-of-equilibrium process where cells passively interact with each other and exert active forces in response to their mechanical environment (4). Such collective behavior drives many biological processes such as embryonic development (5), tissue morphogenesis (6), wound healing (7), and tumor metastasis (8, 9). Although single cell dynamics has been extensively studied (10-12), the movement of multicellular structures could not be simply explained by cell autonomous behaviors (13-16). Instead, intercellular interactions and large-scale propagation of mechanical signals (over several cell sizes) are necessary to understand the emergen...

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Section: Contrast Images (Movie S2mentioning

confidence: 99%

Section: Contrast Images (Movie S2mentioning

confidence: 99%

Emerging modes of collective cell migration induced by geometrical constraints

Vedula

Leong

Lai

et al. 2012

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

415

480

View full text Add to dashboard Cite

show abstract

“…21,22 E-cadherin, encoded by the CDH1 gene on chromosome 16q22, is a signature member of the cadherin family and constitutes a key component of adherens junctions. 23 Herein, we have showed that GRHL2 acted as an oncogene as it was upregulated in about 61% of CRCs and associated with tumor progression due to higher levels of cell proliferation. Knocking down GRHL2 inhibited G 1 /S cell cycle progression in CRC cells, decreased cell proliferation and impaired tumorigenesis in a nude mouse xenograft model.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of GRHL2 inhibits the proliferation of colorectal cancer cells by targeting ZEB1

Quan

Jin

Huang

et al. 2014

Cancer Biology & Therapy

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“…Cadherinassociated α-catenin may play a critical function in actin bundle formation at junctions through direct interactions with other actin-binding proteins or by binding actin filaments directly (Gates and Peifer, 2005). However, some reports claim that cytoplasmic α-catenin, rather than cadherinassociated α-catenin, plays critical roles in actin organization (Drees et al, 2005;Benjamin et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Defining the Roles of .ALPHA.-Catenin in Cell Adhesion and Cytoskeleton Organization: Isolation of F9 Cells Completely Lacking Cadherin-catenin Complex

Ozono

Komiya

Shimamura

et al. 2011

Cell Struct. Funct.

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ABSTRACT. To define the roles of α-catenin in cell-cell adhesion, the E-cadherin, α-catenin, β-catenin, and/or plakoglobin genes were inactivated in F9 teratocarcinoma cells. An E-cadherin-α-catenin fusion protein (Eα) restored full cell-adhesion function and organized the actin-based cytoskeleton and ZO-1, an actin filament binding protein, in F9 cells lacking all endogenous cadherin-catenin complex components. There were two types of cadherin-based cell-adhesion junctions in parental F9 cells, those with ZO-1 and those without ZO-1, and only junctions with ZO-1 were associated with thick actin bundles. Additionally, ZO-1 localized to most Eα-based celladhesion junctions. These data demonstrated that Eα supported cadherin-based cell adhesion and recruited actin bundles and ZO-1 to cell-cell contact sites in the absence of cytoplasmic α-catenin. Moreover, the C-terminal half of α-catenin was involved in the formation of cell-adhesion junctions with ZO-1.

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αE-catenin regulates actin dynamics independently of cadherin-mediated cell–cell adhesion

Abstract: αE-catenin has cell–cell contact–dependent and –independent functions in regulating actin and membrane dynamics.

Cited by 142 publications

References 50 publications

Emerging modes of collective cell migration induced by geometrical constraints

Emerging modes of collective cell migration induced by geometrical constraints

Downregulation of GRHL2 inhibits the proliferation of colorectal cancer cells by targeting ZEB1

Defining the Roles of .ALPHA.-Catenin in Cell Adhesion and Cytoskeleton Organization: Isolation of F9 Cells Completely Lacking Cadherin-catenin Complex

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