scholarly journals Building up actin at adherens junctions

2012 ◽  
Vol 196 (1) ◽  
pp. 3-3
Author(s):  
Ben Short
Keyword(s):  
Adherens Junctions ◽  
Biochemical Approach ◽  
Intercellular Adhesions

A biochemical approach reveals that α-actinin-4 and Arp2/3 team up to assemble actin at intercellular adhesions.

scholarly journals Branched actin networks push against each other at adherens junctions to maintain cell–cell adhesion

2018 ◽  
Vol 217 (5) ◽  
pp. 1827-1845 ◽  
Author(s):  
Nadia Efimova ◽  
Tatyana M. Svitkina
Keyword(s):  
Actin Cytoskeleton ◽  
Actin Polymerization ◽  
Mechanical Load ◽  
Adherens Junctions ◽  
Cell Junctions ◽  
Pull System ◽  
Actin Networks ◽  
Pulling Forces ◽  
Intercellular Adhesions ◽  
Cell Cell

Adherens junctions (AJs) are mechanosensitive cadherin-based intercellular adhesions that interact with the actin cytoskeleton and carry most of the mechanical load at cell–cell junctions. Both Arp2/3 complex–dependent actin polymerization generating pushing force and nonmuscle myosin II (NMII)-dependent contraction producing pulling force are necessary for AJ morphogenesis. Which actin system directly interacts with AJs is unknown. Using platinum replica electron microscopy of endothelial cells, we show that vascular endothelial (VE)-cadherin colocalizes with Arp2/3 complex–positive actin networks at different AJ types and is positioned at the interface between two oppositely oriented branched networks from adjacent cells. In contrast, actin–NMII bundles are located more distally from the VE-cadherin–rich zone. After Arp2/3 complex inhibition, linear AJs split, leaving gaps between cells with detergent-insoluble VE-cadherin transiently associated with the gap edges. After NMII inhibition, VE-cadherin is lost from gap edges. We propose that the actin cytoskeleton at AJs acts as a dynamic push–pull system, wherein pushing forces maintain extracellular VE-cadherin transinteraction and pulling forces stabilize intracellular adhesion complexes.

Recruitment of (β)-catenin to cadherin-mediated intercellular adhesions is involved in myogenic induction

2001 ◽  
Vol 114 (7) ◽  
pp. 1309-1319 ◽  
Author(s):  
P. Goichberg ◽  
M. Shtutman ◽  
A. Ben-Ze'ev ◽  
B. Geiger
Keyword(s):  
Gene Expression ◽  
Myogenic Differentiation ◽  
Adherens Junctions ◽  
Cell Junctions ◽  
Major Constituent ◽  
Sharp Decline ◽  
Transfected Cells ◽  
Intercellular Adhesions ◽  
Late Stages ◽  
Myogenic Induction

Cadherin-mediated cell adhesion is involved in muscle differentiation from early stages of myogenic induction to late stages of myoblast interaction and fusion. (β)-Catenin is a major constituent of cadherin-based adherens junctions and also serves as a signal transduction molecule that regulates gene expression during development. In this study, we explored the involvement of (β)-catenin in myogenic differentiation. We show here that shortly after a switch from growth to differentiation medium, (β)-catenin translocates to cell-cell junctions and its levels increase. We further show that elevation of (β)-catenin levels, induced either by inhibition of its breakdown, using LiCl, or by its overexpression, suppresses the formation of adherens junctions, resulting in a sharp decline in myogenin expression and an arrest of myogenic progression. Recruitment of (β)-catenin to adherens junctions after transfection with N-cadherin restores myogenin expression in the transfected cells. These results suggest that increased cadherin-mediated adhesion and translocation of (β)-catenin to adherens junctions are involved in activating the early steps of myogenic differentiation.

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