Evolution of the Cadherin–Catenin Complex
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Adherens junction
Adherens junction
Conditional gene knockout
Intestinal epithelium
Beta-catenin
Intestinal mucosa
Barrier function
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Nectin
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Capillary endothelial cells express Vascular Endothelial (VE)‐ and Neural (N)‐cadherin, with overlapping functions. VE‐cadherin forms homotypic adhesion between endothelial cells whereas N‐cadherin forms heterotypic adhesion with the surrounding pericytes in capillary endothelia. Endothelial specific deletions of Cdh2 (N‐cadherin) or Cdh5 (VE‐cadherin) in mice demonstrated poorly formed leaky capillaries and in utero death at E9.5 due to defective angiogenesis. These findings raise the question of whether N‐ and VE‐cadherin function independently or whether N‐cadherin activated signaling regulates the assembly of VE‐cadherin and thereby the formation of adherens junctions. We investigated the role of N‐cadherin in the formation of VE‐cadherin junctions using mouse genetic models and identifying N‐cadherin signaling pathways in endothelial monolayers. We show that N‐cadherin functions by interacting with the RhoGEF Trio to activate the RhoGTPases Rac1 and RhoA in nascent adherens junctions, inducing the recruitment of VE‐cadherin. This N‐cadherin activated signaling pathway is essential for maximal VE‐cadherin assembly and the formation of the endothelial junctional barrier. Support or Funding Information Supported by NIH grant R01 HL103922 to Y.A.K.; AHA AWARD 16PRE27260230 to K.K. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .
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ABSTRACT Cultured human keratinocytes maintained in 30 μM Ca2+ do not form adherens junctions; however, when the extracellular Ca2+ concentration is raised to 1 mM, adherens junctions form very rapidly. The formation of a junction involves the coordinate organization of intracellular and extracellular components. Cadherins have been shown to mediate this coordinate organization. In this report we show that E-cadherin organizes the various junctional components by signalling through protein kinase C.
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The mechanism that coordinates different adhesion receptors is poorly understood. We investigated this mechanism by focusing on the nectin-2 and E-cadherin adherens junction receptors. Cadherin is not required for the basic process of nectin junction formation since nectin-2 forms junctions in cadherin-deficient A431D cells. Formation of nectin junctions in these cells, however, becomes regulated by cadherin as soon as E-cadherin is reconstituted. E-cadherin recruits nectin-2 into adherens junctions, where both proteins form distinct but tightly associated clusters. Live-cell imaging showed that the appearance of cadherin clusters often precedes that of nectin clusters at sites of junction assembly. Inactivation of cadherin clustering by different strategies concomitantly suppresses the formation of nectin clusters. Furthermore, cadherin significantly increases the stability of nectin clusters, thereby making them resistant to the BC-12 antibody, which targets the nectin-2 adhesion interface. By testing different cadherin-α-catenin chimeras, we showed that the recruitment of nectin into chimera junctions is mediated by the actin-binding domain of α-catenin. Our data suggests that cadherin regulates-assembly of nectin junctions through α-catenin-induced remodeling of the actin cytoskeleton around the cadherin clusters.
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Cell–cell interaction
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