Three functions of cadherins in cell adhesion - PubMed (original) (raw)
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Three functions of cadherins in cell adhesion
Jean-Léon Maître et al. Curr Biol. 2013.
Abstract
Cadherins are transmembrane proteins that mediate cell-cell adhesion in animals. By regulating contact formation and stability, cadherins play a crucial role in tissue morphogenesis and homeostasis. Here, we review the three major functions of cadherins in cell-cell contact formation and stability. Two of those functions lead to a decrease in interfacial tension at the forming cell-cell contact, thereby promoting contact expansion--first, by providing adhesion tension that lowers interfacial tension at the cell-cell contact, and second, by signaling to the actomyosin cytoskeleton in order to reduce cortex tension and thus interfacial tension at the contact. The third function of cadherins in cell-cell contact formation is to stabilize the contact by resisting mechanical forces that pull on the contact.
Copyright © 2013 Elsevier Ltd. All rights reserved.
Figures
Figure 1
Adhesion tension. Upon cadherin _trans_-binding, opposing plasma membranes are brought closer together, thereby expanding the contact through zippering. Accumulation of cadherins and other proteins at the contact zone can also result in membrane crowding and expansion of the contact zone via lateral pressure. Finally, cadherin accumulation at the contact zone might result in an osmotic-driven movement of proteins outside of the contact zone, resulting in lateral pressure shrinking the contact. The combination of these effects results in the adhesion tension function of cadherins in cell–cell adhesion, which has a direct effect on the surface tension at the cell–cell contact and thereby regulates its size.
Figure 2
Adhesion signaling. Cadherin _trans_-binding triggers local signaling at the contact. This signaling is mediated by p120-catenin activating Rac1 and inhibiting RhoA, and by α-catenin interfering with the function of Arp2/3 in polymerizing actin. Cadherin-mediated signaling is thought to disrupt the contractile actomyosin cortex at the contact, thereby lowering cell–cell interfacial tension and expanding the contact.
Figure 3
Adhesion coupling. When mechanically challenged, the adhesion complex dissociates at its cytoplasmic side. It is not clear whether dissociation occurs between α-catenin and β-catenin or downstream of them. To prevent dissociation, the intracellular part of the adhesion complex can be strengthened either via chemical signaling from p120-catenin, which stabilizes β-catenin–α-catenin interaction or via mechanosensing of α-catenin, which unfolds and recruits vinculin, which again strengthens anchoring to the actin cytoskeleton.
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