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© The Rockefeller University Press, 0021-9525/1997//1663 $5.00
The Journal of Cell Biology, Volume 137, Number 7, , 1997 1663-1681

Article

Cross Talk between Adhesion Molecules: Control of N-cadherin Activity by Intracellular Signals Elicited by β1 and β3 Integrins in Migrating Neural Crest Cells



Frédérique Monier-Gavelle and Jean-Loup Duband

Institut Jacques Monod, Centre National de la Recherche Scientifique (CNRS) et Université Paris 7-Denis Diderot, and Laboratoire de Biologie Moléculaire et Cellulaire du Développement, CNRS et Université Pierre et Marie Curie, 75252 Paris, France

During embryonic development, cell migration and cell differentiation are associated with dynamic modulations both in time and space of the repertoire and function of adhesion receptors, but the nature of the mechanisms responsible for their coordinated occurrence remains to be elucidated. Thus, migrating neural crest cells adhere to fibronectin in an integrin-dependent manner while maintaining reduced N-cadherin–mediated intercellular contacts. In the present study we provide evidence that, in these cells, the control of N-cadherin may rely directly on the activity of integrins involved in the process of cell motion. Prevention of neural crest cell migration using RGD peptides or antibodies to fibronectin and to β1 and β3 integrins caused rapid N-cadherin–mediated cell clustering. Restoration of stable intercellular contacts resulted essentially from the recruitment of an intracellular pool of N-cadherin molecules that accumulated into adherens junctions in tight association with the cytoskeleton and not from the redistribution of a preexisting pool of surface N-cadherin molecules. In addition, agents that cause elevation of intracellular Ca2+ after entry across the plasma membrane were potent inhibitors of cell aggregation and reduced the N-cadherin– mediated junctions in the cells. Finally, elevated serine/ threonine phosphorylation of catenins associated with N-cadherin accompanied the restoration of intercellular contacts. These results indicate that, in migrating neural crest cells, β1 and β3 integrins are at the origin of a cascade of signaling events that involve transmembrane Ca2+ fluxes, followed by activation of phosphatases and kinases, and that ultimately control the surface distribution and activity of N-cadherin. Such a direct coupling between adhesion receptors by means of intracellular signals may be significant for the coordinated interplay between cell–cell and cell–substratum adhesion that occurs during embryonic development, in wound healing, and during tumor invasion and metastasis.

We are extremely grateful to K. Yamada for useful discussions and advice, for providing antibodies, and for critical reading of the manuscript. We also thank B. Geiger for the anti–A-CAM antibodies, F. Sanchez-Madrid for the antibodies to the {alpha}4 integrin subunit, D. Cheresh for the antibodies to the {alpha}Vβ3 integrin, and M. Block for helpful discussions.

Please address all correspondence to Jean-Loup Duband, Equipe Adhésion et Migration Cellulaires, Laboratoire de Biologie Moléculaire et Cellulaire du Développement, CNRS URA 1135 et Université Pierre et Marie Curie, 9 quai Saint-Bernard, 75252 Paris Cedex 05, France. Fax: (33) 1-44-27-34-97. e-mail: duband{at}ccr.jussieu.fr


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