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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Monier-gavelle, F. Duband, J. L. |
| Description | Author Affiliation: Monier-Gavelle F ( Institut Jacques Monod, Centre National de la Recherche Scientifique (CNRS) et Université Paris 7-Denis Diderot, CNRS et Université Pierre et Marie Curie, 75252 Paris, France.) |
| Abstract | 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 $Ca^{2+}$ 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 $Ca^{2+}$ 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. |
| ISSN | 00219525 |
| e-ISSN | 15408140 |
| Journal | The Journal of Cell Biology |
| Issue Number | 7 |
| Volume Number | 137 |
| Language | English |
| Publisher | Rockefeller University Press (United States) |
| Publisher Date | 1997-06-30 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Antigens, CD29 Physiology Antigens, CD Cadherins Cell Adhesion Molecules Cell Movement Neural Crest Embryology Platelet Membrane Glycoproteins Animals Cell Adhesion Coturnix Gene Expression Regulation, Developmental Integrin Beta3 Signal Transduction Research Support, Non-U.S. Gov't Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Medicine |
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