QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Vol. 18, Issue 5, 1734-1743, May 2007

This Article Full Text Full Text (PDF) Supplemental Material All Versions of this Article: E06-08-0766v1 18/5/1734    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Charrasse, S. Articles by Gauthier-Rouvière, C. Search for Related Content PubMed PubMed Citation Articles by Charrasse, S. Articles by Gauthier-Rouvière, C.

M-Cadherin Activates Rac1 GTPase through the Rho-GEF Trio during Myoblast Fusion

Centre de Recherches de Biochimie Macromoléculaire, Centre National de la Recherche Scientifique, IFR 122, 34293 Montpellier, France

Submitted August 31, 2006; Revised February 14, 2007; Accepted February 16, 2007
Monitoring Editor: Anne Ridley

Cadherins are transmembrane glycoproteins that mediate Ca²⁺-dependent homophilic cell–cell adhesion and play crucial role during skeletal myogenesis. M-cadherin is required for myoblast fusion into myotubes, but its mechanisms of action remain unknown. The goal of this study was to cast some light on the nature of the M-cadherin–mediated signals involved in myoblast fusion into myotubes. We found that the Rac1 GTPase activity is increased at the time of myoblast fusion and it is required for this process. Moreover, we showed that M-cadherin–dependent adhesion activates Rac1 and demonstrated the formation of a multiproteic complex containing M-cadherin, the Rho-GEF Trio, and Rac1 at the onset of myoblast fusion. Interestingly, Trio knockdown efficiently blocked both the increase in Rac1-GTP levels, observed after M-cadherin–dependent contact formation, and myoblast fusion. We conclude that M-cadherin–dependent adhesion can activate Rac1 via the Rho-GEF Trio at the time of myoblast fusion.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Address correspondence to: Cécile Gauthier-Rouvière (cecile.gauthier{at}crbm.cnrs.fr)

This article has been cited by other articles:

				M. Laurin, N. Fradet, A. Blangy, A. Hall, K. Vuori, and J.-F. Cote The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo PNAS, October 7, 2008; 105(40): 15446 - 15451. [Abstract] [Full Text] [PDF]

				P. Patwari and R. T. Lee Mechanical Control of Tissue Morphogenesis Circ. Res., August 1, 2008; 103(3): 234 - 243. [Abstract] [Full Text] [PDF]

				K. V. Pajcini, J. H. Pomerantz, O. Alkan, R. Doyonnas, and H. M. Blau Myoblasts and macrophages share molecular components that contribute to cell-cell fusion J. Cell Biol., March 5, 2008; 180(5): 1005 - 1019. [Abstract] [Full Text] [PDF]

				J. Kim, Y. Shao, S. Y. Kim, S. Kim, H. K. Song, J. H. Jeon, H. W. Suh, J. W. Chung, S. R. Yoon, Y. S. Kim, et al. Hypoxia-induced IL-18 Increases Hypoxia-inducible Factor-1{alpha} Expression through a Rac1-dependent NF-{kappa}B Pathway Mol. Biol. Cell, February 1, 2008; 19(2): 433 - 444. [Abstract] [Full Text] [PDF]

				S. Backer, M. Hidalgo-Sanchez, N. Offner, E. Portales-Casamar, A. Debant, P. Fort, C. Gauthier-Rouviere, and E. Bloch-Gallego Trio Controls the Mature Organization of Neuronal Clusters in the Hindbrain J. Neurosci., September 26, 2007; 27(39): 10323 - 10332. [Abstract] [Full Text] [PDF]

				C. A. Moore, C. A. Parkin, Y. Bidet, and P. W. Ingham A role for the Myoblast city homologues Dock1 and Dock5 and the adaptor proteins Crk and Crk-like in zebrafish myoblast fusion Development, September 1, 2007; 134(17): 3145 - 3153. [Abstract] [Full Text] [PDF]