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J. Biol. Chem., Vol. 282, Issue 36, 26266-26274, September 7, 2007

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Polysialylation Increases Lateral Diffusion of Neural Cell Adhesion Molecule in the Cell Membrane^*

Fabien Conchonaud^¶1, Stéphane Nicolas^||**, Marie-Claude Amoureux^||**, Céline Ménager^||**2, Didier Marguet^¶, Pierre-François Lenne, Geneviève Rougon^||**3, and Valéry Matarazzo^||**4

From the ^||Institut de Biologie du Développement de Marseille-Luminy and Centre d'Immunologie de Marseille Luminy, MOSAIC Group, Université de la Méditerranée, 13288 Marseille, ^**CNRS UMR-6216, 13288 Marseille, CNRS UMR-6102, 13288 Marseille, ^¶INSERM UMR-631, 13288 Marseille, Institut Fresnel, Université d'Aix Marseille III, 13397 Marseille, and CNRS UMR-6133, 13397 Marseille, France

Polysialic acid (PSA) is a polymer of N-acetylneuraminic acid residues added post-translationally to the membrane-bound neural cell adhesion molecule (NCAM). The large excluded volume created by PSA polymer is thought to facilitate cell migration by decreasing cell adhesion. Here we used live cell imaging (spot fluorescence recovery after photobleaching and fluorescence correlation spectroscopy) combined with biochemical approaches in an attempt to uncover a link between cell motility and the impact of polysialylation on NCAM dynamics. We show that PSA regulates specifically NCAM lateral diffusion and this is dependent on the integrity of the cytoskeleton. However, whereas the glial-derivative neurotrophic factor chemotactic effect is dependent on PSA, the molecular dynamics of PSA-NCAM is not directly affected by glial-derivative neurotrophic factor. These findings reveal a new intrinsic mechanism by which polysialylation regulates NCAM dynamics and thereby a biological function like cell migration.

Received for publication, September 6, 2006 , and in revised form, July 5, 2007.

^* This work was supported in part by CNRS (to G. R. and D. M.), INSERM (to D. M.), region Provence Alpes Cote d'Azur (to G. R. and D. M.), grants from the "Fondation pour la Recherche sur le Cerveau" and Association pour la Recherche sur la Sclérose en Plaque (to G. R.) and a Marie-Curie International Reintregration grant (to C. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2 and supplemental methods.

¹ Supported by a fellowship from the Research Ministry.

² Supported by a fellowship from "la Ligue contre le Cancer."

⁴ Supported by a fellowship from "la Fondation pour la Recherche Médicale."

³ To whom correspondence should be addressed: IBDML, Case 907, Parc Scientifique de Luminy, 13288 Marseille cedex 9, France. Tel.: 33-491-269-348; Fax: 33-491-269-748; E-mail: rougon{at}ibdm.univ-mrs.fr.

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