MOLECULAR NEUROSCIENCEDystrophin Dp71 in PC12 cell adhesionEnríquez-Aragón, Jose Arturo1; Cerna-Cortés, Joel1; de León, Mario Bermúdez1; García-Sierra, Francisco2; González, Everardo1; Mornet, Dominique3; Cisneros, Bulmaro1 CAAuthor Information 1Department of Genetics and Molecular Biology 2Department of Cell Biology, Centro de Investigación y de Estudios Avanzados del IPN, 07360 México, D. F., México 3Departement de Physiologie des Interactions (EA701), Institut de Biologie, Bvd Henry IV, 34060 Montpellier, France CACorresponding Author: [email protected] Received 7 October 2004; accepted 30 December 2004 NeuroReport: February 28th, 2005 - Volume 16 - Issue 3 - p 235-238 Buy SDC Abstract Previously, we reported that PC12 cells with decreased Dp71 expression (antisense-Dp71 cells) display deficient nerve-growth-factor-induced neurite outgrowth. In this study, we show that disturbed neurite outgrowth of antisense-Dp71 cells is accompanied by decreased adhesion activity on laminin, collagen and fibronectin. In wild-type cells, the immunostaining of Dp71 and β1-integrin overlaps in the basal area contacting the substrate, but staining of both proteins decrease in the antisense-Dp71 cells. Morphology of antisense-Dp71 cells at the electron microscopic level is characterized by the lack of filopodia, cellular projections involved in adhesion. Our findings suggest that Dp71 is required for the efficient PC12 cell attachment to β1-integrin-dependent substrata and that decreased adhesion activity of the antisense-Dp71 cells could determine their deficiency to extend neurites. © 2005 Lippincott Williams & Wilkins, Inc.