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J. Biol. Chem., Vol. 279, Issue 30, 30923-30926, July 23, 2004

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Semaphorin 3A Stimulates Neurite Extension and Regulates Gene Expression in PC12 Cells^*

Jens C. Schwamborn, Roberto Fiore, Dominique Bagnard, Joachim Kappler¶, Christian Kaltschmidt||, and Andreas W. Püschel**

From the Institut für Allgemeine Zoologie und Genetik, Westfälische Wilhelms-Universität Münster, Schlossplatz 5, D-48149 Münster, Germany, the INSERM U575-Physiopathologie du Système Nerveux, Groupe de Physiologie Moléculaire de la Régénération Nerveuse (PMRN), Centre de Neurochimie, 5 Rue Blaise Pascal, 67084 Strasbourg, France, the ^¶Institut für Physiologische Chemie, Rheinische Friedrich-Wilhelms-Universität Bonn, Nussallee 11, D-53115 Bonn, Germany, and the ^||Institut für Neurobiochemie, Universität Witten/Herdecke, Stockumer Strasse 10, D-58448 Witten, Germany

The secreted semaphorin 3A (Sema3A) is a member of a large family of proteins that act as guidance signals for axons and dendrites. While the receptors and signaling pathways that mediate the repulsive effects of semaphorins are beginning to be understood in some detail, the mechanisms that are responsible for the ability of Sema3A to stimulate the extension of dendrites remain to be elucidated. Here we show that PC12 cells, a model widely used to study neuronal differentiation, can be used to dissect this pathway. Sema3A is as effective as nerve growth factor in stimulating the extension of neurites from PC12 cells. We show that Sema3A is able to regulate gene expression and identify mitochondria as a novel target of Sema3A signaling. Pharmacological block of mitochondrial reactive oxygen species production abolishes the extension of neurites in response to Sema3A. These results show that the characterization of transcripts that are regulated by axon guidance signals may help to identify novel components of their signaling pathways.

Received for publication, February 23, 2004 , and in revised form, May 17, 2004.

^* This work was supported by a grant from the Deutsche Forschungsgemeinschaft (SFB 492 (to A. W. P.)) and by a Boehringer Ingelheim Foundation fellowship (to J. C. S.). 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 Experimental Procedures, Fig. S1, Tables 1–5, and Refs. 1–3.

^** To whom correspondence should be addressed at: Inst. für Allgemeine Zoologie und Genetik, Westfälische Wilhelms-Universität, Schlossplatz 5, D-48149 Münster, Germany. Tel.: 49-251-83-23872; Fax: 49-0251-83-24723; E-mail: apuschel{at}uni-muenster.de.

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