The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase

DOI PDF 被引用文献6件
  • Uwe Schlomann
    Institut für Allgemeine Zoologie und Genetik, Westfalische Wilhelms-Universität Münster, Schlossplatz 5, D-48149 Münster, Germany
  • Jens C. Schwamborn
    Institut für Allgemeine Zoologie und Genetik, Westfalische Wilhelms-Universität Münster, Schlossplatz 5, D-48149 Münster, Germany
  • Myriam Müller
    Institut für Allgemeine Zoologie und Genetik, Westfalische Wilhelms-Universität Münster, Schlossplatz 5, D-48149 Münster, Germany
  • Reinhard Fässler
    Department of Molecular Medicine, Max-Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany
  • Andreas W. Püschel
    Institut für Allgemeine Zoologie und Genetik, Westfalische Wilhelms-Universität Münster, Schlossplatz 5, D-48149 Münster, Germany

書誌事項

公開日
2009-06-15
DOI
  • 10.1242/jcs.038232
公開者
The Company of Biologists

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<jats:p>The rate and direction of axon and dendrite growth depend on multiple guidance signals and growth factors. Semaphorin 3A (Sema3A) acts as a repellent for axons and attractant for dendrites. Here, we show that the requirement for integrin engagement distinguishes the response of axons and dendrites to Sema3A in hippocampal neurons. Sema3A promotes the extension of hippocampal dendrites by a pathway that requires focal adhesion kinase (FAK). The stimulation of dendrite growth and FAK phosphorylation by Sema3A depend on integrin engagement. Unlike their function as a target of Sema3A during the collapse of axonal growth cones, integrins facilitate the stimulation of dendrite extension. Conditional inactivation of the genes encoding β1 integrin or FAK blocks the growth-promoting effect of Sema3A but not the collapse of axonal growth cones. Our results demonstrate that different pathways mediate the stimulation of dendrite growth and the collapse of axonal growth cones by Sema3A.</jats:p>

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