EphB receptors regulate dendritic spine morphogenesis through the recruitment/phosphorylation of  FAK and RhoA activation

doi:10.1074/jbc.M511756200

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Papers In Press, published online ahead of print November 18, 2005
J. Biol. Chem, 10.1074/jbc.M511756200
Submitted on October 31, 2005
Revised on November 17, 2005
Accepted on November 18, 2005

EphB receptors regulate dendritic spine morphogenesis through the recruitment/phosphorylation of FAK and RhoA activation

Michael L. Moeller, Yang Shi, Louis F. Reichardt, and Iryna M. Ethell

Biomedical Sciences, University of California Riverside, Riverside, CA 92521

Corresponding Author: iryna.ethell{at}ucr.edu

Dendritic filopodia are small protrusions on the surface of neuronal dendrites that transform into dendritic spines upon synaptic contact with axon terminals. The formation of dendritic spines is a critical aspect of synaptic development. Dendritic spine morphogenesis is characterized by filopodia shortening followed by the formation of mature mushroom-shaped spines. Here we show that activation of the EphB receptor tyrosine kinases in cultured hippocampal neurons by their ephrin-B ligands induces morphogenesis of dendritic filopodia into dendritic spines. This appears to occur through assembly of an EphB-associated protein complex that includes focal adhesion kinase (FAK), Src, Grb2, and paxillin and the subsequent activations of FAK, Src, paxillin and RhoA. Furthermore, Cre-mediated knockout of loxP-flanked fak or RhoA inhibition blocks EphB-mediated morphogenesis of dendritic filopodia. Finally, EphB-mediated RhoA activation is disrupted by FAK knockdown. These data suggest that EphB receptors are upstream regulators of FAK in dendritic filopodia, and that FAK-mediated RhoA activation contributes to assembly of actin filaments in dendritic spines.

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