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The Journal of Neuroscience, January 10, 2007, 27(2):355-365; doi:10.1523/JNEUROSCI.3209-06.2006

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Cellular/Molecular
A WAVE-1 and WRP Signaling Complex Regulates Spine Density, Synaptic Plasticity, and Memory

Scott H. Soderling,^1,2 Eric S. Guire,² Stefanie Kaech,³ Jon White,^1,2 Fang Zhang,^1,2 Kevin Schutz,^1,2 Lorene K. Langeberg,^1,2 Gary Banker,³ Jacob Raber,⁴ and John D. Scott^1,2

¹Howard Hughes Medical Institute, ²Vollum Institute, ³Center for Research on Occupational and Environmental Toxicology, and ⁴Departments of Behavioral Neuroscience and Neurology and Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Portland, Oregon 97239

Correspondence should be addressed to either of the following: Scott H. Soderling, Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, Email: s.soderling{at}cellbio.duke.edu; or John D. Scott, Vollum Institute L-474, Oregon Health & Science University, Portland, OR 97239, Email: scott{at}ohsu.edu

The scaffolding protein WAVE-1 (Wiskott-Aldrich syndrome protein family member 1) directs signals from the GTPase Rac through the Arp2/3 complex to facilitate neuronal actin remodeling. The WAVE-associated GTPase activating protein called WRP is implicated in human mental retardation, and WAVE-1 knock-out mice have altered behavior. Neuronal time-lapse imaging, behavioral analyses, and electrophysiological recordings from genetically modified mice were used to show that WAVE-1 signaling complexes control aspects of neuronal morphogenesis and synaptic plasticity. Gene targeting experiments in mice demonstrate that WRP anchoring to WAVE-1 is a homeostatic mechanism that contributes to neuronal development and the fidelity of synaptic connectivity. This implies that signaling through WAVE-1 complexes is essential for neural plasticity and cognitive behavior.

Key words: WAVE-1; WRP; actin; Arp2/3; dendritic spine; synaptic plasticity

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Received July 26, 2006; revised Nov. 17, 2006; accepted Nov. 19, 2006.

Correspondence should be addressed to either of the following: Scott H. Soderling, Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, Email: s.soderling{at}cellbio.duke.edu; or John D. Scott, Vollum Institute L-474, Oregon Health & Science University, Portland, OR 97239, Email: scott{at}ohsu.edu

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