Phosphorylation of WAVE1 regulates actin polymerization and dendritic spine morphology

Yong Kim, Jee Young Sung, Ilaria Ceglia, Ko-Woon Lee, Jung-Hyuck Ahn, Jonathan M. Halford, Amie M. Kim, Seung P. Kwak, Jong Bae Park, Sung Ho Ryu, Annette Schenck, Barbara Bardoni, John D. Scott, Angus C. Nairn and Paul Greengard ()
Additional contact information
Yong Kim: The Rockefeller University
Jee Young Sung: The Rockefeller University
Ilaria Ceglia: The Rockefeller University
Ko-Woon Lee: The Rockefeller University
Jung-Hyuck Ahn: The Rockefeller University
Jonathan M. Halford: The Rockefeller University
Amie M. Kim: The Rockefeller University
Seung P. Kwak: Wyeth Research
Jong Bae Park: Pohang University of Science and Technology
Sung Ho Ryu: Pohang University of Science and Technology
Annette Schenck: Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP
Barbara Bardoni: Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP
John D. Scott: Howard Hughes Medical Institute, Vollum Institute
Angus C. Nairn: The Rockefeller University
Paul Greengard: The Rockefeller University

Nature, 2006, vol. 442, issue 7104, 814-817

Abstract: Abstract WAVE1—the Wiskott–Aldrich syndrome protein (WASP)-family verprolin homologous protein 1—is a key regulator of actin-dependent morphological processes1 in mammals, through its ability to activate the actin-related protein (Arp2/3) complex. Here we show that WAVE1 is phosphorylated at multiple sites by cyclin-dependent kinase 5 (Cdk5) both in vitro and in intact mouse neurons. Phosphorylation of WAVE1 by Cdk5 inhibits its ability to regulate Arp2/3 complex-dependent actin polymerization. Loss of WAVE1 function in vivo or in cultured neurons results in a decrease in mature dendritic spines. Expression of a dephosphorylation-mimic mutant of WAVE1 reverses this loss of WAVE1 function in spine morphology, but expression of a phosphorylation-mimic mutant does not. Cyclic AMP (cAMP) signalling reduces phosphorylation of the Cdk5 sites in WAVE1, and increases spine density in a WAVE1-dependent manner. Our data suggest that phosphorylation/dephosphorylation of WAVE1 in neurons has an important role in the formation of the filamentous actin cytoskeleton, and thus in the regulation of dendritic spine morphology.

Date: 2006
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DOI: 10.1038/nature04976

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