Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 8, Pages 3112-3116Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0712180105
Keywords
cdk5; filopodia; depolarization; phosphorylation; NMDA receptor
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Funding
- NIA NIH HHS [P01 AG009464, AG09464] Funding Source: Medline
- NIDA NIH HHS [DA10044, P01 DA010044] Funding Source: Medline
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Mitochondrial fission and trafficking to dendritic protrusions have been implicated in dendritic spine development. Here, we show that Wiskott-Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1) controls depolarization-induced mitochondrial movement into dendritic spines and filopodia and regulates spine morphogenesis. Depolarization-induced degradation of the p35 regulatory subunit of cyclin-dependent kinase 5 (Cdk5), with the resultant decreased inhibitory phosphorylation on WAVE1, depend on NMDA receptor activation. Thus, WAVE1 dephosphorylation and activation are likely associated with mitochondrial redistribution and spine morphogenesis.
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