WAVE1 controls neuronal activity-induced mitochondrial distribution in dendritic spines.
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Where this comes from
- Record sourced from PubMed, PMID 18287015.
- Also identified by DOI 10.1073/pnas.0712180105 and PMC identifier 2268593.
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Abstract
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.
Medical subject headings
- Dendritic Spines
- Hippocampus
- Mitochondria
- Wiskott-Aldrich Syndrome Protein Family