WAVE1 controls neuronal activity-induced mitochondrial distribution in dendritic spines.

Authors: Sung, Jee Young  Engmann, Olivia  Teylan, Merilee A  Nairn, Angus C  Greengard, Paul  Kim, Yong 
Citation: Sung JY, etal., Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3112-6. doi: 10.1073/pnas.0712180105. Epub 2008 Feb 14.
Pubmed: (View Article at PubMed) PMID:18287015
DOI: Full-text: DOI:10.1073/pnas.0712180105

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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CRRD Object Information
CRRD ID: 13702174
Created: 2018-07-18
Species: All species
Last Modified: 2018-07-18
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.