WAVE1 controls neuronal activity-induced mitochondrial distribution in dendritic spines.
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.
Sung
Jee Young
JY
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Engmann
Olivia
O
Teylan
Merilee A
MA
Nairn
Angus C
AC
Greengard
Paul
P
Kim
Yong
Y
D000818:Animals; D049229:Dendritic Spines / Q000502:physiology*; D006624:Hippocampus / Q000166:cytology*; D007091:Image Processing, Computer-Assisted; D008856:Microscopy, Fluorescence; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D010766:Phosphorylation; D034622:RNA Interference; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D051300:Wiskott-Aldrich Syndrome Protein Family / Q000378:metabolism*
D016194:Receptors, N-Methyl-D-Aspartate; C114864:WASF1 protein, human; D051300:Wiskott-Aldrich Syndrome Protein Family