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Vasodilator‐stimulated phosphoprotein (VASP) is recruited into dendritic spines via G‐actin‐dependent mechanism and contributes to spine enlargement and stabilization
Author(s) -
Iwasaki Kanako,
Obashi Kazuki,
Okabe Shigeo
Publication year - 2020
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.14634
Subject(s) - dendritic spine , phosphoprotein , microbiology and biotechnology , actin remodeling of neurons , actin , actin cytoskeleton , spine (molecular biology) , biology , cytoskeleton , actin remodeling , dendritic filopodia , phosphorylation , hippocampal formation , chemistry , neuroscience , cell , biochemistry
Actin organization and dynamics are modulated by diverse actin regulators during dendritic spine development. To understand the molecular network that regulates actin organization and spine morphology, it is important to investigate dynamic redistribution of actin regulators during spine development. One of the actin regulators, vasodilator‐stimulated phosphoprotein (VASP), has multiple functions in actin regulation and is known to regulate spine morphology. However, dynamics and temporal regulation of VASP during spine development have not been clarified. In this study, we performed time‐lapse imaging of mouse hippocampal dissociated neurons to analyse the change in localization of VASP during spine development. We found that accumulation of VASP within spines precedes the start of persistent F‐actin increase, which are temporally coupled with spine enlargement. Using domain deletion or mutation constructs of VASP, we revealed that the interaction with G‐actin is important for the preceding accumulation of VASP. Furthermore, we showed that accumulation of VASP contributes to actin enrichment within spines and stabilization of spine morphology by dominant negative experiments. These data suggest that G‐actin‐dependent VASP recruitment has dual functions in spine development, enlargement and stabilization, through the interaction with actin and other cytoskeletal regulators.