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A role of GRK5 in neuronal morphogenesis: promoting actin bundling and targeting bundles to membrane structures
Author(s) -
Wang Feifei,
Chen Yuejun,
long Hui,
Wu Ziyan,
Ma lan
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.972.9
Subject(s) - microbiology and biotechnology , morphogenesis , cytoskeleton , actin , biology , actin cytoskeleton , dendritic spine , actin remodeling of neurons , kinase , scaffold protein , actin remodeling , chemistry , signal transduction , neuroscience , biochemistry , cell , hippocampal formation , gene
The extensive membrane remodeling and cytoskeleton dynamics are both required in neuronal morphogenesis, but how these two processes are coordinated spatio‐temporally during neuronal development is largely unknown. Overexpression and depletion studies in neuronal cells indicate that G protein coupled receptor (GPCR) kinase 5 (GRK5), is critical for neuritogenesis, dendrite branching, and maturation of dendritic spines, and the effects are largely independent of its kinase activity. Furthermore, GRK5 promotes F‐actin bundling at membranes of dynamic neuronal structures through interacting with both F‐actin and PI(4,5)P2. Disruption either of the F‐actin and PI(4,5)P2 binding properties of GRK5 results in decreased dendritic arborization and maturation of dendritic spines, indicating GRK5 is not acting as a kinase, but rather provides a key link between the plasma membrane and actin cytoskeleton. Our results reveal that GRK5 functions as a molecular scaffold to promote the formation of actin bundles and targeting them to membranes at dynamic neuronal structures and demonstrate its physiological significance in neuronal morphogenesis.