The F-BAR protein Rapostlin regulates dendritic spine formation in hippocampal neurons.

摘要: Pombe Cdc15 homology proteins, characterized by Fer/CIP4 Bin-Amphiphysin-Rvs/extended (F-BAR/EFC) domains with membrane invaginating property, play critical roles in a variety of reorganization processes. Among them, Rapostlin/formin-binding protein 17 (FBP17) has attracted increasing attention as coordinator endocytosis. Here we found that Rapostlin was expressed the developing rat brain, including hippocampus, late developmental stages when accelerated dendritic spine formation and maturation occur. In primary cultured hippocampal neurons, knockdown shRNA or overexpression Rapostlin-QQ, an F-BAR domain mutant no ability to induce invagination, led significant decrease density. Expression shRNA-resistant wild-type effectively restored density whereas expression deletion mutants lacking kinase C-related region 1 (HR1) Src 3 (SH3) did not. addition, Rapostlin-QQ reduced uptake transferrin neurons. Knockdown Rnd2, which binds HR1 Rapostlin, also uptake. These results suggest Rnd2 cooperatively regulate Indeed, enhanced Rapostlin-induced tubular invagination. We conclude whose activity is regulated plays key role through regulation dynamics.