APache Is an AP2-Interacting Protein Involved in Synaptic Vesicle Trafficking and Neuronal Development

A Piccini, E Castroflorio, Pierluigi Valente, FC Guarnieri, D Aprile, C Michetti, M Bramini, G Giansante, B Pinto, A Savardi, F Cesca, A Bachi, A Cattaneo, JD Wren, A Fassio, F Valtorta, Fabio Benfenati, S Giovedì

Research output: Contribution to journalArticlepeer-review


Synaptic transmission is critically dependent on synaptic vesicle (SV) recycling. Although the precise mechanisms of SV retrieval are still debated, it is widely accepted that a fundamental role is played by clathrin-mediated endocytosis, a form of endocytosis that capitalizes on the clathrin/adaptor protein complex 2 (AP2) coat and several accessory factors. Here, we show that the previously uncharacterized protein KIAA1107, predicted by bioinformatics analysis to be involved in the SV cycle, is an AP2-interacting clathrin-endocytosis protein (APache). We found that APache is highly enriched in the CNS and is associated with clathrin-coated vesicles via interaction with AP2. APache-silenced neurons exhibit a severe impairment of maturation at early developmental stages, reduced SV density, enlarged endosome-like structures, and defects in synaptic transmission, consistent with an impaired clathrin/AP2-mediated SV recycling. Our data implicate APache as an actor in the complex regulation of SV trafficking, neuronal development, and synaptic plasticity. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
Original languageEnglish
Pages (from-to)3596-3611
Number of pages16
JournalCell Reports
Issue number12
Publication statusPublished - 2017


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