Regulation of KIF1A-Driven Dense Core Vesicle Transport: Ca2+/CaM Controls DCV Binding and Liprin-α/TANC2 Recruits DCVs to Postsynaptic Sites

• DOI: 10.1016/j.celrep.2018.06.071
• Publication Date: 2018-07-17T14:45:48Z
• Authors: Riccardo Stucchi; Gabriela Plucińska; Jessica J.A. Hummel; Eitan E. Zahavi; Irune Guerra San ...; Oleg Klykov; Richard A. Scheltema; A.F. Maarten Alte...; Casper C. Hoogenraad
• Keywords: Vesicular Transport Proteins; Kinesin

Tight regulation of neuronal transport allows for cargo binding and release at specific cellular locations. The mechanisms by which motor proteins are loaded on vesicles how cargoes captured appropriate sites remain unclear. To better understand KIF1A-driven dense core vesicle (DCV) is regulated, we identified the KIF1A interactome focused three partners, calcium protein calmodulin (CaM) two synaptic scaffolding proteins: liprin-α TANC2. We showed that calcium, acting via CaM, enhances to DCVs increases motility. In contrast, TANC2 not part KIF1A-cargo complex but capture dendritic spines. Furthermore, found mutations—reported in patients with different neuropsychiatric disorders—abolish interaction KIF1A. propose a model Ca2+/CaM regulates recruit KIF1A-transported vesicles.