Complexin arrests a pool of docked vesicles for fast Ca2+ -dependent release

• Verfasst von: Malsam, Jörg [VerfasserIn]
• Verfasst von: Parisotto, Daniel [VerfasserIn]
• Verfasst von: Malsam, Andrea [VerfasserIn]
• Verfasst von: Krause, Jean Michel [VerfasserIn]
• Verfasst von: Söllner, Thomas [VerfasserIn]
• Titel: Complexin arrests a pool of docked vesicles for fast Ca2+ -dependent release
• Verf.angabe: Jörg Malsam, Daniel Parisotto, Tanmay A. M. Bharat, Andrea Scheutzow, Jean Michel Krause, John A. G. Briggs and Thomas H. Söllner
• E-Jahr: 2012
• Jahr: 15. June 2012
• Umfang: 12 S.
• Fussnoten: Die Zahl 2 und das Zeichen + sind im Text hochgestellt ; Gesehen am 11.10.2018
• Titel Quelle: Enthalten in: European Molecular Biology OrganizationThe EMBO journal
• Ort Quelle: [London] : Nature Publishing Group UK, 1982
• Jahr Quelle: 2012
• Band/Heft Quelle: 31(2012), 15, Seite 3270-3281
• ISSN Quelle: 1460-2075
• DOI: doi:10.1038/emboj.2012.164
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: exocytosis
• Sach-SW: fusion
• Sach-SW: reconstitution
• Sach-SW: SNARE
• Sach-SW: synaptic vesicle
• K10plus-PPN: 1581764871

Abstract

Regulated exocytosis requires that the assembly of the basic membrane fusion machinery is temporarily arrested. Synchronized membrane fusion is then caused by a specific trigger—a local rise of the Ca2+ concentration. Using reconstituted giant unilamellar vesicles (GUVs), we have analysed the role of complexin and membrane‐anchored synaptotagmin 1 in arresting and synchronizing fusion by lipid‐mixing and cryo‐electron microscopy. We find that they mediate the formation and consumption of docked small unilamellar vesicles (SUVs) via the following sequence of events: Synaptotagmin 1 mediates v‐SNARE‐SUV docking to t‐SNARE‐GUVs in a Ca2+‐independent manner. Complexin blocks vesicle consumption, causing accumulation of docked vesicles. Together with synaptotagmin 1, complexin synchronizes and stimulates rapid fusion of accumulated docked vesicles in response to physiological Ca2+ concentrations. Thus, the reconstituted assay resolves both the stimulatory and inhibitory function of complexin and mimics key aspects of synaptic vesicle fusion.