Accessory and Central α-helices of Complexin Selectively Activate Ca 2+ Triggering of Synaptic Exocytosis

Complexins, binding to assembling soluble NSF-attachment protein receptor (SNARE) complexes, activate Ca triggered exocytosis and clamp spontaneous release in the presynaptic terminal. Functions of complexin are structural dependent and mechanistically distinct. To further understand the functional/structural dependence of complexin, here we show that the accessory and central α-helices of complexin are sufficient in activation of Ca triggered vesicle fusion but not in clamping spontaneous release. Targeting the two α-helices to synaptic vesicle suppresses spontaneous release, thus further emphasizing the importance of curvature membrane localization in clamping function.