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 Ca2+ 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 alpha-helices of complexin are sufficient in activation of Ca2+ triggered vesicle fusion but not in clamping spontaneous release. Targeting the two alpha-helices to synaptic vesicle suppresses spontaneous release, thus further emphasizing the importance of curvature membrane localization in clamping function.