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Accessory and Central ?-helices of Complexin Selectively Activate Ca2+ Triggering of Synaptic Exocytosis.


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

SUBMITTER: Yu Y 

PROVIDER: S-EPMC5834437 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Accessory and Central α-helices of Complexin Selectively Activate Ca<sup>2+</sup> Triggering of Synaptic Exocytosis.

Yu Yi Y   Chen Su S   Mo Xiaoqiang X   Gong Jihong J   Li Chenhong C   Yang Xiaofei X  

Frontiers in molecular neuroscience 20180226


Complexins, binding to assembling soluble NSF-attachment protein receptor (SNARE) complexes, activate Ca<sup>2+</sup> 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<sup>2+</sup> triggered vesicle fusion but not in  ...[more]

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