Frontiers in Molecular Neuroscience (Feb 2018)

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

  • Yi Yu,
  • Su Chen,
  • Xiaoqiang Mo,
  • Jihong Gong,
  • Chenhong Li,
  • Xiaofei Yang

DOI
https://doi.org/10.3389/fnmol.2018.00061
Journal volume & issue
Vol. 11

Abstract

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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 α-helices of complexin are sufficient in activation of Ca2+ 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.

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