Jorquera Lab

This Week in The Journal

• ​Cellular/Molecular

Complexin Influences Ca2+ Dependence of Vesicle Release

Fusion of vesicles to the plasma membrane is driven by formation of SNARE complexes composed of proteins residing in vesicular and target membranes. Formation of this complex brings the membranes together and delivers energy sufficient to drive fusion. Fusion can occur spontaneously, but at synapses, complexin clamps vesicles when the SNARE complex is partially formed; then, when calcium enters the terminal, synaptotagmin drives synchronous fusion of multiple vesicles. Experiments by Jorquera et al. demonstrate how complexin and synaptotagmin cooperate to regulate spontaneous (spike-independent) and evoked vesicle release in Drosophila larvae. Knocking out complexin increased the frequency of spontaneous vesicle release at neuromuscular junctions, thus reducing the size of the readily releasable pool and the proportion of vesicles released synchronously during spikes. Surprisingly, complexin knockout also reduced the calcium dependence of release. Furthermore, knocking out synaptotagmin rescued spontaneous release rates in complexin-null larvae. Altogether, the results suggest that synaptotagmin can facilitate vesicle fusion independently of calcium, but complexin makes synaptotagmin–SNARE interactions calcium dependent.