(A) Working model of the endogenous presynaptic active zones; (B) RIM+ELKS knockout leads to loss of many active zone scaffolds and to impaired vesicle docking, priming, and release;(C) Reconstitution of synaptic function is mediated by β4-Zn fusion protein that docks primed vesicles close to Ca2+ channels in the absence of most active zone scaffolds.
Next：Munc13 supports fusogenicity of non-docked vesicles at synapses with disrupted active zones
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