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VAMP2/Munc18-1 domain 3a interaction controls the nanoscale reorganization underpinning vesicular priming

Meunier, F. A.; Jiang, A.; Gormal, R. S.; Kasula, R.; Blum, A.; Salla-Martret, M.; Chai, Y. J.; Wallis, T. P.; Brouillet, J. Z.; Padmanabhan, P.; Weeratunga, S.; Livingstone, E.; Mollazade, M.; Joensuu, M.; Martinez-Marmol, R.; Collins, B.

2023-09-11 neuroscience
10.1101/2023.09.10.556776 bioRxiv
Show abstract

SNARE-mediated secretory vesicle (SV) exocytosis underpins neuronal communication. Munc18-1 orchestrates SNARE complex formation by controlling the opening of syntaxin-1A. How the SV-plasma membrane interface becomes fusion-competent at the nanoscale level is poorly understood. Here, we propose that the interaction of Munc18-1 with VAMP2 during vesicular docking triggers nanoscale re-organization which renders the SV-plasma membrane interface fusion-competent. We identified and mutated key residues in Munc18-1 domain 3a (A297 and T304) hypothesised to impair its interaction with VAMP2. Munc18-1A297H, and to a lesser extent Munc18-1T304H, constrained SVs on the plasma membrane and reduced stimulated secretion, under re-expression conditions in Munc18-1/2 double knockout neurosecretory cells. Moreover, the de-clustering of Munc18-1 in response to activity was lost for both mutants. The interaction of VAMP2 with the Munc18-1 domain 3a therefore controls the re-organization of the nanoscale environment of the docked SV-plasma membrane interface, fostering syntaxin-1A opening and Munc18-1 release to ensure that SNARE assembly only occurs within the confinement of docked vesicles.

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