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Stable positioning of Unc13 restricts synaptic vesicle fusion to defined release sites to promote synchronous neurotransmission.

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons96560

Göttfert,  F.
Department of NanoBiophotonics, MPI for Biophysical Chemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons15210

Hell,  S. W.
Department of NanoBiophotonics, MPI for Biophysical Chemistry, Max Planck Society;

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Zitation

Reddy-Alla, S., Böhme, M. A., Reynolds, E., Beis, C., Grasskamp, A. T., Mampell, M. M., et al. (2017). Stable positioning of Unc13 restricts synaptic vesicle fusion to defined release sites to promote synchronous neurotransmission. Neuron, 95(6), 1350-1364. doi:10.1016/j.neuron.2017.08.016.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002D-E274-A
Zusammenfassung
Neural information processing depends on precisely timed, Ca2+-activated synaptic vesicle exocytosis from release sites within active zones (AZs), but molecular details are unknown. Here, we identify that the (M)Unc13-family member Unc13A generates release sites and show the physiological relevance of their restrictive AZ targeting. Super-resolution and intravital imaging of Drosophila neuromuscular junctions revealed that (unlike the other release factors Unc18 and Syntaxin-1A) Unc13A was stably and precisely positioned at AZs. Local Unc13A levels predicted single AZ activity. Different Unc13A portions selectively affected release site number, position, and functionality. An N-terminal fragment stably localized to AZs, displaced endogenous Unc13A, and reduced the number of release sites, while a C-terminal fragment generated excessive sites at atypical locations, resulting in reduced and delayed evoked transmission that displayed excessive facilitation. Thus, release site generation by the Unc13A C terminus and their specific AZ localization via the N terminus ensure efficient transmission and prevent ectopic, temporally imprecise release.