Published December 10, 2024 | Version v1
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Research data supporting "Synaptophysin accelerates synaptic vesicle fusion by expanding the membrane upon neurotransmitter loading"

  • 1. ROR icon Universitätsmedizin Göttingen
  • 2. ROR icon University of Virginia
  • 3. ROR icon Charité - Universitätsmedizin Berlin
  • 4. University of Virginia School of Medicine
  • 5. Max-Planck-Institute for Multidisciplinary Sciences
  • 6. ROR icon Leibniz-Forschungsinstitut für Molekulare Pharmakologie
  • 7. University of Virginia, Charlottesville
  • 8. ROR icon Max Planck Institute for Multidisciplinary Sciences

Description

Research data supporting Preobraschenski et al. "Synaptophysin accelerates synaptic vesicle fusion by expanding the membrane upon neurotransmitter loading"

Synaptic transmission is mediated by the exocytotic release of neurotransmitters stored in synaptic vesicles (SVs). SVs filled with neurotransmitters preferentially undergo exocytosis but it is unclear how this is achieved. Here we show that during transmitter loading SVs substantially increase in size, which is reversible and requires synaptophysin, an abundant membrane protein with unclear function. SVs are larger when synaptophysin is knocked out, and conversely, liposomes are smaller when reconstituted with synaptophysin. Moreover, transmitter loading of SVs accelerates fusion in vitro which is abolished when synaptophysin is lacking despite near normal transmitter uptake. We conclude that synaptophysin functions as a curvature-promoting entity in the SV membrane, allowing for major lateral expansion of the SV membrane during neurotransmitter filling, thus increasing their propensity for exocytosis.

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