ArticleProceedings of the National Academy of Sciences of the United States of America2015
Transmembrane tethering of synaptotagmin to synaptic vesicles controls multiple modes of neurotransmitter release.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Regulation of spontaneous neurotransmission and homeostatic synaptic plasticity by synaptotagmin-1 disease variants at the SNARE primary interface.bioRxiv : the preprint server for biology · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Optogenetic neuromuscular actuation of a miniature electronic biohybrid robot.Science robotics · 2025Article
- Developmental and physiological impacts of pathogenic human huntingtin protein in the nervous system.Neurobiology of disease · 2024Article
- Role of calcium-sensor proteins in cell membrane repair.Bioscience reports · 2023Review
- Vesicle trafficking and vesicle fusion: mechanisms, biological functions, and their implications for potential disease therapy.Molecular biomedicine · 2022Review
- Synaptotagmin 1 oligomerization via the juxtamembrane linker regulates spontaneous and evoked neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Truncation of the otoferlin transmembrane domain alters the development of hair cells and reduces membrane docking.Molecular biology of the cell · 2021Article
- Function of Drosophila Synaptotagmins in membrane trafficking at synapses.Cellular and molecular life sciences : CMLS · 2021Review
- A novel dual Ca2+ sensor system regulates Ca2+-dependent neurotransmitter release.The Journal of cell biology · 2021Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Membrane Association and Functional Mechanism of Synaptotagmin-1 in Triggering Vesicle Fusion.Biophysical journal · 2020Article
- Article
- Synaptic aging disrupts synaptic morphology and function in cerebellar Purkinje cells.Neural regeneration research · 2018Article
- Molecular Mechanisms of Fast Neurotransmitter Release.Annual review of biophysics · 2018Review
- The First 100 nm Inside the Pre-synaptic Terminal Where Calcium Diffusion Triggers Vesicular Release.Frontiers in synaptic neuroscience · 2018Review
- Synaptotagmin isoforms confer distinct activation kinetics and dynamics to chromaffin cell granules.The Journal of general physiology · 2017Article
- Paternal spatial training enhances offspring's cognitive performance and synaptic plasticity in wild-type but not improve memory deficit in Alzheimer's mice.Scientific reports · 2017Article
- Regulation of Exocytotic Fusion Pores by SNARE Protein Transmembrane Domains.Frontiers in molecular neuroscience · 2017Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Synaptotagmin 1 (Syt1) is a synaptic vesicle integral membrane protein that regulates neurotransmitter release by activating fast synchronous fusion and suppressing slower asynchronous release. The cytoplasmic C2 domains of Syt1 interact with SNAREs and plasma membrane phospholipids in a Ca(2+)-dependent manner and can substitute for full-length Syt1 in in vitro membrane fusion assays. To determine whether synaptic vesicle tethering of Syt1 is required for normal fusion in vivo, we performed a structure-function study with tethering mutants at the Drosophila larval neuromuscular junction. Transgenic animals expressing only the cytoplasmic C2 domains or full-length Syt1 tethered to the plasma membrane failed to restore synchronous synaptic vesicle fusion, and also failed to clamp spontaneous vesicle release. In addition, transgenic animals with shorter, but not those with longer, linker regions separating the C2 domains from the transmembrane segment abolished Syt1's ability to activate synchronous vesicle fusion. Similar defects were observed when C2 domain alignment was altered to C2B-C2A from the normal C2A-C2B orientation, leaving the tether itself intact. Although cytoplasmic and plasma membrane-tethered Syt1 variants could not restore synchronous release in syt1 null mutants, they were very effective in promoting fusion through the slower asynchronous pathway. As such, the subcellular localization of Syt1 within synaptic terminals is important for the temporal dynamics that underlie synchronous and asynchronous neurotransmitter release.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.