ArticleProceedings of the National Academy of Sciences of the United States of America2010
Differential regulation of synchronous versus asynchronous neurotransmitter release by the C2 domains of synaptotagmin 1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Disease-causing mutations in Synaptotagmin can act via dominant-negative, gain-of-function or haploinsufficient mechanisms.bioRxiv : the preprint server for biology · 2026Article
- CRISPR-SWITCH (silent mutations with intention to create heterozygotes): a strategy for monoallelic genome editing and generation of aFrontiers in genome editing · 2026Article
- Synaptotagmin-1 serves as a primary ZnNature communications · 2025Article
- Molecular Dynamics Simulations of the SNARE Complex Interacting with Synaptotagmin, Complexin, and Lipid Bilayers.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Calcium Sensors of Neurotransmitter Release.Advances in neurobiology · 2023Article
- Alpha-Synuclein is Involved in DYT1 Dystonia Striatal Synaptic Dysfunction.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Expanding the genotype and phenotype spectrum of SYT1-associated neurodevelopmental disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2022Article
- 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
- Synaptotagmin 7 switches short-term synaptic plasticity from depression to facilitation by suppressing synaptic transmission.Scientific reports · 2021Article
- SNARE complex alters the interactions of the CaBiophysical journal · 2021Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Article
- The role of the C2A domain of synaptotagmin 1 in asynchronous neurotransmitter release.PloS one · 2020Article
- Synaptotagmin-1 enables frequency coding by suppressing asynchronous release in a temperature dependent manner.Scientific reports · 2019Article
- Structural basis for the clamping and CaNature communications · 2019Article
- Short-term synaptic depression can increase the rate of information transfer at a release site.PLoS computational biology · 2019Article
- SNT-1 Functions as the CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Article
- Drosophila studies support a role for a presynaptic synaptotagmin mutation in a human congenital myasthenic syndrome.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic vesicle fusion at many synapses has been kinetically separated into two distinct Ca(2+)-dependent temporal components consisting of a rapid synchronous phase followed by a slower asynchronous component. Mutations in the synaptic vesicle Ca(2+) sensor Synaptotagmin 1 (Syt 1) reduce synchronous neurotransmission while enhancing the slower asynchronous phase of release. Syt 1 regulation of vesicle fusion requires interactions mediated by its tandem cytoplasmic C2 domains (C2A and C2B). Although Ca(2+) binding by Syt 1 is predicted to drive synchronous release, it is unknown if Ca(2+) interactions with either C2 domain is required for suppression of asynchronous release. To determine if Ca(2+) binding by Syt 1 regulates these two phases of release independently, we performed electrophysiological analysis of transgenically expressed Syt 1 mutated at Ca(2+) binding sites in C2A or C2B in the background of Drosophila Syt 1-null mutants. Transgenic animals expressing mutations that disrupt Ca(2+) binding to C2A fully restored the synchronous phase of neurotransmitter release, whereas the asynchronous component was not suppressed. In contrast, rescue with Ca(2+)-binding mutants in C2B displayed little rescue of the synchronous release component, but reduced asynchronous release. These results suggest that the tandem C2 domains of Syt 1 play independent roles in neurotransmission, as Ca(2+) binding to C2A suppresses asynchronous release, whereas Ca(2+) binding to C2B mediates synchronous fusion.
Indexed as
Identifiers
What OpenQuestion holds
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.