ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Genetic analysis of synaptotagmin C2 domain specificity in regulating spontaneous and evoked neurotransmitter release.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 79 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
- Calcium-sensitive synaptotagmin 11-lipid interaction modulates exo-endocytosis.Nature communications · 2025Article
- Identifying potential biomarkers in the hippocampus of chronic fatigue syndrome rats treated with moxibustion at Zusanli (ST36): a proteomics study.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- A lever hypothesis for Synaptotagmin-1 action in neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Correlation between evoked neurotransmitter release and adaptive functions in SYT1-associated neurodevelopmental disorder.EBioMedicine · 2024Article
- Dynamic formation of the protein-lipid prefusion complex.Biophysical journal · 2024Article
- Dynamic Formation of the Protein-Lipid Pre-fusion Complex.bioRxiv : the preprint server for biology · 2024Article
- Lethal variant in the C2A domain may cause severe SYT1-associated neurodevelopmental disorder in the newborns.Neurogenetics · 2024Article
- Oxidative Stress and Dopaminergic Metabolism: A Major PD Pathogenic Mechanism and Basis of Potential Antioxidant Therapies.CNS & neurological disorders drug targets · 2024Review
- The Core Complex of the CaJournal of molecular biology · 2023Review
- Calcium Sensors of Neurotransmitter Release.Advances in neurobiology · 2023Article
- Synaptotagmin rings as high-sensitivity regulators of synaptic vesicle docking and fusion.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Polybasic Patches in Both C2 Domains of Synaptotagmin-1 Are Required for Evoked Neurotransmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Expression and distribution of synaptotagmin family members in the zebrafish retina.The Journal of comparative neurology · 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
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- New recessive mutations inNeurology. Genetics · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic vesicle fusion mediates communication between neurons and is triggered by rapid influx of Ca(2+). The Ca(2+)-triggering step for fusion is regulated by the synaptic vesicle transmembrane protein Synaptotagmin 1 (Syt1). Syt1 contains two cytoplasmic C2 domains, termed C2A and C2B, which coordinate Ca(2+) binding. Although C2A and C2B share similar topology, binding of Ca(2+) ions to the C2B domain has been suggested as the only critical trigger for evoked vesicle release. If and how C2A domain function is coordinated with C2B remain unclear. In this study, we generated a panel of Syt1 chimeric constructs in Drosophila to delineate the unique and shared functions of each C2 domain in regulation of synaptic vesicle fusion. Expression of Syt 1 transgenes containing only individual C2 domains, or dual C2A-C2A or C2B-C2B chimeras, failed to restore Syt1 function in a syt1(-/-) null mutant background, indicating both C2A and C2B are specifically required to support fast synchronous release. Mutations that disrupted Ca(2+) binding to both C2 domains failed to rescue evoked release, but supported synaptic vesicle docking and endocytosis, indicating that these functions of Syt1 are Ca(2+)-independent. The dual C2 domain Ca(2+)-binding mutant also enhanced spontaneous fusion while dramatically increasing evoked release when coexpressed with native Syt1. Together, these data indicate that synaptic transmission can be regulated by Syt1 multimerization and that both C2 domains of Syt1 are uniquely required for modulating Ca(2+)-independent spontaneous fusion and Ca(2+)-dependent synchronous release.
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