ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
An Engineered Metal Sensor Tunes the Kinetics of Synaptic Transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Alternative splicing of synaptotagmin 7 regulates oligomerization and short-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Baker-Gordon Syndrome-Associated Synaptotagmin-1 Mutations Reduce Synaptic Strength in Mouse Primary and Human-Induced Neuronal Culture Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Identification of a Novel Signature Based on Ferritinophagy-Related Genes to Predict Prognosis in Lung Adenocarcinoma: Focus on AHNAK2.Bioengineering (Basel, Switzerland) · 2024Article
- The juxtamembrane linker of synaptotagmin 1 regulates CaNature communications · 2024Article
- The juxtamembrane linker of synaptotagmin 1 regulates CabioRxiv : the preprint server for biology · 2023Article
- Expanding Phenotype ofMolecular syndromology · 2023Article
- Synaptotagmin 9 Modulates Spontaneous Neurotransmitter Release in Striatal Neurons by Regulating Substance P Secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The Core Complex of the CaJournal of molecular biology · 2023Review
- Vesicular release probability sets the strength of individual Schaffer collateral synapses.Nature communications · 2022Article
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- Article
- Increased miR-34c mediates synaptic deficits by targeting synaptotagmin 1 through ROS-JNK-p53 pathway in Alzheimer's Disease.Aging cell · 2020Article
- Resolving kinetic intermediates during the regulated assembly and disassembly of fusion pores.Nature communications · 2020Article
- Synaptotagmin 17 controls neurite outgrowth and synaptic physiology via distinct cellular pathways.Nature communications · 2019Article
- Phosphatidylinositol 4,5-bisphosphate drives CaThe Journal of biological chemistry · 2019Article
- The high-affinity calcium sensor synaptotagmin-7 serves multiple roles in regulated exocytosis.The Journal of general physiology · 2018Review
- Molecular Mechanisms of Fast Neurotransmitter Release.Annual review of biophysics · 2018Review
- Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Ca(2+) sensor synaptotagmin-1 (syt-1) regulates neurotransmitter release by interacting with anionic phospholipids. Here we test the idea that the intrinsic kinetics of syt-membrane interactions determine, in part, the time course of synaptic transmission. To tune the kinetics of this interaction, we grafted structural elements from the slowest isoform, syt-7, onto the fastest isoform, syt-1, resulting in a chimera with intermediate kinetic properties. Moreover, the chimera coupled a physiologically irrelevant metal, Sr(2+), to membrane fusion in vitro. When substituted for syt-1 in mouse hippocampal neurons, the chimera slowed the kinetics of synaptic transmission. Neurons expressing the chimera also evinced rapid and efficient Sr(2+) triggered release, in contrast to the weak response of neurons expressing syt-1. These findings reveal presynaptic sensor-membrane interactions as a major factor regulating the speed of the release machinery. Finally, the chimera failed to clamp the elevated spontaneous fusion rate exhibited by syt-1 KO neurons, indicating that the metal binding loops of syt-1 regulate the two modes of release by distinct mechanisms. SIGNIFICANCE STATEMENT: In calcium, synaptotagmin-1 triggers neurotransmitter release by interacting with membranes. Here, we demonstrate that intrinsic properties of this interaction control the time course of synaptic transmission. We engineered a "chimera" using synaptotagmin-1 and elements of a slower isoform, synaptotagmin-7. When expressed in neurons, the chimera slowed the rate of neurotransmitter release. Furthermore, unlike native synaptotagmin-1, the chimera was able to function robustly in the presence of strontium-a metal not present in cells. We exploited this ability to show that a key function of synaptotagmin-1 is to penetrate cell membranes. This work sheds light on fundamental mechanisms of neurotransmitter release.
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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.