ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Dual roles of the C2B domain of synaptotagmin I in synchronizing Ca2+-dependent neurotransmitter release.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 157 citations in OpenAlex.
- Synaptic Vesicle Recycling at the Developing Presynapse.Journal of neurochemistry · 2025Review
- Mechanisms that regulate the C1-C2B mutual inhibition control functional switch of UNC-13.eLife · 2025Article
- Correlation between evoked neurotransmitter release and adaptive functions in SYT1-associated neurodevelopmental disorder.EBioMedicine · 2024Article
- A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter release.Molecular psychiatry · 2024Article
- Expanding the genetic and phenotypic spectrum of Baker-Gordon syndrome: a newJournal of genetics · 2024Article
- 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
- Calcium Sensors of Neurotransmitter Release.Advances in neurobiology · 2023Article
- Vesicle trafficking and vesicle fusion: mechanisms, biological functions, and their implications for potential disease therapy.Molecular biomedicine · 2022Review
- 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
- Synaptic Secretion and Beyond: Targeting Synapse and Neurotransmitters to Treat Neurodegenerative Diseases.Oxidative medicine and cellular longevity · 2022Review
- Microphysiological Modeling of the Structure and Function of Neuromuscular Transmitter Release Sites.Frontiers in synaptic neuroscience · 2022Review
- The neuronal calcium sensor Synaptotagmin-1 and SNARE proteins cooperate to dilate fusion pores.eLife · 2021Article
- Function of Drosophila Synaptotagmins in membrane trafficking at synapses.Cellular and molecular life sciences : CMLS · 2021Review
- SNARE complex alters the interactions of the CaBiophysical journal · 2021Article
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- Berberine exerts antidepressant-like effects via regulating miR-34a-synaptotagmin1/Bcl-2 axis.Chinese herbal medicines · 2021Article
- Synaptotagmin-1 membrane binding is driven by the C2B domain and assisted cooperatively by the C2A domain.Scientific reports · 2020Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Although the vesicular protein synaptotagmin I contains two Ca2+-binding domains (C2A and C2B), Ca2+ binding to the C2B domain is more important for triggering synchronous neurotransmitter release. We have used point mutagenesis to determine the functional contributions of the five negatively charged aspartate (Asp) residues that constitute the Ca2+-binding sites in the C2B domain of synaptotagmin I. Transfecting wild-type synaptotagmin I DNA into cultured hippocampal neurons from synaptotagmin I knock-out mice rescued Ca2+-dependent synchronous transmitter release and reduced a slower, asynchronous component of release, indicating that synaptotagmin I suppresses asynchronous release. Mutating either the second or third Asp residues of the C2B domain potently inhibited the ability of synaptotagmin I to rescue synchronous release but did not change its ability to suppress asynchronous release. Synaptotagmin I with mutations in the first or fourth Asp residues of the C2B domain partially rescued synchronous release and partially suppressed asynchronous release, whereas neutralizing the fifth Asp residue had no effect on the ability of synaptotagmin I to rescue transmitter release. Thus, we conclude that the C2B domain of synaptotagmin I regulates neurotransmitter release in at least two ways. Synchronous release absolutely requires binding of Ca2+ to the second and third Asp residues in this domain. For the suppression of asynchronous release, Ca2+ binding to the C2B domain of synaptotagmin I apparently is not necessary because mutation of the second Asp residue inhibits Ca2+ binding, yet still allows this protein to suppress asynchronous 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.