ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Munc13-1 C1 domain activation lowers the energy barrier for synaptic vesicle fusion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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130 citing papers in PubMed, 235 citations in OpenAlex.
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- Resolving endogenous protein organization in cells with nanometer resolution.Nature communications · 2026Article
- Selective, genetically induced increase in synaptic vesicle priming.Science advances · 2026Article
- Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Temporal Coding rather than Circuit Wiring allows Hippocampal CA3 Neurons to Dynamically Distinguish Different Cortical Inputs.bioRxiv : the preprint server for biology · 2026Article
- Munc13-1 couples DAG and CaScience advances · 2026Article
- Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function.Nature genetics · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- PKC-dependent enhancement of glutamate input to VTA dopamine neurons in 3xTg-AD mice.bioRxiv : the preprint server for biology · 2025Article
- Monoamine-induced diacylglycerol signaling rapidly accumulates Unc13 in nanoclusters for fast presynaptic potentiation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Presynaptic αNeuron · 2025Article
- Mechanisms that regulate the C1-C2B mutual inhibition control functional switch of UNC-13.eLife · 2025Article
- Synapse-specific catecholaminergic modulation of neuronal glutamate release.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mutations of Single Residues in the Complexin N-terminus Exhibit Distinct Phenotypes in Synaptic Vesicle Fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Differential SNARE chaperoning by Munc13-1 and Munc18-1 dictates fusion pore fate at the release site.Nature communications · 2024Article
- Control of Munc13-1 Activity by Autoinhibitory Interactions Involving the Variable N-terminal Region.Journal of molecular biology · 2024Article
- Tomosyns attenuate SNARE assembly and synaptic depression by binding to VAMP2-containing template complexes.Nature communications · 2024Article
- Article
70 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Synapses need to encode a wide dynamic range of action potential frequencies. Essential vesicle priming proteins of the Munc13 (mammalian Unc13) family play an important role in adapting vesicle supply to variable demand and thus influence short-term plasticity characteristics and synaptic function. Structure-function analyses of Munc13s have identified a "catalytic" C-terminal domain and several N-terminal modulatory domains, including a diacylglycerol/phorbol ester [4beta-phorbol-12, 13-dibutyrate (PDBu)] binding C1 domain. Although still allowing basal priming, a Munc13-1 C1 domain mutation (H567K) prevents PDBu induced potentiation of evoked transmitter release, leads to strong depression during trains of synaptic activity, and causes perinatal lethality in mice. To understand the mechanism of C1 domain-mediated modulation of Munc13 function, we examined how PDBu increases neurotransmitter release. Analyses of osmotically induced release as well as Ca2+ triggered and spontaneous release showed that PDBu increases the vesicular release rate without affecting the size of the readily releasable vesicle pool, linking C1 domain activation to a lowering of the energy barrier for vesicle fusion. PDBu binding-deficient mutant Munc13-1(H567K) synapses mirrored the vesicular release properties of PDBu-potentiated wild-type synapses, indicating that Munc13-1(H567K) is a gain-of-function mutant, which conformationally mimics the PDBu-activated state of Munc13-1. We propose a PKC analogous two-state model of regulation of Munc13s, in which the basal state of Munc13s is disinhibited by C1 domain activation into a state of facilitated vesicle release, regardless of whether the release is spontaneous or action potential triggered.
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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.