ArticleNature neuroscience2016
Active zone scaffolds differentially accumulate Unc13 isoforms to tune Ca(2+) channel-vesicle coupling.
Article in Nature neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed.
- Undoing of firing rate adaptation enables invariant population codes.Science advances · 2026Article
- Btbd11 regulates glutamatergic synapse organization in GABAergic inhibitory interneurons.bioRxiv : the preprint server for biology · 2026Article
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- Semi-automatic 3D-quantification of in-vivo synapse formation.BMC bioinformatics · 2026Article
- The nanoscale mobility of calcium channels is driven by readily releasable synaptic vesicles to support precise neurotransmission in livebioRxiv : the preprint server for biology · 2026Article
- An unexpected specialization of the active zone scaffold RIM at high release synapses.bioRxiv : the preprint server for biology · 2026Article
- Single nucleotide variants inBiochemistry and biophysics reports · 2026Article
- Deployment of endocytic machinery to periactive zones of nerve terminals is independent of active zone assembly and evoked release.bioRxiv : the preprint server for biology · 2026Article
- Article
- Scales of Postsynaptic Nanostructure: Molecules, Nanoclusters, and Nanodomains.Advances in neurobiology · 2026Review
- Active Zone Maturation Controls Presynaptic Output and Release Mode and Is Regulated by Neuronal Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function.Nature genetics · 2025Article
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Independently engaging protein tethers of different length enhance synaptic vesicle trafficking to the plasma membrane.The Journal of physiology · 2025Article
- Munc13-1 restoration mitigates presynaptic pathology in spinal muscular atrophy.Nature communications · 2025Article
- Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Myosin 15 participates in assembly and remodeling of the presynapse.The Journal of cell biology · 2025Article
- Loss of synaptic Munc13-1 underlies neurotransmission abnormalities in spinal muscular atrophy.Cellular and molecular life sciences : CMLS · 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
- Trans-synaptic molecular context of NMDA receptor nanodomains.Nature communications · 2025Article
79 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain function relies on fast and precisely timed synaptic vesicle (SV) release at active zones (AZs). Efficacy of SV release depends on distance from SV to Ca(2+) channel, but molecular mechanisms controlling this are unknown. Here we found that distances can be defined by targeting two unc-13 (Unc13) isoforms to presynaptic AZ subdomains. Super-resolution and intravital imaging of developing Drosophila melanogaster glutamatergic synapses revealed that the Unc13B isoform was recruited to nascent AZs by the scaffolding proteins Syd-1 and Liprin-α, and Unc13A was positioned by Bruchpilot and Rim-binding protein complexes at maturing AZs. Unc13B localized 120 nm away from Ca(2+) channels, whereas Unc13A localized only 70 nm away and was responsible for docking SVs at this distance. Unc13A(null) mutants suffered from inefficient, delayed and EGTA-supersensitive release. Mathematical modeling suggested that synapses normally operate via two independent release pathways differentially positioned by either isoform. We identified isoform-specific Unc13-AZ scaffold interactions regulating SV-Ca(2+)-channel topology whose developmental tightening optimizes synaptic transmission.
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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.