ArticlePLoS biology2007
Open syntaxin docks synaptic vesicles.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 199 citations in OpenAlex.
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- Munc13- and SNAP25-dependent molecular bridges play a key role in synaptic vesicle priming.Science advances · 2023Article
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- CaV1 and CaV2 calcium channels mediate the release of distinct pools of synaptic vesicles.eLife · 2023Article
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- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- Functional Roles of UNC-13/Munc13 and UNC-18/Munc18 in Neurotransmission.Advances in neurobiology · 2023Review
- Munc13 supports fusogenicity of non-docked vesicles at synapses with disrupted active zones.eLife · 2022Article
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- Endogenous tagging of Unc-13 reveals nanoscale reorganization at active zones during presynaptic homeostatic potentiation.Frontiers in cellular neuroscience · 2022Article
- LncRNA/miRNA/mRNA ceRNA network analysis in spinal cord injury rat with physical exercise therapy.PeerJ · 2022Article
- rab-27 acts in an intestinal pathway to inhibit axon regeneration in C. elegans.PLoS genetics · 2021Article
- A novel dual Ca2+ sensor system regulates Ca2+-dependent neurotransmitter release.The Journal of cell biology · 2021Article
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43 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Synaptic vesicles dock to the plasma membrane at synapses to facilitate rapid exocytosis. Docking was originally proposed to require the soluble N-ethylmaleimide-sensitive fusion attachment protein receptor (SNARE) proteins; however, perturbation studies suggested that docking was independent of the SNARE proteins. We now find that the SNARE protein syntaxin is required for docking of all vesicles at synapses in the nematode Caenorhabditis elegans. The active zone protein UNC-13, which interacts with syntaxin, is also required for docking in the active zone. The docking defects in unc-13 mutants can be fully rescued by overexpressing a constitutively open form of syntaxin, but not by wild-type syntaxin. These experiments support a model for docking in which UNC-13 converts syntaxin from the closed to the open state, and open syntaxin acts directly in docking vesicles to the plasma membrane. These data provide a molecular basis for synaptic vesicle docking.
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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.