ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Munc18-1: sequential interactions with the fusion machinery stimulate vesicle docking and priming.
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 70 papers.
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Who cites it
70 citing papers in PubMed.
- Functional differences of Munc18 isoforms reflect their affinities for the exocytosis site.Cellular and molecular life sciences : CMLS · 2026Article
- Fusion Pores as Regulators of Quantal Size and Cellular Physiology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Impaired Aggrephagy, Interrupted Vesicular Trafficking, and Cellular Stress, Lead to Protein Aggregation, and Synaptic Dysfunction in Cerebellum of Children and Adults with Idiopathic Autism.Cerebellum (London, England) · 2025Article
- Syntaxin 3B: A SNARE Protein Required for Vision.International journal of molecular sciences · 2024Review
- SIP30 involvement in vesicle exocytosis from PC12 cells.Biochemistry and biophysics reports · 2024Article
- Article
- Construction of the metabolism-related models for predicting prognosis and infiltrating immune phenotype in lung squamous cell carcinoma.Journal of Cancer · 2023Article
- Functional Roles of UNC-13/Munc13 and UNC-18/Munc18 in Neurotransmission.Advances in neurobiology · 2023Review
- Reexamination of N-terminal domains of syntaxin-1 in vesicle fusion from central murine synapses.eLife · 2021Article
- Article
- PTP-MEG2 regulates quantal size and fusion pore opening through two distinct structural bases and substrates.EMBO reports · 2021Article
- Article
- The fusion pore, 60 years after the first cartoon.FEBS letters · 2018Review
- Syntaxin clusters at secretory granules in a munc18-bound conformation.Molecular biology of the cell · 2018Article
- How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018Review
- Evidence for a conserved inhibitory binding mode between the membrane fusion assembly factors Munc18 and syntaxin in animals.The Journal of biological chemistry · 2017Article
- MiR-335 overexpression impairs insulin secretion through defective priming of insulin vesicles.Physiological reports · 2017Article
- Munc13-1 and Munc18-1 together prevent NSF-dependent de-priming of synaptic vesicles.Nature communications · 2017Article
- Early Golgi Abnormalities and Neurodegeneration upon Loss of Presynaptic Proteins Munc18-1, Syntaxin-1, or SNAP-25.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
10 more citing papers are in PubMed but not listed here.
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8 authors.
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Abstract
Exocytosis of secretory or synaptic vesicles is executed by a mechanism including the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) proteins. Munc18-1 is a part of this fusion machinery, but its role is controversial because it is indispensable for fusion but also inhibits the assembly of purified SNAREs in vitro. This inhibition reflects the binding of Munc18-1 to a closed conformation of the target-SNARE syntaxin1. The controversy would be solved if binding to closed syntaxin1 were shown to be stimulatory for vesicle fusion and/or additional essential interactions were identified between Munc18-1 and the fusion machinery. Here, we provide evidence for both notions by dissecting sequential steps of the exocytotic cascade while expressing Munc18 variants in the Munc18-1 null background. In Munc18-1 null chromaffin cells, vesicle docking is abolished and syntaxin levels are reduced. A mutation that diminished Munc18 binding to syntaxin1 in vitro attenuated the vesicle-docking step but rescued vesicle priming in excess of docking. Conversely, expressing the Munc18-2 isoform, which also displays binding to closed syntaxin1, rescued vesicle docking identical with Munc18-1 but impaired more downstream vesicle priming steps. All Munc18 variants restored syntaxin1 levels at least to wild-type levels, showing that the docking phenotype is not caused by syntaxin1 reduction. None of the Munc18 variants affected vesicle fusion kinetics or fusion pore duration. In conclusion, binding of Munc18-1 to closed syntaxin1 stimulates vesicle docking and a distinct interaction mode regulates the consecutive priming step.
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