ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Targeted mutations in the syntaxin H3 domain specifically disrupt SNARE complex function in synaptic transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 60 citations in OpenAlex.
- Syntaxin-3 Regulates Tight Junction Assembly in Human Retinal Pigment Epithelium.Cell biochemistry and function · 2026Article
- Disrupting stroke-induced GAT-1-syntaxin1A interaction promotes functional recovery after stroke.Cell reports. Medicine · 2024Article
- A mouse model of human TLR4 D299G/T399I SNPs reveals mechanisms of altered LPS and pathogen responses.The Journal of experimental medicine · 2021Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- CRMP2-Neurofibromin Interface Drives NF1-related Pain.Neuroscience · 2018Article
- v-SNARE function in chromaffin cells.Pflugers Archiv : European journal of physiology · 2018Review
- Electrophysiological analysis of synaptic transmission in Drosophila.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- Distinct Functions of Syntaxin-1 in Neuronal Maintenance, Synaptic Vesicle Docking, and Fusion in Mouse Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Molecular underpinnings of synaptic vesicle pool heterogeneity.Traffic (Copenhagen, Denmark) · 2015Review
- Cytotoxicity of botulinum neurotoxins reveals a direct role of syntaxin 1 and SNAP-25 in neuron survival.Nature communications · 2013Article
- Differential regulation of synchronous versus asynchronous neurotransmitter release by the C2 domains of synaptotagmin 1.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Electrophysiological recording in the Drosophila embryo.Journal of visualized experiments : JoVE · 2009Article
- Harvesting and preparing Drosophila embryos for electrophysiological recording and other procedures.Journal of visualized experiments : JoVE · 2009Article
- Interactions between neuronal fusion proteins explored by molecular dynamics.Biophysical journal · 2008Article
- Vesicle priming and recruitment by ubMunc13-2 are differentially regulated by calcium and calmodulin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Bidirectional modulation of transmitter release by calcium channel/syntaxin interactions in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Sequential N- to C-terminal SNARE complex assembly drives priming and fusion of secretory vesicles.The EMBO journal · 2006Article
- Structural transitions in the synaptic SNARE complex during Ca2+-triggered exocytosis.The Journal of cell biology · 2006Article
- Dual roles of the C2B domain of synaptotagmin I in synchronizing Ca2+-dependent neurotransmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Ceramidase regulates synaptic vesicle exocytosis and trafficking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The cytoplasmic H3 helical domain of syntaxin is implicated in numerous protein-protein interactions required for the assembly and stability of the SNARE complex mediating vesicular fusion at the synapse. Two specific hydrophobic residues (Ala-240, Val-244) in H3 layers 4 and 5 of mammalian syntaxin1A have been suggested to be involved in SNARE complex stability and required for the inhibitory effects of syntaxin on N-type calcium channels. We have generated the equivalent double point mutations in Drosophila syntaxin1A (A243V, V247A; syx(4) mutant) to examine their significance in synaptic transmission in vivo. The syx(4) mutant animals are embryonic lethal and display severely impaired neuronal secretion, although non-neuronal secretion appears normal. Synaptic transmission is nearly abolished, with residual transmission delayed, highly variable, and nonsynchronous, strongly reminiscent of transmission in null synaptotagmin I mutants. However, the syx(4) mutants show no alterations in synaptic protein levels in vivo or syntaxin partner binding interactions in vitro. Rather, syx(4) mutant animals have severely impaired hypertonic saline response in vivo, an assay indicating loss of fusion-competent synaptic vesicles, and in vitro SNARE complexes containing Syx(4) protein have significantly compromised stability. These data suggest that the same residues required for syntaxin-mediated calcium channel inhibition are required for the generation of fusion-competent vesicles in a neuronal-specific mechanism acting at synapses.
Indexed as
Identifiers
11717347PMC6763887W2125575826What OpenQuestion holds
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.