ArticlePLoS biology2018
Nitric oxide-mediated posttranslational modifications control neurotransmitter release by modulating complexin farnesylation and enhancing its clamping ability.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Influence of nitrate supplementation on motor unit activity during recovery following a sustained ischemic contraction in recreationally active young males.European journal of nutrition · 2024Trial
- Effect of nitrate supplementation on skeletal muscle motor unit activity during isometric blood flow restriction exercise.European journal of applied physiology · 2022Trial
- Ramalin Ameliorates Alzheimer's Disease Pathology by Targeting BACE1, HDAC6, and MAPK Pathways.MedComm · 2026Article
- Protein farnesylation: from molecular mechanisms to therapeutic targeting in cancer, aging, and beyond.Frontiers in pharmacology · 2026Review
- Microglial activation induces nitric oxide signalling and alters protein S-nitrosylation patterns in extracellular vesicles.Journal of extracellular vesicles · 2024Article
- Cyclic nucleotide-induced bidirectional long-term synaptic plasticity in Drosophila mushroom body.The Journal of physiology · 2024Article
- Cyclic nucleotide-induced bidirectional long-term synaptic plasticity inbioRxiv : the preprint server for biology · 2024Article
- Function and regulation of nitric oxide signaling in Drosophila.Molecules and cells · 2024Review
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.Cell reports · 2023Article
- Medium-Chain Fatty Acids Rescue Motor Function and Neuromuscular Junction Degeneration in aCells · 2023Article
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.bioRxiv : the preprint server for biology · 2023Article
- Membrane Binding Induces Distinct Structural Signatures in the Mouse Complexin-1C-Terminal Domain.Journal of molecular biology · 2023Article
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- Neuroinflammatory Modulation of Extracellular Vesicle Biogenesis and Cargo Loading.Neuromolecular medicine · 2022Review
- Determinants of synapse diversity revealed by super-resolution quantal transmission and active zone imaging.Nature communications · 2022Article
- Nitrergic modulation of ion channel function in regulating neuronal excitability.Channels (Austin, Tex.) · 2021Article
- Inhibition of neuroinflammatory nitric oxide signaling suppresses glycation and prevents neuronal dysfunction in mouse prion disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Systems biology reveals reprogramming of the S-nitroso-proteome in the cortical and striatal regions of mice during aging process.Scientific reports · 2020Article
- Glutamate at the Vertebrate Neuromuscular Junction: From Modulation to Neurotransmission.Cells · 2019Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) regulates neuronal function and thus is critical for tuning neuronal communication. Mechanisms by which NO modulates protein function and interaction include posttranslational modifications (PTMs) such as S-nitrosylation. Importantly, cross signaling between S-nitrosylation and prenylation can have major regulatory potential. However, the exact protein targets and resulting changes in function remain elusive. Here, we interrogated the role of NO-dependent PTMs and farnesylation in synaptic transmission. We found that NO compromises synaptic function at the Drosophila neuromuscular junction (NMJ) in a cGMP-independent manner. NO suppressed release and reduced the size of available vesicle pools, which was reversed by glutathione (GSH) and occluded by genetic up-regulation of GSH-generating and de-nitrosylating glutamate-cysteine-ligase and S-nitroso-glutathione reductase activities. Enhanced nitrergic activity led to S-nitrosylation of the fusion-clamp protein complexin (cpx) and altered its membrane association and interactions with active zone (AZ) and soluble N-ethyl-maleimide-sensitive fusion protein Attachment Protein Receptor (SNARE) proteins. Furthermore, genetic and pharmacological suppression of farnesylation and a nitrosylation mimetic mutant of cpx induced identical physiological and localization phenotypes as caused by NO. Together, our data provide evidence for a novel physiological nitrergic molecular switch involving S-nitrosylation, which reversibly suppresses farnesylation and thereby enhances the net-clamping function of cpx. These data illustrate a new mechanistic signaling pathway by which regulation of farnesylation can fine-tune synaptic release.
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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.