ArticleProceedings of the National Academy of Sciences of the United States of America2013
Deconstructing complexin function in activating and clamping Ca2+-triggered exocytosis by comparing knockout and knockdown phenotypes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 98 citations in OpenAlex.
- A primordial synaptotagmin-independent function of complexin in regulated exocytosis.Nature communications · 2026Article
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- Article
- Mutations of Single Residues in the Complexin N-terminus Exhibit Distinct Phenotypes in Synaptic Vesicle Fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Membrane Binding Induces Distinct Structural Signatures in the Mouse Complexin-1C-Terminal Domain.Journal of molecular biology · 2023Article
- Complexins: Ubiquitously Expressed Presynaptic Regulators of SNARE-Mediated Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- Spontaneous neurotransmission at evocable synapses predicts their responsiveness to action potentials.Frontiers in cellular neuroscience · 2023Article
- Neuronal SNARE complex assembly guided by Munc18-1 and Munc13-1.FEBS open bio · 2022Review
- Vesicle trafficking and vesicle fusion: mechanisms, biological functions, and their implications for potential disease therapy.Molecular biomedicine · 2022Review
- Stability profile of the neuronal SNARE complex reflects its potency to drive fast membrane fusion.Biophysical journal · 2022Article
- Article
- Stochastic Properties of Spontaneous Synaptic Transmission at Individual Active Zones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The complexin C-terminal amphipathic helix stabilizes the fusion pore open state by sculpting membranes.Nature structural & molecular biology · 2022Article
- SNARE Regulatory Proteins in Synaptic Vesicle Fusion and Recycling.Frontiers in molecular neuroscience · 2021Review
- Complexin Suppresses Spontaneous Exocytosis by Capturing the Membrane-Proximal Regions of VAMP2 and SNAP25.Cell reports · 2020Article
- Synergistic roles of Synaptotagmin-1 and complexin in calcium-regulated neuronal exocytosis.eLife · 2020Article
- Synaptotagmin 1 oligomers clamp and regulate different modes of neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Complexin I knockout rats exhibit a complex neurobehavioral phenotype including profound ataxia and marked deficits in lifespan.Pflugers Archiv : European journal of physiology · 2020Article
- Synaptotagmin 1 clamps synaptic vesicle fusion in mammalian neurons independent of complexin.Nature communications · 2019Article
- Structural basis for the clamping and CaNature communications · 2019Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 2 countries.
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Abstract
Complexin, a presynaptic protein that avidly binds to assembled SNARE complexes, is widely acknowledged to activate Ca(2+)-triggered exocytosis. In addition, studies of invertebrate complexin mutants and of mouse neurons with a double knockdown (DKD) of complexin-1 and -2 suggested that complexin maintains the readily releasable pool (RRP) of vesicles and clamps spontaneous exocytosis. In contrast, studies of mouse neurons with a double knockout (DKO) of complexin-1 and -2, largely carried out in hippocampal autapses, did not detect changes in the RRP size or in spontaneous exocytosis. To clarify complexin function, we here directly compared in two different preparations, cultured cortical and olfactory bulb neurons, the phenotypes of complexin DKD and DKO neurons. We find that complexin-deficient DKD and DKO neurons invariably exhibit a ~50% decrease in vesicle priming. Moreover, the DKD consistently increased spontaneous exocytosis, but the DKO did so in cortical but not olfactory bulb neurons. Furthermore, the complexin DKD but not the complexin DKO caused a compensatory increase in complexin-3 and -4 mRNA levels; overexpression of complexin-3 but not complexin-1 increased spontaneous exocytosis. Complexin-3 but not complexin-1 contains a C-terminal lipid anchor attaching it to the plasma membrane; addition of a similar lipid anchor to complexin-1 converted complexin-1 from a clamp into an activator of spontaneous exocytosis. Viewed together, our data suggest that complexin generally functions in priming and Ca(2+) triggering of exocytosis, and additionally contributes to the control of spontaneous exocytosis dependent on the developmental history of a neuron and on the subcellular localization of the complexin.
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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.