ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Dystrobrevin controls neurotransmitter release and muscle Ca(2+) transients by localizing BK channels in Caenorhabditis elegans.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Variants in DTNA cause a mild, dominantly inherited muscular dystrophy.Acta neuropathologica · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Regulation of Ryanodine Receptor-Dependent Neurotransmitter Release by AIP, Calstabins, and Presenilins.Advances in neurobiology · 2023Article
- Regulation of Neurotransmitter Release by KAdvances in neurobiology · 2023Article
- Melatonin promotes sleep by activating the BK channel inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Calnexin revealed as an ether-a-go-go chaperone by getting mutant worms up and going.The Journal of general physiology · 2018Article
- Serotonin Disinhibits aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- HRPU-2, a Homolog of Mammalian hnRNP U, Regulates Synaptic Transmission by Controlling the Expression of SLO-2 Potassium Channel inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- BKIP-1, an auxiliary subunit critical to SLO-1 function, inhibits SLO-2 potassium channel in vivo.Scientific reports · 2017Article
- AIP limits neurotransmitter release by inhibiting calcium bursts from the ryanodine receptor.Nature communications · 2017Article
- Presynaptic BK channels control transmitter release: physiological relevance and potential therapeutic implications.The Journal of physiology · 2016Review
- Role of CYP eicosanoids in the regulation of pharyngeal pumping and food uptake in Caenorhabditis elegans.Journal of lipid research · 2015Article
- Presynaptic BK channel localization is dependent on the hierarchical organization of alpha-catulin and dystrobrevin and fine-tuned by CaV2 calcium channels.BMC neuroscience · 2015Article
- Regulation of synaptic transmission at the Caenorhabditis elegans M4 neuromuscular junction by an antagonistic relationship between two calcium channels.G3 (Bethesda, Md.) · 2014Article
- SLO-2 potassium channel is an important regulator of neurotransmitter release in Caenorhabditis elegans.Nature communications · 2014Article
- Conserved single residue in the BK potassium channel required for activation by alcohol and intoxication in C. elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- BK channel opening involves side-chain reorientation of multiple deep-pore residues.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Track-a-worm, an open-source system for quantitative assessment of C. elegans locomotory and bending behavior.PloS one · 2013Article
- Postsynaptic current bursts instruct action potential firing at a graded synapse.Nature communications · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Dystrobrevin is a major component of a dystrophin-associated protein complex. It is widely expressed in mammalian tissues, including the nervous system, in which it is localized to the presynaptic nerve terminal with unknown function. In a genetic screen for suppressors of a lethargic phenotype caused by a gain-of-function isoform of SLO-1 in Caenorhabditis elegans, we isolated multiple loss-of-function (lf) mutants of the dystrobrevin gene dyb-1.dyb-1(lf) phenocopied slo-1(lf), causing increased neurotransmitter release at the neuromuscular junction, increased frequency of Ca(2+) transients in body-wall muscle, and abnormal locomotion behavior. Neuron- and muscle-specific rescue experiments suggest that DYB-1 is required for SLO-1 function in both neurons and muscle cells. DYB-1 colocalized with SLO-1 at presynaptic sites in neurons and dense body regions in muscle cells, and dyb-1(lf) caused SLO-1 mislocalization in both types of cells without altering SLO-1 protein level. The neuronal phenotypes of dyb-1(lf) were partially rescued by mouse α-dystrobrevin-1. These observations revealed novel functions of the BK channel in regulating muscle Ca(2+) transients and of dystrobrevin in controlling neurotransmitter release and muscle Ca(2+) transients by localizing the BK channel.
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