ArticleThe Journal of biological chemistry2011
The dystrophin-associated protein complex maintains muscle excitability by regulating Ca(2+)-dependent K(+) (BK) channel localization.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Wnt-Ror-Dvl signalling and the dystrophin complex organize planar-polarized membrane compartments in C. elegans muscles.Nature communications · 2024Article
- Optimized lentiviral vector to restore full-length dystrophin via a cell-mediated approach in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2022Article
- Involvement of muscle satellite cell dysfunction in neuromuscular disorders: Expanding the portfolio of satellite cell-opathies.European journal of translational myology · 2022Article
- Shank promotes action potential repolarization by recruiting BK channels to calcium microdomains.eLife · 2022Article
- Post-translational Modification in Muscular Dystrophies.Advances in experimental medicine and biology · 2022Article
- Melatonin promotes sleep by activating the BK channel inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Transcriptome changes during the initiation and progression of Duchenne muscular dystrophy in Caenorhabditis elegans.Human molecular genetics · 2020Article
- Calnexin revealed as an ether-a-go-go chaperone by getting mutant worms up and going.The Journal of general physiology · 2018Article
- AIP limits neurotransmitter release by inhibiting calcium bursts from the ryanodine receptor.Nature communications · 2017Article
- Duchenne and Becker Muscular Dystrophies: A Review of Animal Models, Clinical End Points, and Biomarker Quantification.Toxicologic pathology · 2017Review
- ERG-28 controls BK channel trafficking in the ER to regulate synaptic function and alcohol response ineLife · 2017Article
- SLO BK Potassium Channels Couple Gap Junctions to Inhibition of Calcium Signaling in Olfactory Neuron Diversification.PLoS genetics · 2016Article
- 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
- In vivo single-molecule imaging identifies altered dynamics of calcium channels in dystrophin-mutant C. elegans.Nature communications · 2014Article
- C. elegans Punctin specifies cholinergic versus GABAergic identity of postsynaptic domains.Nature · 2014Article
- Positive modulation of a Cys-loop acetylcholine receptor by an auxiliary transmembrane subunit.Nature neuroscience · 2012Article
- Interaction of α-catulin with dystrobrevin contributes to integrity of dystrophin complex in muscle.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
The dystrophin-associated protein complex (DAPC) consists of several transmembrane and intracellular scaffolding elements that have been implicated in maintaining the structure and morphology of the vertebrate neuromuscular junction (NMJ). Genetic linkage analysis has identified loss-of-function mutations in DAPC genes that give rise to degenerative muscular dystrophies. Although much is known about the involvement of the DAPC in maintaining muscle integrity, less is known about the precise contribution of the DAPC in cell signaling events. To better characterize the functional role of the DAPC at the NMJ, we used electrophysiology, immunohistochemistry, and fluorescent labeling to directly assess cholinergic synaptic transmission, ion channel localization, and muscle excitability in loss-of-function (lf) mutants of Caenorhabditis elegans DAPC homologues. We found that all DAPC mutants consistently display mislocalization of the Ca(2+)-gated K(+) channel, SLO-1, in muscle cells, while ionotropic acetylcholine receptor (AChR) expression and localization at the NMJ remained unaltered. Synaptic cholinergic signaling was also not significantly impacted across DAPC(lf) mutants. Consistent with these findings and the postsynaptic mislocalization of SLO-1, we observed an increase in muscle excitability downstream of cholinergic signaling. Based on our results, we conclude that the DAPC is not involved in regulating AChR architecture at the NMJ, but rather functions to control muscle excitability, in an activity-dependent manner, through the proper localization of SLO-1 channels.
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