ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Dystrophin is required for appropriate retrograde control of neurotransmitter release at the Drosophila neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Optical coherence tomography findings in Duchenne muscular dystrophy.BMC ophthalmology · 2026Article
- Genome-Wide Association Study and transcriptome analysis reveals a complex gene network that regulates opsin gene expression and cell fate determination inbioRxiv : the preprint server for biology · 2024Article
- Synaptic defects in a drosophila model of muscular dystrophy.Frontiers in cellular neuroscience · 2024Article
- Advancements in 2D and 3D In Vitro Models for Studying Neuromuscular Diseases.International journal of molecular sciences · 2023Review
- Signaling through the dystrophin glycoprotein complex affects the stress-dependent transcriptome in Drosophila.Disease models & mechanisms · 2023Article
- The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021Review
- Defects of full-length dystrophin trigger retinal neuron damage and synapse alterations by disrupting functional autophagy.Cellular and molecular life sciences : CMLS · 2021Article
- Modelling Neuromuscular Diseases in the Age of Precision Medicine.Journal of personalized medicine · 2020Review
- Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways.Human molecular genetics · 2017Article
- Cognitive dysfunction in Duchenne muscular dystrophy: a possible role for neuromodulatory immune molecules.Journal of neurophysiology · 2016Review
- C-terminal Src Kinase Gates Homeostatic Synaptic Plasticity and Regulates Fasciclin II Expression at the Drosophila Neuromuscular Junction.PLoS genetics · 2016Article
- Dystrophin induced cognitive impairment: mechanisms, models and therapeutic strategies.Annals of neurosciences · 2015Review
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- Homeostatic plasticity at the Drosophila neuromuscular junction.Neuropharmacology · 2014Review
- Regeneration of soft tissues is promoted by MMP1 treatment after digit amputation in mice.PloS one · 2013Article
- Extracellular matrix and its receptors in Drosophila neural development.Developmental neurobiology · 2011Review
- New dystrophin/dystroglycan interactors control neuron behavior in Drosophila eye.BMC neuroscience · 2011Article
- The RhoGAP crossveinless-c interacts with Dystrophin and is required for synaptic homeostasis at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the human dystrophin gene cause the Duchenne and Becker muscular dystrophies. The Dystrophin protein provides a structural link between the muscle cytoskeleton and extracellular matrix to maintain muscle integrity. Recently, Dystrophin has also been found to act as a scaffold for several signaling molecules, but the roles of dystrophin-mediated signaling pathways remain unknown. To further our understanding of this aspect of the function of dystrophin, we have generated Drosophila mutants that lack the large dystrophin isoforms and analyzed their role in synapse function at the neuromuscular junction. In expression and rescue studies, we show that lack of the large dystrophin isoforms in the postsynaptic muscle cell leads to elevated evoked neurotransmitter release from the presynaptic apparatus. Overall synapse size, the size of the readily releasable vesicle pool as assessed with hypertonic shock, and the number of presynaptic neurotransmitter release sites (active zones) are not changed in the mutants. Short-term synaptic facilitation of evoked transmitter release is decreased in the mutants, suggesting that the absence of dystrophin results in increased probability of release. Absence of the large dystrophin isoforms does not lead to changes in muscle cell morphology or alterations in the postsynaptic electrical response to spontaneously released neurotransmitter. Therefore, postsynaptic glutamate receptor function does not appear to be affected. Our results indicate that the postsynaptically localized scaffolding protein Dystrophin is required for appropriate control of neuromuscular synaptic homeostasis.
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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.