ArticleScientific reports2011
Hyperthermic seizures and aberrant cellular homeostasis in Drosophila dystrophic muscles.
Article in Scientific reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Signaling through the dystrophin glycoprotein complex affects the stress-dependent transcriptome in Drosophila.Disease models & mechanisms · 2023Article
- Article
- Profiling of the muscle-specific dystroglycan interactome reveals the role of Hippo signaling in muscular dystrophy and age-dependent muscle atrophy.BMC medicine · 2020Article
- The roles of dystroglycan in the nervous system: insights from animal models of muscular dystrophy.Disease models & mechanisms · 2018Review
- miRNA-based buffering of the cobblestone-lissencephaly-associated extracellular matrix receptor dystroglycan via its alternative 3'-UTR.Nature communications · 2014Article
- Measurement of metabolic rate in Drosophila using respirometry.Journal of visualized experiments : JoVE · 2014Article
- Stress-induced ECM alteration modulates cellular microRNAs that feedback to readjust the extracellular environment and cell behavior.Frontiers in genetics · 2013Review
- Dg-Dys-Syn1 signaling in Drosophila regulates the microRNA profile.BMC cell biology · 2012Article
- New dystrophin/dystroglycan interactors control neuron behavior in Drosophila eye.BMC neuroscience · 2011Article
- Dystrophin Orchestrates the Epigenetic Profile of Muscle Cells Via miRNAs.Frontiers in genetics · 2011Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In humans, mutations in the Dystrophin Glycoprotein Complex (DGC) cause muscular dystrophies (MDs) that are associated with muscle loss, seizures and brain abnormalities leading to early death. Using Drosophila as a model to study MD we have found that loss of Dystrophin (Dys) during development leads to heat-sensitive abnormal muscle contractions that are repressed by mutations in Dys's binding partner, Dystroglycan (Dg). Hyperthermic seizures are independent from dystrophic muscle degeneration and rely on neurotransmission, which suggests involvement of the DGC in muscle-neuron communication. Additionally, reduction of the Ca(2+) regulator, Calmodulin or Ca(2+) channel blockage rescues the seizing phenotype, pointing to Ca(2+) mis-regulation in dystrophic muscles. Also, Dys and Dg mutants have antagonistically abnormal cellular levels of ROS, suggesting that the DGC has a function in regulation of muscle cell homeostasis. These data show that muscles deficient for Dys are predisposed to hypercontraction that may result from abnormal neuromuscular junction signaling.
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