ArticleDisease models & mechanisms2023
Signaling through the dystrophin glycoprotein complex affects the stress-dependent transcriptome in Drosophila.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- A Landscape ofBiology · 2026Review
- Skeletal muscle adaptation to microgravity: how altered mechanical cues drive catabolic signaling.EMBO reports · 2026Review
- Low expression of SGCA promotes lung squamous cell carcinoma malignant progression.Scientific reports · 2025Article
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- Exploring the Wilderness within: An Integrative Metabolomics and Transcriptomics Study on Near-Wild and ColonizedInsects · 2024Article
- Article
- From adhesion complex to signaling hub: the dual role of dystroglycan.Frontiers in molecular biosciences · 2023Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deficiencies in the human dystrophin glycoprotein complex (DGC), which links the extracellular matrix with the intracellular cytoskeleton, cause muscular dystrophies, a group of incurable disorders associated with heterogeneous muscle, brain and eye abnormalities. Stresses such as nutrient deprivation and aging cause muscle wasting, which can be exacerbated by reduced levels of the DGC in membranes, the integrity of which is vital for muscle health and function. Moreover, the DGC operates in multiple signaling pathways, demonstrating an important function in gene expression regulation. To advance disease diagnostics and treatment strategies, we strive to understand the genetic pathways that are perturbed by DGC mutations. Here, we utilized a Drosophila model to investigate the transcriptomic changes in mutants of four DGC components under temperature and metabolic stress. We identified DGC-dependent genes, stress-dependent genes and genes dependent on the DGC for a proper stress response, confirming a novel function of the DGC in stress-response signaling. This perspective yields new insights into the etiology of muscular dystrophy symptoms, possible treatment directions and a better understanding of DGC signaling and regulation under normal and stress conditions.
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Registered trials
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