ArticleProceedings of the National Academy of Sciences of the United States of America2022
Dystrophin missense mutations alter focal adhesion tension and mechanotransduction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 32 citations in OpenAlex.
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- Repairing the defective folding of alpha-sarcoglycan is needed to promote myogenic cell engraftment in 3D artificial muscle models of LGMDR3.Skeletal muscle · 2025Article
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- Mechanotransduction and Skeletal Muscle Atrophy: The Interplay Between Focal Adhesions and Oxidative Stress.International journal of molecular sciences · 2025Review
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Pan-Cancer Analysis of KANK2: Clinical and Molecular Insights into Tumor Progression and Therapeutic Implications.Journal of Cancer · 2025Article
- Development of label-free cell tracking for discrimination of the heterogeneous mesenchymal migration.PloS one · 2025Article
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- Comparison of vinculin tension in cellular monolayers and three-dimensional multicellular aggregates.Biomedical optics express · 2024Article
- The Role of Biophysical Factors in Organ Development: Insights from Current Organoid Models.Bioengineering (Basel, Switzerland) · 2024Review
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- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- Duchenne muscular dystrophy treatment with lentiviral vector containing mini-dystrophin gene in vivo.MedComm · 2024Article
- Analysis of common and characteristic actions ofJournal of ginseng research · 2023Review
- RAD-TGTs: high-throughput measurement of cellular mechanotype via rupture and delivery of DNA tension probes.Nature communications · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Dystrophin is an essential muscle protein that contributes to cell membrane stability by mechanically linking the actin cytoskeleton to the extracellular matrix via an adhesion complex called the dystrophin-glycoprotein complex. The absence or impaired function of dystrophin causes muscular dystrophy. Focal adhesions (FAs) are also mechanosensitive adhesion complexes that connect the cytoskeleton to the extracellular matrix. However, the interplay between dystrophin and FA force transmission has not been investigated. Using a vinculin-based bioluminescent tension sensor, we measured FA tension in transgenic C2C12 myoblasts expressing wild-type (WT) dystrophin, a nonpathogenic single nucleotide polymorphism (SNP) (I232M), or two missense mutations associated with Duchenne (L54R), or Becker muscular dystrophy (L172H). Our data revealed cross talk between dystrophin and FAs, as the expression of WT or I232M dystrophin increased FA tension compared to dystrophin-less nontransgenic myoblasts. In contrast, the expression of L54R or L172H did not increase FA tension, indicating that these disease-causing mutations compromise the mechanical function of dystrophin as an FA allosteric regulator. Decreased FA tension caused by these mutations manifests as defective migration, as well as decreased Yes-associated protein 1 (YAP) activation, possibly by the disruption of the ability of FAs to transmit forces between the extracellular matrix and cytoskeleton. Our results indicate that dystrophin influences FA tension and suggest that dystrophin disease-causing missense mutations may disrupt a cellular tension-sensing pathway in dystrophic skeletal muscle.
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