ArticleBiology open2015
The evolution of the dystroglycan complex, a major mediator of muscle integrity.
Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- The missense mutation C667F in murine β-dystroglycan causes embryonic lethality, myopathy and blood-brain barrier destabilization.Disease models & mechanisms · 2024Article
- The α-dystroglycan N-terminus is a broad-spectrum antiviral agent against SARS-CoV-2 and enveloped viruses.Antiviral research · 2024Article
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- GANAB andInternational journal of molecular sciences · 2022Review
- Article
- High degree of conservation of the enzymes synthesizing the laminin-binding glycoepitope of α-dystroglycan.Open biology · 2021Article
- Cellular Reprogramming and Immortality: Expression Profiling Reveals Putative Genes Involved in Turritopsis dohrnii's Life Cycle Reversal.Genome biology and evolution · 2021Article
- Limb-girdle muscular dystrophy due to GMPPB mutations: A case report and comprehensive literature review.Bosnian journal of basic medical sciences · 2020Review
- Profiling of the muscle-specific dystroglycan interactome reveals the role of Hippo signaling in muscular dystrophy and age-dependent muscle atrophy.BMC medicine · 2020Article
- Proteomics analysis of Trichoplusia ni midgut epithelial cell brush border membrane vesicles.Insect science · 2019Article
- A molecular overview of the primary dystroglycanopathies.Journal of cellular and molecular medicine · 2019Review
- Analysis of α-Dystroglycan/LG Domain Binding Modes: Investigating Protein Motifs That Regulate the Affinity of Isolated LG Domains.Frontiers in molecular biosciences · 2019Review
- Structural flexibility of human α-dystroglycan.FEBS open bio · 2017Article
- Expansion of divergent SEA domains in cell surface proteins and nucleoporin 54.Protein science : a publication of the Protein Society · 2017Article
- Phylogenetic evidence for the modular evolution of metazoan signalling pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- An evaluation of the evolution of the gene structure of dystroglycan.BMC research notes · 2017Article
- The effect of the pathological V72I, D109N and T190M missense mutations on the molecular structure of α-dystroglycan.PloS one · 2017Article
- Muscle involvement in limb-girdle muscular dystrophy with GMPPB deficiency (LGMD2T).Neurology. Genetics · 2016Article
- Diversity of Cnidarian Muscles: Function, Anatomy, Development and Regeneration.Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basement membrane (BM) extracellular matrices are crucial for the coordination of different tissue layers. A matrix adhesion receptor that is important for BM function and stability in many mammalian tissues is the dystroglycan (DG) complex. This comprises the non-covalently-associated extracellular α-DG, that interacts with laminin in the BM, and the transmembrane β-DG, that interacts principally with dystrophin to connect to the actin cytoskeleton. Mutations in dystrophin, DG, or several enzymes that glycosylate α-DG underlie severe forms of human muscular dystrophy. Nonwithstanding the pathophysiological importance of the DG complex and its fundamental interest as a non-integrin system of cell-ECM adhesion, the evolution of DG and its interacting proteins is not understood. We analysed the phylogenetic distribution of DG, its proximal binding partners and key processing enzymes in extant metazoan and relevant outgroups. We identify that DG originated after the divergence of ctenophores from porifera and eumetazoa. The C-terminal half of the DG core protein is highly-conserved, yet the N-terminal region, that includes the laminin-binding region, has undergone major lineage-specific divergences. Phylogenetic analysis based on the C-terminal IG2_MAT_NU region identified three distinct clades corresponding to deuterostomes, arthropods, and mollusks/early-diverging metazoans. Whereas the glycosyltransferases that modify α-DG are also present in choanoflagellates, the DG-binding proteins dystrophin and laminin originated at the base of the metazoa, and DG-associated sarcoglycan is restricted to cnidarians and bilaterians. These findings implicate extensive functional diversification of DG within invertebrate lineages and identify the laminin-DG-dystrophin axis as a conserved adhesion system that evolved subsequent to integrin-ECM adhesion, likely to enhance the functional complexity of cell-BM interactions in early metazoans.
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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.