ArticleDisease models & mechanisms2014
Impaired embryonic motility in dusp27 mutants reveals a developmental defect in myofibril structure.
Article in Disease models & mechanisms, 2014. 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, 28 citations in OpenAlex.
- Dual Specificity Phosphatase 27 Regulates Pluripotency and Meso-Endodermal Differentiation by Interacting with Transcription Factor CP2 Like-1 in Embryonic Stem Cells.International journal of stem cells · 2025Article
- In vivo profiling of the endothelium using 'AngioTag' zebrafish.Angiogenesis · 2025Article
- High throughput machine learning pipeline to characterize larval zebrafish motor behavior.PloS one · 2025Article
- Dual-specificity phosphatases 13 and 27 as key switches in muscle stem cell transition from proliferation to differentiation.Stem cells (Dayton, Ohio) · 2024Article
- Article
- A cerebellar-prepontine circuit for tonic immobility triggered by an inescapable threat.Science advances · 2022Article
- The progress of research into pseudophosphatases.Frontiers in public health · 2022Review
- The Roles of Pseudophosphatases in Disease.International journal of molecular sciences · 2021Review
- Gene alteration in zebrafish exposed to a mixture of substances of abuse.Environmental pollution (Barking, Essex : 1987) · 2021Article
- In vivo assessment of contractile strength distinguishes differential gene function in skeletal muscle of zebrafish larvae.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
An essential step in muscle fiber maturation is the assembly of highly ordered myofibrils that are required for contraction. Much remains unknown about the molecular mechanisms governing the formation of the contractile apparatus. We identified an early embryonic motility mutant in zebrafish caused by integration of a transgene into the pseudophosphatase dual specificity phosphatase 27 (dusp27) gene. dusp27 mutants exhibit near complete paralysis at embryonic and larval stages, producing extremely low levels of spontaneous coiling movements and a greatly diminished touch response. Loss of dusp27 does not prevent somitogenesis but results in severe disorganization of the contractile apparatus in muscle fibers. Sarcomeric structures in mutants are almost entirely absent and only rare triads are observed. These findings are the first to implicate a functional role of dusp27 as a gene required for myofiber maturation and provide an animal model for analyzing the mechanisms governing myofibril assembly.
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Registered trials
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