The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Dystrophin is required for the formation of stable muscle attachments in the zebrafish embryo
Open accessAbstract
A class of recessive lethal zebrafish mutations has been identified in which normal skeletal muscle differentiation is followed by a tissue-specific degeneration that is reminiscent of the human muscular dystrophies. Here, we show that one of these mutations, sapje, disrupts the zebrafish orthologue of the X-linked human Duchenne muscular dystrophy(DMD) gene. Mutations in this locus cause Duchenne or Becker muscular dystrophies in human patients and are thought to result in a dystrophic pathology through disconnecting the cytoskeleton from the extracellular matrix in skeletal muscle by reducing the level of dystrophin protein at the sarcolemma. This is thought to allow tearing of this membrane, which in turn leads to cell death. Surprisingly, we have found that the progressive muscle degeneration phenotype of sapje mutant zebrafish embryos is caused by the failure of embryonic muscle end attachments. Although a role for dystrophin in maintaining vertebrate myotendinous junctions (MTJs) has been postulated previously and MTJ structural abnormalities have been identified in the Dystrophin-deficient mdx mouse model, in vivo evidence of pathology based on muscle attachment failure has thus far been lacking. This zebrafish mutation may therefore provide a model for a novel pathological mechanism of Duchenne muscular dystrophy and other muscle diseases.
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Metadata
- Authors
- Bassett, D. I., Bryson-Richardson, R. J., Daggett, D. F., Gautier, P., Keenan, D. G., & Currie, P. D.
- Venue
- Development
- Publisher
- The Company of Biologists
- Published
- 2003-12-01
- Volume
- 130
- Issue
- 23
- Pages
- 5851-5860
- ISSN
- 0950-1991 (ISSN-L)
- 1477-9129
- OpenAlex
- W2018753432
- Cited by
- 270
- References
- 39
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- bronze
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