Expression of myosin heavy chain isoforms and myogenesis of intrafusal fibres in rat muscle spindles
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
- MeSH
- Immunoenzyme Techniques MeSH
- Isoenzymes metabolism MeSH
- Muscle Fibers, Skeletal cytology metabolism MeSH
- Muscle, Skeletal cytology growth & development innervation metabolism MeSH
- Rats MeSH
- Morphogenesis MeSH
- Myosins biosynthesis metabolism MeSH
- Neurons, Efferent physiology MeSH
- Muscle Development MeSH
- Hindlimb MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Isoenzymes MeSH
- Myosins MeSH
This review concerns the pattern of expression and regulation of myosin heavy chain (MHC) isoforms in intrafusal fibres of rat muscle spindles detected by immunocytochemistry. The three types of intrafusal fibres--nuclear bag1, nuclear bag2, and nuclear chain fibres--are unique in co-expressing several MHCs including special isoforms such as slow tonic and alpha cardiac-like MHC and isoforms typical of muscle development, such as embryonic and neonatal MHC. The distinct intrafusal fibre types appear sequentially during rat hind limb development, the nuclear bag2 precursors being first identifiable at 17-18 days in utero as the only primary myotubes expressing slow tonic MHC. Sensory innervation is required for the expression of "spindle-specific" MHC isoforms. Motor innervation contributes to the diversity in distribution of the different MHCs along the length of the nuclear bag fibres. It is suggested that unique populations of myoblasts are destined to become intrafusal fibres during development in the rat hind limb muscles and that the regional heterogeneity in MHC expression is related both to sensory and motor innervation and to the properties of the myoblast lineages. These distinct features make intrafusal fibres an attractive in situ model for investigating myogenesis, myofibrillogenesis, and the mechanisms regulating MHC expression.
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