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PubMed1999

Red muscle development of gilthead sea bream Sparus aurata (L.): structural and ultrastructural morphometry.

The transverse red and white muscle area, the superficial red muscle fibres area and their percentages of mitochondria (%mit), myofibrils (%myof) and sarcoplasm (%sarc) were determined in the Mediterranean teleost gilthead sea bream, Sparus aurata (L.). Fish aged from hatching to 78 days were studied. The proportional growth of the red and white muscles was higher for the red muscle in the first half of the larval stage (1-35 days). Then the opposite relationship was observed. The hypertrophic growth of the superficial muscle fibres was continuous except in the first week after hatching. The percentage of mitochondria and percentage of myofibrils showed a significant change just after the half of the larval stage. Whereas the %mit of the superficial muscle fibres was higher than %myof from the first week after hatching to 35 days (average 66.64%), then the %mit decreased significantly and at 73-78 days both parameters were close to an average value of 50%. The meaning of these morphological changes is discussed in relation to the functional role of the red muscle of larvae and the onset of the gills respiration.

Aging↗
PubMed1981

Muscle development in the human fetus as exemplified by m. sartorius: a quantitative study.

M. sartorius was removed from 21 human fetuses ranging from 7.0 to 35.0 cm crown-rump length (CR). Various gross amd cellular changes (as seen in a transverse section) which take place in developing human skeletal muscle were quantified. The weights, lengths and cross sectional areas (at mid-length level) of m. sartorius were found to exhibit allometric relationship with CR and body weight (BW). Initially (7.5 cm CR) myotubes were more numerous and larger (40 micrometer 2 cross sectional area) than the myofibres (about 26 micrometer 2). This situation was soon reversed, however, so that at about 19 cm CR myotubes were only a very small proportion of the total muscle cell population and somewhat smaller than the myofibres in cross sectional area. At about 21 cm CR all myotube appearance was lost, whilst the total number of myofibres increased rapidly up to about 22.5 cm CR, and thereafter the rate slowed down. This stage (22.5 cm CR) seemed, in fact, to be about the time when hypertrophy of myofibres started to markedly replace hyperplasia as the main factor contributing to total muscle cross sectional area increase, although there was still a 6% contribution from hyperplasia at 35 cm CR. At 18 to 22 cm CR there were no more myofibres in the smallest size class (2-3 micrometer diameter). This may be an indication that real hyperplasia had ceased at this point so that beyond this the hyperplasia seen was only apparent and represented longitudinal growth of existing myofibres. Throughout the period studied the amount of intercellular space decreased (at a declining rate) from about 62% at 7 cm CR to about 21% at 35 cm CR. Results on counts of nuclei suggested that total muscle nuclear proliferation slowed down in later gestation. Myofibril number was not related to myotube size but increased, though at a declining rate, with myofibre size. All the muscle parameters mentioned were plotted against CR, and sometimes BW, and regression equations given wherever possible.

Body Weight↗
PubMed1996

Combinatorial control of muscle development by basic helix-loop-helix and MADS-box transcription factors.

Members of the MyoD family of muscle-specific basic helix-loop-helix (bHLH) proteins function within a genetic pathway to control skeletal muscle development. Mutational analyses of these factors suggested that their DNA binding domains mediated interaction with a coregulator required for activation of muscle-specific transcription. Members of the myocyte enhancer binding factor 2 (MEF2) family of MADS-box proteins are expressed at high levels in muscle and neural cells and at lower levels in several other cell types. MEF2 factors are unable to activate muscle gene expression alone, but they potentiate the transcriptional activity of myogenic bHLH proteins. This potentiation appears to be mediated by direct interactions between the DNA binding domains of these different types of transcription factors. Biochemical and genetic evidence suggests that MEF2 factors are the coregulators for myogenic bHLH proteins. The presence of MEF2 and cell-specific bHLH proteins in other cell types raises the possibility that these proteins may also cooperate to regulate other programs of cell-specific gene expression. We present a model to account for such cooperative interactions.

Amino Acid Sequence↗
PubMed1985

Myosin switches in skeletal muscle development of an urodelan amphibian, Pleurodeles waltlii. Comparison with a mammalian, Mus musculus.

The isomyosins from dorsal axial muscle, which appear successively through metamorphosis of P.waltlii, are shown to be composed of identical fast-type light chains but of distinct heavy subunits. We observe that this modification goes with a change in ATPase activity as also in the case of mouse. Metamorphosis in amphibian as well as birth in mammalian are thus both accompanied by the synthesis of new myosins of higher catalytic efficiency.

Animals↗
PubMed1994

Genetic analysis of the Drosophila single-minded gene reveals a central nervous system influence on muscle development.

The Drosophila single-minded gene is expressed in the embryonic central nervous system midline cells and plays a critical role in central nervous system development. Additional expression of single-minded is found in a subset of ventral muscle precursor cells. Null mutations of single-minded result in an alteration of the ventral oblique muscles, such that muscle fibers form inside the embryo above the central nervous system. This defect is due to the mislocalization of a subset of mesodermal precursor cells. The muscle defect observed in single-minded null mutations is not due to the absence of single-minded expression in muscle precursor cells and likely results from an influence of the central nervous system on ventral muscle development.

Animals↗
PubMed1995

The inositol 1,4,5-triphosphate receptor expression in Drosophila suggests a role for IP3 signalling in muscle development and adult chemosensory functions.

Inositol 1,4,5-triphosphate (IP3) is generated as a second messenger in many diverse cellular signalling pathways. In general these signalling pathways activate a membrane-bound phospholipase C, which cleaves the phospholipid phosphatidylinositol bisphosphate to generate IP3 and diacylglycerol. IP3 binds to a specific intracellular receptor, which is a membrane protein and a ligand-gated Ca2+ channel, that causes Ca2+ release from intracellular stores. The inositol 1,4,5-triphosphate receptor (IP3R) is thus an integral part of the IP3 signalling pathway and can be used as a marker to identify biological processes that use IP3 as a second messenger. We have used an affinity-purified antibody, directed against a bacterial fusion protein and containing 339 amino acids of the Drosophila IP3R, to detect this protein in adult heads and during embryonic and pupal development. Our results suggest that in Drosophila the IP3 signalling pathway is used during muscle development, primarily when myoblasts undergo rapid multiplication, in both embryos and pupae. In adults, IP3 is probably a second messenger in more than one sensory transduction pathway, as well as in other as yet undefined brain and muscle functions.

Animals↗
PubMed1986

The earliest form of C-protein expressed during striated muscle development is immunologically the same as cardiac-type C-protein.

A monoclonal antibody (C-315) specific for cardiac-type C-protein was prepared and, in combination with other antibodies specific for fast and slow skeletal muscle C-proteins, it was used to investigate the expression of C-protein isoforms in developing striated muscle cells in vivo and in vitro. During embryonic development of skeletal muscles, a C-protein recognized by C-315 appeared first but only transiently, it being replaced subsequently by two other isoforms recognized by the antibodies to slow and fast skeletal muscle C-proteins in a fiber-type specific manner as previously demonstrated (Obinata et al. (1984) Develop. Biol. 101, 116-124). In contrast, only cardiac-type C-protein was detected in cardiac muscle throughout the developmental stages. When myogenesis in vitro was monitored using the same antibodies, C-315 binding appeared first in multinucleated myotubes as in vivo which was followed by the sequential expression of two other C-protein variants. The reactivity of C-315 as well as that of anti-slow and anti-fast skeletal C-protein antibodies persisted during muscle development in culture. Thus, this study demonstrates that the earliest form of C-protein expressed in striated muscles may either be a cardiac-type isoform or a unique embryonic protein containing an epitope in common with the adult cardiac-type protein, and that transitions of C-protein isoform expression characteristic of each fiber-type occur during muscle development in vivo but not in vitro.

Animals↗
PubMed1990

Junctional acetylcholine receptor channel open time is not presynaptically regulated in developing muscle.

The role of motor innervation in controlling the development of acetylcholine receptor (AChR) channel open time was tested by examining synaptic current durations in transplanted muscles of Xenopus tadpoles. The presumptive lower jaw region, which gives rise to the interhyoideus muscle, was transplanted to the tail, overlying the myotomal muscle cells. The transplanted muscles became innervated, presumably by spinal nerves which normally innervate myotomal muscle. Despite development in the presence of foreign innervation, synaptic currents in the transplanted interhyoideus were predominantly long in duration and resembled those in the normally innervated interhyoideus. They did not resemble those in the myotomal muscle, where synaptic currents are brief. The apparent lack of neural influence on development of AChR function in muscle contrasts with the evidence for presynaptic control of AChR open time in frog sympathetic ganglia. This may reflect a fundamental difference between nerve and muscle in the regulation of postsynaptic function.

Animals↗
PubMed1998

Muscle development: electrical control of gene expression.

The electrical activity resulting from stimulation by motor neurons regulates gene expression in skeletal muscle fibres. A recent study has suggested a mechanism by which distinct patterns of electrical stimulus might be integrated to control the contractile properties of these fibres.

Animals↗
PubMed1985

Specific regulation of N-CAM/D2-CAM cell adhesion molecule during skeletal muscle development.

The expression of the N-CAM/D2-CAM cell adhesion molecule was studied in skeletal muscle. In cell cultures derived from adult human muscle N-CAM/D2-CAM was found at the cell surface of myoblasts and myotubes but not fibroblasts, showing that N-CAM/D2-CAM is a specific gene product of muscle. Western blots showed that the anti N-CAM/D2-CAM antibody reacted with a single protein band of 180 000 daltons in these cultures that differed in mobility from the broad band of 150 000-200 000 daltons found in brain. N-CAM/D2-CAM is also expressed by muscle at certain stages of development. Human foetal muscle of 10 and 20 weeks gestation showed N-CAM/D2-CAM around developing myofibres while both fast and slow adult muscle fibres did not express N-CAM/D2-CAM, suggesting that the protein is down regulated during myofibre maturation. This was studied further in developing rat muscle where N-CAM/D2-CAM was found on myofibres in the day 1 neonate, but had disappeared by day 9. N-CAM/D2-CAM is, however, re-expressed in human muscle disease where there is muscle regeneration such as in polymyositis, and here is associated with classic regenerating myofibres. N-CAM/D2-CAM expression is temporally regulated and is expressed only at times of synapse formation consistent with the idea that it may be involved in early nerve-muscle interactions.

Antigens, Surface↗
PubMedDate not supplied

Muscle development in mdx mutant mice.

Mechanical and contractile properties of tibialis anterior (TA) muscles from X-linked muscular dystrophic (mdx) mutant mice at different stages of development are compared to those of muscles from normal control animals. There is no difference between the tension output, speeds of contraction and relaxation, and weight of TA muscles from mutant adults and normal control animals. However, it is found that in 3-4-week-old mutant animals, tension output and muscle weight are very much reduced, and half relaxation time is prolonged. Thus, during this stage of development, muscles from mdx mice do not function properly. Histological examination of these muscles provides further evidence that, in these animals, rapid muscle destruction occurs at a particular time of development and that it is followed by complete recovery. This new mutant therefore presents an interesting case of muscle destruction and rapid regeneration. However, it is not an adequate model for Duchenne muscular dystrophy.

Animals↗
PubMed1994

Cardiac phenotypic markers expressed in early stages of both cardiac and skeletal muscle development.

We have examined changes in the expression of chicken myosin heavy chain (MHC) mRNAs in the heart and skeletal muscles during normal development and in regenerating adult muscles. cDNA clones isolated from adult heart and regenerating skeletal muscle libraries revealed more than 98% sequence homology in the 3' untranslated regions. Using specific cDNA probes we have detected ventricular MHC transcripts in the heart and in early developmental stages of fast as well as slow skeletal muscles. The expression of ventricular MHC mRNA in skeletal muscles is especially significant since, in contrast to mammals, the avian ventricular and slow MHC mRNAs are encoded by different genes.

Animals↗
PubMed2000

Biogenesis of giant mitochondria during insect flight muscle development in the locust, Locusta migratoria (L.). Transcription, translation and copy number of mitochondrial DNA.

The biogenesis of giant mitochondria in flight muscle of Locusta migratoria (L.) was analyzed at the molecular level. During the 2 weeks between the beginning of the last larval stage and the imago capable of sustained flight, individual mitochondria have been shown to enlarge 30-fold and the fractional mitochondrial volume of muscle cells increases fourfold [Brosemer, R.W., Vogell, W. and Bücher, Th. (1963) Biochem. Z. 338, 854-910]. Within the same period, the activity of cytochrome c oxidase, containing subunits encoded on mitochondrial DNA, increased twofold. However, no significant change in mitochondrial DNA copy number, and even a threefold decrease in mitochondrial transcripts, was observed. Mitochondrial translation rate, measured in isolated organelles, was twofold higher in larval muscle, which can be explained only partly by the higher content of mitochondrial RNAs. Thus, rather unusually, in this system of mitochondrial differentiation, the mitochondrial biosynthetic capacity correlates with the rate of organelle biogenesis rather than the steady-state concentration of a marker enzyme. The copy number of mitochondrial DNA does not seem to play a major role in determining either mitochondrial transcript levels or functional mass.

Animals↗
PubMed1992

Inactivation of MyoD in mice leads to up-regulation of the myogenic HLH gene Myf-5 and results in apparently normal muscle development.

The myogenic basic HLH transcription factor family of genes, composed of MyoD, myogenin, Myf-5, and Myf-6, are thought to regulate skeletal muscle differentiation. To understand the role of MyoD in myogenesis, we have introduced a null mutation of MyoD into the germline of mice. Surprisingly, mice lacking MyoD are viable and fertile. Histological examination of skeletal muscle failed to reveal any morphological abnormalities in these mice. Furthermore, Northern analysis revealed normal levels of skeletal muscle-specific mRNAs. Significantly, Myf-5 mRNA levels are elevated in postnatal mutant mice. Normally, Myf-5 expression becomes markedly reduced at day 12 of gestation when MyoD mRNA first appears. This suggests that Myf-5 expression is repressed by MyoD. Our results indicate that MyoD is dispensable for skeletal muscle development in mice, revealing some degree of functional redundancy in the control of the skeletal myogenic developmental program.

Animals↗