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At least 163 records · Page 9Linked to original sources
PubMed1994

The expression pattern of contractile and intermediate filament proteins in developing skeletal muscle and rhabdomyosarcoma of childhood: diagnostic and prognostic utility.

In order to investigate whether rhabdomyosarcoma (RMS) can be related to equivalent stages of skeletal muscle development, muscle tissue of 21 human foetuses and 112 primary RMSs were characterized immunohistochemically using antibodies directed against vimentin, desmin, muscle-specific actin (HHF35), sarcomeric actin (sr-actin), smooth muscle actin (sm-actin), and troponin-T. During fetal skeletal muscle development, all myotubes/fibres of the first and second generations expressed desmin, HHF35, and sr-actin. Vimentin was almost exclusively present in immature primary and secondary myotubes/fibres. Troponin-T was expressed in immature myotubes/fibres of the first and second generations as well as mature fibres of the second generation. Sm-actin was never expressed. Vimentin was expressed in 96 per cent of primary and 98 per cent of relapsed RMS; HHF35 in 96 and 98 per cent, respectively; desmin in 95 and 100 per cent; troponin-T in 82 and 75 per cent; sr-actin in 71 and 86 per cent; and sm-actin in 13 and 17 per cent. The proportion of RMS cells reacting with vimentin, HHF35, and desmin was consistently higher than those expressing sr-actin and troponin-T. Neither the shape nor size of neoplastic RMS cells nor the histopathological types were related to the expression pattern of the investigated markers. RMS with aberrant expression of two or more markers predicted a worse prognosis than RMS in which at most one marker was aberrantly expressed (25 per cent and 54 per cent 10-year survival, P = 0.01). These results demonstrate that HHF35, desmin, sr-actin, and troponin-T have the potential to confirm the commitment of the tumours to the myogenic pathway which supports the diagnosis of RMS. However, it was impossible to relate RMS to equivalent stages of skeletal muscle development. Aberrant marker expression by RMS cells correlated significantly with patients' survival.

Actins↗
PubMed1996

Three zebrafish MEF2 genes delineate somitic and cardiac muscle development in wild-type and mutant embryos.

The zebrafish is an important experimental system for vertebrate embryology, and is well suited to the molecular analysis of muscle development. Transcription factors, such as the MEF2s, regulate skeletal and cardiac muscle-specific genes during development. We report the identification of three zebrafish MEF2 genes which, like their mammalian counterparts, encode factors that function as DNA-binding transcriptional activators of muscle specific promoters. The pattern of MEF2 expression in zebrafish defines discrete cell populations in the developing somites and heart and has mechanistic implications for developmental regulation of the MEF2 genes, when compared with other species. Alteration of MEF2 expression in two mutants affecting somitogenesis provides insight into the control of muscle formation in the embryo.

Amino Acid Sequence↗
PubMed1988

Shedding of cytoplasmic actins by developing muscle cells.

Young myotubes develop spots or macules of actin and alpha actinin under and adjacent to slender actin strands. Macules are found only before sarcomere formation. They contain cytoplasmic actin, small amounts of alpha actin, and alpha actinin but are devoid of tubulin, myosin and vimentin. In the electron microscope, they are seen to contain small filaments but no other organelles. Macules are found on the culture dish and in the culture medium, as well as on the lower and lateral surfaces of the cells. Both emetine and cycloheximide, at doses that inhibit protein synthesis, accelerate formation and shedding of macules. This presents the first observation of a cellular system in which the changeover from a generalized cytoskeleton to a tissue-specific cytoskeleton involves shedding of the cytoplasmic isoforms of cytoskeletal proteins.

Actins↗
PubMed1985

Muscle development in the grasshopper embryo. III. Sequential origin of the flexor tibiae muscle pioneers.

The flexor (FlTi) and extensor (ETi) tibiae are antagonist muscles located in the femur of the metathoracic leg of the grasshopper. Both are complex, consisting of an array of bundles of muscle fibers connecting the ectoderm of the wall of the femur with their respective apodemes. In the previous paper (E. E. Ball and C. S. Goodman, 1985, Dev. Biol. 111, 399-416) we described the embryonic development of the ETi muscle, focusing in particular on its syncytial origin from a giant supramuscle pioneer which later divides into an array of individual muscle pioneers. Here we describe the embryonic development of the FlTi muscle. In contrast to the development of the ETi muscle, the array of individual muscle pioneers for the FlTi does not have a syncytial origin but rather arises by sequential recruitment from the mass of smaller, undifferentiated mesoderm cells. The FlTi MPs first appear as two cells symmetrically placed on the corners of the FlTi apodeme at around 37%. A third MP is then added between these two; this third MP later dies. Subsequent growth occurs by symmetrical addition of MPs distally along the sides of the developing apodeme and by enlargement of the individual MPs. Initially each MP contains only a single nucleus; by about 50% there are at least two to three nuclei per MP and each is surrounded by a cluster of smaller, undifferentiated mesoderm cells. Each MP develops into a bundle of muscle fibers by a cycle of fusion and division. The individual mesoderm cells surrounding each MP fuse with it starting at about 60%. At the same time, the large MP begins to divide into smaller muscle fibers.

Animals↗
PubMed1997

Ectopic expression of MEF2 in the epidermis induces epidermal expression of muscle genes and abnormal muscle development in Drosophila.

Myocyte-specific enhancer-binding factor 2 (MEF2) is a myogenic regulatory factor in vertebrates and Drosophila. Whereas the role of MEF2 in regulating vertebrate myogenesis and muscle genes has been extensively studied, little is known of the role of MEF2 in regulating Drosophila myogenesis. We have shown in a recent analysis of the regulation of the Drosophila Tropomyosin I (TmI) gene in transgenic flies that MEF2 is a positive regulator of TmI expression in the somatic body-wall muscles of embryos, larvae, and adults. To understand further the role of MEF2 in myogenesis and test the role of MEF2 in regulating TmI expression, we have used the yeast GAL4/UAS system to generate embryos in which MEF2 is ectopically expressed in tissues where it is not normally expressed or embryos in which MEF2 is overexpressed in the mesoderm and muscles. We observe that ectopic expression of MEF2 in the epidermis and the ventral midline cells in embryos activates the expression of TmI and other muscle genes in these tissues and that this activation is stage-dependent suggesting a requirement for additional factors. Furthermore, ectopic expression of MEF2 in the epidermis results in a decrease in the expression of signaling molecules in the epidermis and a failure of the embryo to properly form body-wall muscles. These results indicate that MEF2 can function out of context in the epidermis to induce the expression of muscle genes and interfere with a requirement for the epidermis in muscle development. We also find that the level of MEF2 in the mesoderm and/or muscles in embryos is critical to body-wall muscle formation; however, no effect is observed on the development of the visceral muscle or dorsal vessel.

Animals↗
PubMed2001

Regulation of myosin heavy chain expression during rat skeletal muscle development in vitro.

Signals that determine fast- and slow-twitch phenotypes of skeletal muscle fibers are thought to stem from depolarization, with concomitant contraction and activation of calcium-dependent pathways. We examined the roles of contraction and activation of calcineurin (CN) in regulation of slow and fast myosin heavy chain (MHC) protein expression during muscle fiber formation in vitro. Myotubes formed from embryonic day 21 rat myoblasts contracted spontaneously, and approximately 10% expressed slow MHC after 12 d in culture, as seen by immunofluorescent staining. Transfection with a constitutively active form of calcineurin (CN*) increased slow MHC by 2.5-fold as determined by Western blot. This effect was attenuated 35% by treatment with tetrodotoxin and 90% by administration of the selective inhibitor of CN, cyclosporin A. Conversely, cyclosporin A alone increased fast MHC by twofold. Cotransfection with VIVIT, a peptide that selectively inhibits calcineurin-induced activation of the nuclear factor of activated T-cells, blocked the effect of CN* on slow MHC by 70% but had no effect on fast MHC. The results suggest that contractile activity-dependent expression of slow MHC is mediated largely through the CN-nuclear factor of activated T-cells pathway, whereas suppression of fast MHC expression may be independent of nuclear factor of activated T-cells.

Animals↗
PubMed1995

Posthatching growth and pectoralis muscle development in broiler strain chickens, bantam chickens and the reciprocal crosses between them.

Body weight, pectoralis muscle weight, pectoralis protein and DNA concentration, and plasma GH and IGF-I concentrations of broiler chicks (BrBr), bantam chicks (BaBa) and reciprocal crosses between them (BaBr and BrBa) were measured between 0 and 42 days after hatching. At hatch, body weight and pectoralis weight of the two types of chicks from broiler eggs (BrBr and BaBr) were equal to each other but greater than the two types of chicks from bantam eggs (BaBa and BrBa), which were not different from each other. BrBr chicks grew more rapidly than crossbreds and BaBa chicks grew more slowly. Weights of the reciprocal crosses (BaBr and BrBa) were markedly different at day of age, but converged by day 14. The increase in pectoralis muscle mass of BrBr chicks exceeded that of the reciprocal crosses which in turn exceeded that of BaBa chicks. The increase in pectoralis DNA content and protein content followed the same pattern. The DNA unit size, as expressed by the protein:DNA ratio, was markedly lower in pure bantam chicks from 14 to 42 days of ages, whereas the unit size did not differ between the intermediate sized reciprocal crosses and the large bodied broiler chicks. Differences in muscle mass were primarily achieved by differences in the number of DNA units although a difference in unit size was also a factor. There were no clear relationships between growth and plasma growth hormone or insulin-like growth factor I concentrations. Thus while satellite cell proliferation is primarily responsible for genotypic differences in muscle mass, the plasma growth hormone-IGF-I axis does not appear to be regulating their proliferation.

Age Factors↗
PubMed1996

Uncoupling of Grb2 from the Met receptor in vivo reveals complex roles in muscle development.

Hepatocyte growth factor (HGF) and its receptor, the Met tyrosine kinase, are determinants of placenta, liver, and muscle development. Here, we show that Met function in vivo requires signaling via two carboxy-terminal tyrosines. Mutation of both residues in the mouse genome caused embryonal death, with placenta, liver, and limb muscle defects, mimicking the phenotype of met null mutants. In contrast, disrupting the consensus for Grb2 binding allowed development to proceed to term without affecting placenta and liver but caused a striking reduction in limb muscle coupled to a generalized deficit of secondary fibers. These data show that the requirements for Met signaling vary depending on the tissue and reveal a novel role for HGF/ Met in late myogenesis.

Adaptor Proteins, Signal Transducing↗
PubMed1975

Physiological properties of junctions between nerve and muscle developing during salamander limb regeneration.

1. Physiological properties of developing nerve-muscle junctions were studied in regenerating limbs of adult salamanders. 2. During the period of synapse formation the muscle fibres had diameters of 4-10 mum, resting potentials of minus 90 to minus 100 mV and input resistances of 10-50 Momega. Some, but not all, pairs of adjacent muscle fibres were electrically coupled. 3. At the stage when muscle fibres could first be identified, some of them were not innervated, at least as determined by electrophysiological criteria. 4. During muscle innervation the neuromuscular synapses were encountered in several intermediate phases of maturity. (i) At the least mature junctions small spontaneous synaptic potentials occurred, but stimulation of the motor nerve trunk did not evoke synchronous transmitter release. (ii) At other junctions maximal nerve stimulation evoked only a single end-plate potential of low quantum content. (iii) More mature fibres received synaptic input from as many as four motor neurons, which could be distinguished by their discrete stimulus thresholds. 5. During this period of synapse development the fibres lacked an action potential but often showed a prolonged response to depolarization. 6. Fibres in normal adult muscles had from one to three synaptic inputs, were not electrically coupled, and responded to depolarization with an action potential.

Action Potentials↗
PubMed1998

Expression of myogenic regulatory factors during muscle development of Xenopus: myogenin mRNA accumulation is limited strictly to secondary myogenesis.

To clarify the acquisition of the adult muscle pattern in Xenopus laevis, in situ hybridization and reverse transcriptase-polymerase chain reaction were used to correlate the time course of gene expression for myogenic regulatory factors (Myf-5, MyoD, and myogenin) with the expression of contractile protein (myosin heavy chain; MHC) genes during hindlimb formation compared with their expression in dorsal body muscles. After the precocious expression of Myf-5 and MyoD mRNA in limb bud (stage 50), myogenin mRNA strongly accumulated later at paddle stages (stages 52/53) concomitantly with the accumulation of both the larval and the adult MHC mRNAs. In dorsal body muscles, as early as stage 52, myogenin transcripts accumulated in a few small, secondary myofibers expressing the adult MHC mRNA that were located along the dorsomedial edge, but they were never detected in the large, primary myofibers of the body expressing the larval MHC mRNA. During metamorphosis, the areas expressing both the adult MHC and the myogenin transcripts gradually expanded from the dorsomedial edge to the ventral side of the dorsal body muscles, accounting for the progression of the secondary "adult" myogenesis described previously (Nishikawa and Hayashi [1994] Dev. Biol. 165:86-94). This work shows that, in Xenopus, the accumulation of myogenin mRNA is restricted to secondary myogenesis, including the formation of new muscles in developing limbs as well as in dorsal muscles during body remodeling. This shows that myogenin is not required for primary myogenesis, and it suggests a crucial role for myogenin in the terminal differentiation program, including myoblast fusion and the activation of adult-type muscle genes.

Animals↗
PubMed1993

The Splotch mutation interferes with muscle development in the limbs.

Homozygosity for the Splotch mutation causes neural tube and neural crest defects in mice. It has been demonstrated that Splotch mutant mice carry mutations in the homeodomain of the Pax-3 gene. Pax-3 is expressed in the neural tube, some neural crest derivatives, the mesenchyme of the limb bud and the somites. We have examined the development of the somite-derived skeletal muscles in homozygotes carrying the Splotch (Sp1H) mutation. Our results suggest that the Splotch mutation affects the development of skeletal muscles in a region-specific way: 1. The expression of the CMZ transgene in homozygotes reveals a disorganisation of the dermomyotome in whole stained embryos. 2. The axial musculature is reduced in size along a rostro-caudal gradient. 3. The muscle anlagen in the limbs develop much more slowly. Muscles of the head and the ventral body wall are normally developed in the mutant on day 13.5 of gestation. Recently, it has been shown that the myogenic precursors of the limbs are derived from the lateral half of the somite. The specific disturbance of muscle development in the limbs of Splotch mutants thus suggests a role for Pax-3 in the organisation of the somite, the production of trophic factors in the limb mesenchyme or an alteration of myogenic and mesenchymal cells.

Animals↗
PubMed1997

Opposing effects of activin A and follistatin on developing skeletal muscle cells.

Activin and the activin-binding protein follistatin modulate a variety of biological processes and are abundant at sites of muscle development. Activin and follistatin were expressed in developing chick pectoral muscle in vivo and in primary cell culture. Addition of recombinant activin inhibited muscle development in a dose-dependent manner as measured by the number of nuclei in myosin heavy chain positive cells and creatine phosphokinase activity. Conversely, follistatin potentiated muscle development. The effects of activin were found to be distinct from those of the related protein transforming growth factor (TGF) beta1. Muscle development was repressed by activin at all time points investigated and did not recover with the removal of activin following a limited exposure. In contrast, while myogenic differentiation in TGFbeta1 was initially repressed, muscle marker expression recovered to control levels--even in the continued presence of TGFbeta1. Fibroblast growth factor (FGF) had little effect on inhibiton of muscle development caused by activin A. However, inhibition of development produced by TGFbeta increased with increasing concentrations of FGF. Finally, early expression of myoD and myf5 mRNA by muscle cultures in the presence of activin and follistatin was analyzed. Activin-treated cultures expressed reduced myoD and myf5 levels at 1.5 days after plating. Myf5 levels in follistatin-treated cultures were elevated, but, surprisingly, these cultures showed a reduction in myoD levels. These data suggest that endogenously expressed activin and follistatin are important modulators of muscle development.

Activins↗
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↗