Muscular dysgenesis the role of calcium channels in muscle development.
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The regulation and action of myostatin as a negative regulator of muscle development during avian embryogenesis.
Myostatin is a potent inhibitor of muscle growth. Genetic deletion of Myostatin leads to massive hyperplasia and hypertrophy of skeletal muscle. However, the overall muscle pattern is preserved. We show that, during chick embryonic development, Myostatin is expressed at stages and positions unlikely to influence qualitative muscle development. In the somites, Myostatin is predominantly expressed in a central domain of the dermomyotome but not at the dorsomedial and ventrolateral lips, where most cells for myotomal elongation are recruited. During limb bud development, Myostatin is transiently expressed at early stages in both myogenic and nonmyogenic regions. Myostatin is reexpressed during limb bud development at a time when splitting of muscle is underway. Heterotopically developed wing buds that fail to form muscle still express Myostatin. This demonstrates that, in the limb, not all Myostatin-expressing cells are of myogenic origin. Ectoderm and Sonic hedgehog have different effects on the expression of Myostatin dependent on stages at which the operation was performed and the length of the postoperative period. Finally, we show that application of Myostatin protein into the developing limb bud results in a down-regulation of Pax-3 and Myf-5, both genes associated with proliferation of myogenic cells; and, furthermore, Myostatin also prevents the expression of MyoD, a gene associated with muscle differentiation. The long-term effect of Myostatin treatment leads to a deficiency of limb muscle. Therefore, Myostatin negatively affects gene expression of transcription factors, which are necessary for establishing myogenic cell identity.
Animals↗
Muscle development, insulin-like growth factor-I and myostatin mRNA levels in chickens selected for increased breast muscle yield.
Insulin-like growth factor-I (IGF-I) and myostatin (MSTN) are paracrine regulators of muscle growth. The present study was conducted to relate their expression with muscle fibre development in chickens selected for high breast meat yield and their controls. Both mRNA levels were measured by real-time RT-PCR in the Pectoralis major (PM) muscle between 14 days in ovo and 6 weeks post-hatch and in the Sartorius (SART) muscle between 2 and 6 weeks. The data show that PM growth was slow during in ovo development and rapid in the early post-hatch period. Chickens from the selected genotype exhibited significantly higher breast muscle yields from 2 to 6 weeks of age, and muscle fibre hypertrophy. In the PM, IGF-I and MSTN mRNA levels decreased markedly around hatch, while the IGF-I/MSTN ratio increased, suggesting that it could contribute to the explosive growth observed in the early post-hatch period. Between 4 and 6 weeks of age in selected chickens, IGF-I mRNA levels were significantly higher (p=0.04) with a similar trend in MSTN mRNA levels (p=0.07) in the PM muscle but not in the SART muscle. Our results support the hypothesis that the relative levels of IGF-I and MSTN mRNA may participate to set muscle growth rate along development, while other factors are required to explain differences between genotypes.
Animals↗
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↗
Role of calcineurin in striated muscle: development, adaptation, and disease.
Striated muscles, cardiac and skeletal muscles, use calcium as a second messenger to respond and adapt to environmental stimuli. Elevations in intracellular calcium activate calcineurin, a serine/threonine phosphatase, resulting in expression of a set of genes involved in remodeling striated muscle. Activation of calcineurin in hearts produces cardiac hypertrophy, and in skeletal muscle promotes cell differentiation and transforms fiber type specificity. In this review we discuss the effects of calcineurin activity on development, adaptation, and disease of striated muscle.
Adaptation, Physiological↗
A temporal map of transcription factor activity: mef2 directly regulates target genes at all stages of muscle development.
Dissecting components of key transcriptional networks is essential for understanding complex developmental processes and phenotypes. Genetic studies have highlighted the role of members of the Mef2 family of transcription factors as essential regulators in myogenesis from flies to man. To understand how these transcription factors control diverse processes in muscle development, we have combined chromatin immunoprecipitation analysis with gene expression profiling to obtain a temporal map of Mef2 activity during Drosophila embryonic development. This global approach revealed three temporal patterns of Mef2 enhancer binding, providing a glimpse of dynamic enhancer use within the context of a developing embryo. Our results provide mechanistic insight into the regulation of Mef2's activity at the level of DNA binding and suggest cooperativity with the bHLH protein Twist. The number and diversity of new direct target genes indicates a much broader role for Mef2, at all stages of myogenesis, than previously anticipated.
Animals↗
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↗
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↗
Mastophorus muris (Nematoda: Spirurina): Ultrastructure of somatic muscle development.
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Aging↗
Regulatory factors in the control of muscle development.
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Animals↗
Molecular analysis of gastrointestinal smooth muscle development.
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Animals↗
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↗
Effect of selection for growth rate on myosin heavy chain temporal and spatial localization during turkey breast muscle development.
The temporal and spatial localization of the heavy chain fast form of myosin was studied during turkey pectoralis major muscle development in a randombred control line (RBC2), a subline (F) of RBC2 selected only for increased 16-wk BW, a commercial sire line (B), and reciprocal crosses of the F and B lines. Pectoralis major muscle samples were obtained from three females and three males from each group in a manner to avoid contraction. After fixing and sectioning, the muscle samples were stained with a monoclonal antibody to determine the temporal and spatial localization of the heavy chain fast form of myosin. The percentage of muscle fibers at 25 d of incubation and 1 wk posthatch expressing the fast form of myosin heavy chain was calculated. The average percentage of muscle fibers expressing the fast form of myosin heavy chain for all genetic lines combined at embryonic d 25 for males was 76.1 and for females 66.6, whereas at 1 wk posthatch the average percentage for males was 24.2 and 36.1 for females. No interaction of sex and genetic group was noted at either age. At 25 d of embryonic development and at 1 wk of age, additive and nonadditive genetic effects were important in the inheritance of the fast form of myosin heavy chain. Heterosis was negative at both ages but significant at 1 wk of age. By 4 wk posthatch, all the muscle fibers in each genetic group were expressing the myosin heavy chain fast form, and no sex differences were observed. At 16 wk posthatch muscle fiber fragmentation was noted in the samples having reduced endomysial spacing. In the fragmenting muscle fiber areas, expression of the heavy chain fast form of myosin was observed. These muscle fiber changes were predominant in the growth selected F-line suggesting that growth selection may be associated with muscle damage.
Animal Husbandry↗
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↗
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↗
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↗
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↗
Response of broilers selected on carcass quality to dietary protein supply: live performance, muscle development, and circulating insulin-like growth factors (IGF-I and -II).
The effect of dietary protein supply on muscle development and circulating concentrations of insulin-like growth factors (IGF)-I and -II was examined in chickens selected for increased breast yield and decreased fatness (quality, QL) and in its control line (CL). CL and QL chickens were fed isoenergetic diets containing 121.5 or 215.8 g CP/kg during a 12-d period; comparisons were performed at 33 d of age. Birds given the high protein diet grew faster, ate less feed, had lower feed conversion ratio (FCR), and higher muscle weights than their counterparts given the low protein diet. The muscle weight response to protein supply differed between muscles in both lines, with pectoralis major appearing more sensitive than sartorius. The response of the gastrocnemius muscle depended on the line. Selection for carcass quality increased (P < 0.01) body weight, growth rate, feed intake, pectoralis major and sartorius muscle weights, and pectoralis major muscle proportion. There was, however, no line difference in FCR or in sartorius muscle proportion. The weight and proportion of the gastrocnemius muscle were higher (P < 0.05) in the QL than the CL chickens on the high protein diet, but there was no line difference for the low protein diet. Plasma levels of IGF-I, and to a lesser extent IGF-II, were lower (P < 0.01) in protein-restricted chickens. No difference in circulating IGF-II was observed between the lines. Concentrations of IGF-I were higher (P < 0.05) in QL than CL chickens, which may contribute to improved body composition for this genotype.
Animal Feed↗