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PubMed1993

Myosin expression in semitendinosus muscle during fetal development of cattle: immunocytochemical and electrophoretic analyses.

The pattern of expression of different types of myosin and the development of different muscle cell populations were studied in the semitendinosus muscle of cattle from 39 d of gestation to 30 d of post-natal life. Monoclonal antibodies specific to different myosin heavy chains were used. Two cell generations were identified during myogenesis. They appeared successively and were characterized by different patterns of expression of myosins. The first population, which was present from the first stage studied (39 d of gestation), gave rise to type I fibers, which, in the mature animal, express only slow myosin. A second generation became differentiated at about 120 d of fetal life and then developed into type II fibers (IIa, IIb or IIc). The beginning of differentiation was characterized in all the cell populations by the expression of specific types of embryonic or fetal myosins. A comparison of these results with findings from previous works shows a marked similarity between species in the pattern of myogenesis but great differences in the length of the different stages of development. In this respect, myogenesis in cattle closely resembles that in man.

Animals↗
PubMed1988

Regulation of acetylcholine receptor channel function during development of skeletal muscle.

The nicotinic acetylcholine (ACh) receptor channel mediates synaptic transmission at the neuromuscular junction. During the development of skeletal muscle, ACh receptors undergo changes in distribution, antigenic determinants, degradation rate, and function. Now that these developmental hallmarks have been identified, attention has turned toward understanding both the structural bases for such changes and the role of nerve in triggering these changes. Recently, a much clearer understanding of one of these developmental processes, namely, the alterations in channel function, has emerged through both sensitive patch-clamp measurements and the application of recombinant DNA technology. In light of these new advances, we now reevaluate the processes governing the developmental changes in the functional properties of the ACh receptor.

Electric Conductivity↗
PubMed1991

A sensitive period in gestation for nicotine acceleration of neuromuscular maturation.

Nicotine, administered to pregnant Sprague-Dawley rat dams during gestation, altered the maturation of the developing extensor digitorum longus (EDL) muscle-peroneal nerve complex of the 2-week-old offspring. Initial isometric twitch time to peak and rate of rise of tension and tetanus time to peak tension of the group treated with nicotine during gestational (G) days G3-G8 were faster than controls indicating accelerated maturation of EDL muscle. Contractile parameters of the group treated with nicotine during G9-G13, a period immediately prior to muscle innervation, differed little from control. Nicotine administered during G14-G21 significantly increased twitch and tetanus tension and twitch rate of rise. There was little to no effect on motor unit size or number of motor units with nicotine during any of the three prenatal periods. Thus, while late prenatal nicotine administration primarily altered the strength of muscle, early gestational administration of nicotine increased the rate of muscle development suggesting a possible sensitive period for the accelerative action of nicotine on muscle maturation at this time.

Animals↗
PubMed2001

Insulin-like growth factor-mediated muscle differentiation: collaboration between phosphatidylinositol 3-kinase-Akt-signaling pathways and myogenin.

The differentiation and maturation of skeletal muscle require interactions between signaling pathways activated by hormones and growth factors and an intrinsic regulatory network controlled by myogenic transcription factors. Insulin-like growth factors (IGFs) play key roles in muscle development in the embryo and in regeneration in the adult. To study mechanisms of IGF action in muscle, we developed a myogenic cell line that overexpresses IGF-binding protein-5. C2BP5 cells remain quiescent in low serum differentiation medium until the addition of IGF-I. Here we use this cell line to identify signaling pathways controlling IGF-mediated differentiation. Induction of myogenin by IGF-I and myotube formation were prevented by the phosphatidylinositol (PI) 3-kinase inhibitor, LY294002, even when included 2 days after growth factor addition, whereas expression of active PI 3-kinase could promote differentiation in the absence of IGF-I. Differentiation also was induced by myogenin but was blocked by LY294002. The differentiation-promoting effects of IGF-I were mimicked by a modified membrane-targeted inducible Akt-1 (iAkt), and iAkt was able to stimulate differentiation of C2 myoblasts and primary mouse myoblasts incubated with otherwise inhibitory concentrations of LY294002. These results show that an IGF-regulated PI 3-kinase-Akt pathway controls muscle differentiation by mechanisms acting both upstream and downstream of myogenin.

Animals↗
PubMed2000

Lbx1 is required for muscle precursor migration along a lateral pathway into the limb.

In mammalian embryos, myogenic precursor cells emigrate from the ventral lip of the dermomyotome and colonize the limbs, tongue and diaphragm where they differentiate and form skeletal muscle. Previous studies have shown that Pax3, together with the c-Met receptor tyrosine kinase and its ligand Scatter Factor (SF) are necessary for the migration of hypaxial muscle precursors in mice. Lbx1 and Pax3 are co-expressed in all migrating hypaxial muscle precursors, raising the possibility that Lbx1 regulates their migration. To examine the function of Lbx1 in muscle development, we inactivated the Lbx1 gene by homologous recombination. Mice lacking Lbx1 exhibit an extensive loss of limb muscles, although some forelimb and hindlimb muscles are still present. The pattern of muscle loss suggests that Lbx1 is not required for the specification of particular limb muscles, and the muscle defects that occur in Lbx1(-/-) mice can be solely attributed to changes in muscle precursor migration. c-Met is expressed in Lbx1 mutant mice and limb muscle precursors delaminate from the ventral dermomyotome but fail to migrate laterally into the limb. Muscle precursors still migrate ventrally and give rise to tongue, diaphragm and some limb muscles, demonstrating Lbx1 is necessary for the lateral, but not ventral, migration of hypaxial muscle precursors. These results suggest that Lbx1 regulates responsiveness to a lateral migration signal which emanates from the developing limb.

Animals↗
PubMed1995

Calcitonin gene-related peptide (CGRP) in the developing mouse limb.

The mitogenic effects of neuropeptides and their localization to developing tissues suggest an important role for these peptides during gestation. We examined the expression and action of the neuropeptide calcitonin gene-related peptide (CGRP) in the developing mouse limb bud, an excellent model system for studying musculoskeletal development. CGRP immunoreactivity (CGRP-ir) was detected in the developing limb at day 16.5 of gestation (E 16.5) and was limited to nerve fibers surrounding blood vessels, within the developing muscle or in close proximity to the developing cartilaginous skeleton. Although CGRP-ir was not observed until E 16.5, limb buds were responsive to CGRP as early as E 11.5. Within 5 min of exposure to CGRP (10(-8) to 10(-7) M) a 2--3-fold increase in cyclic AMP (cAMP) levels was observed. This CGRP-induced increase in cAMP was abolished by the addition of human CGRP8-37, a CGRP receptor antagonist. This result suggests that the effect on cAMP was mediated by the interaction of CGRP with CGRP receptors. Our findings indicate that mouse limbs are responsive to CGRP when they are composed of primarily undifferentiated mesenchyme and that CGRP-ir appears at a later stage of development in association with cartilage and muscle differentiation.

Animals↗
PubMed1983

Quantitative regulation of acetylcholinesterase development in the muscle lineage cells of cleavage-arrested ascidian embryos.

Some embryos of Ciona intestinalis which were permanently cleavage-arrested with cytochalasin B at the 1-cell, 4-cell, or 8-cell stages produced, after 12 or 16 h of development time (18 degrees C), a level of muscle acetylcholinesterase activity equal to that found in normal early and later larval stage embryos of the same age. Enzyme activity was measured quantitatively in single whole embryos by a colorimetric procedure using microdensitometry. Quantitative regulation of a differentiation end product indicated that the usual transcriptional and translational control mechanisms for that histospecific protein continued to operate normally in the cleavage-arrested embryos. Acetylcholinesterase expression was apparently regulated independently of the usual cell cytoplasmic volume in the muscle lineage cells and possibly also independently of the normal nuclear number in the lineage. There is an egg cytoplasmic determinant that is segregated into the muscle lineage cells during cleavage and which appears to specify the pathway of larval muscle development. Quantitative control of muscle acetylcholinesterase is possibly one of the consequences of how the agent releases genetic expression in the presumptive muscle cells. Quantitative regulation was not, however, a general functional activity of cleavage-arrested embryos. Mitochondrial cytochrome oxidase, an enzyme whose development is believed to be unaffected by cytoplasmic determinants, was not regulated quantitatively in cleavage-arrested embryos. Cytochrome oxidase activity of cleavage-arrested embryos, measured in single whole embryos by a colorimetric microdensitometry assay, increased only slightly during 16 h of development time whereas the activity in normal control embryos doubled during that time.

Acetylcholinesterase↗
PubMed1969

The histogenesis of rat intercostal muscle.

Intercostal muscle from fetal and newborn rats was examined with the electron microscope. At 16 days' gestation, the developing muscle was composed of primary generations of myotubes, many of which were clustered together in groups. Within these groups, the membranes of neighboring myotubes were interconnected by specialized junctions, including tight junctions. Morphologically undifferentiated cells surrounded the muscle groups, frequently extended pseudopodia along the interspace between adjacent myotubes, and appeared to separate neighboring myotubes from one another. At 18 and 20 days' gestation, the muscle was also composed of groups of cells but the structure of the groups differed from that of the groups observed at 16 days. Single, well differentiated myotubes containing much central glycogen and peripheral myofibrils dominated each group. These large cells were interpreted as primary myotubes. Small, less differentiated muscle cells and undifferentiated cells clustered around their walls. Each cluster was ensheated by a basal lamina. The small cells were interpreted as primordia of new generations of muscle cells which differentiated by appositional growth along the walls of the large primary myotubes. All generations of rat intercostal muscle cells matured to myofibers between 20 days' gestation and birth. Coincidentally, large and small myofibers diverged from each other, leading to disintegration of the groups of muscle cells. Undifferentiated cells frequently occurred in the interspaces between neighboring muscle cells at the time of separation. Myofibers arising at different stages of muscle histogenesis intermingled in a checkerboard fashion as a result of this asynchronous mode of development. The possibility of fusion between neighboring muscle cells in this developing system is discussed.

Animals↗
PubMed1991

Expression of the muscle regulatory factor MRF4 during somite and skeletal myofiber development.

The muscle regulatory factors MRF4, myogenin, myf-5, and MyoD constitute a family of proteins that can function as muscle-specific transcriptional activators. Although this gene family has been extensively studied, a specific role for each factor during myogenesis remains to be determined. Understanding how these factors function requires a detailed analysis of their expression patterns during development. Toward this goal, we examined the temporal pattern of expression of MRF4 and the other factors in the rat myogenic cell line L6J1-C, in newborn rat primary muscle cell cultures and in fetal and postnatal rat limb muscle. Our results demonstrate that MyoD, myogenin, and myf-5 transcripts accumulate maximally at various stages of myoblast differentiation and decline to low expression levels in adult muscle tissue. In contrast, MRF4 transcript accumulation is restricted to cell cultures containing multinucleate myofibers, and its expression in vivo increases sharply during late fetal muscle development. This level of MRF4 expression is maintained in the adult which, together with decreased expression of the other three muscle regulatory factors, makes MRF4 the predominant factor in adult muscle. In situ hybridization of mouse embryo tissue sections indicates that MRF4 transcripts accumulate in the limb beginning 13.5 days post coitum, which is 2 days later than the initial appearance of myogenin and MyoD transcripts. Hybridization to earlier stages of development reveals, however, that MRF4 mRNA initially is present in the myotomal compartment of the somites, just after myogenin but 2 days prior to MyoD expression. Unlike myogenin and MyoD, MRF4 expression declines in the myotomes at the time that multinucleate axial muscles begin to form in this region, although during later development MRF4 is expressed in the myofibers of axial muscles at levels comparable to those in the limb. Differences in the expression patterns for MRF4, myogenin, myf-5 and MyoD between myotomal and other skeletal muscle development suggest that the relative timing of expression for each muscle regulatory factor may control the distinct phenotypes associated with myotomal myocytes and multinucleate myofibers.

Aging↗
PubMed1987

Development of a muscle actin specified by maternal and zygotic mRNA in ascidian embryos.

In this investigation, we characterize the embryonic and adult actins and describe the embryonic expression of a muscle actin in the ascidian Styela. Two-dimensional polyacrylamide gel electrophoresis showed that embryos, tadpole larvae, and adult organs contain three major and two minor isoforms of actin. Two of the major isoforms, which are present in the mantle, branchial sac, alimentary tract, and gonads of adults and in eggs, embryos, and heads and tails of tadpoles, are likely to be cytoplasmic actins. The third major isoform, which was enriched in the mantle and branchial sac of adults and localized primarily in the tails of tadpoles, is a muscle actin. The muscle actin isoform was not detected in eggs and early embryos. Radioactivity incorporation studies showed that the cytoplasmic actins were synthesized throughout early development, but muscle actin synthesis was first detected between the 16- and 64-cell stages, 2-3 hr after fertilization. Two lines of evidence indicate that embryonic muscle actin synthesis is directed in part by maternal mRNA. First, poly(A)+ RNA isolated from unfertilized eggs directed the synthesis of muscle actin in an mRNA-dependent reticulocyte lysate. Second, muscle actin was synthesized in anucleate egg fragments. Arguments are also presented that muscle actin synthesis is not directed exclusively by maternal mRNA. It is concluded that embryonic and adult Styela exhibit actin heterogeneity, that one of the actin isoforms is a muscle actin, and that the muscle actin is synthesized during embryogenesis under the direction of maternal and zygotic mRNA.

Actins↗
PubMed1987

Cellular development of skeletal muscle of rats during recovery from prolonged undernutrition.

The cellular basis for growth retardation of skeletal muscle was studied in male Sprague-Dawley rats. At birth, animals were assigned to control (C) or food-restricted (R) groups. During lactation, food intake of the pups was reduced by limiting intake of the mother to 50% of controls. After weaning, pups received 40% of ad libitum intakes until 120 d of age. From 120 to 316 d, all animals were fed ad libitum. At 120 d, body weight of the R group was 41% of C and muscle and adipose weights were 54 and 16% of C, respectively. Muscle DNA in the R group was 47% of C, but protein-to-DNA ratio was normal. Fiber number was not different between C and R groups; however, muscle length and fiber cross-sectional area were 85 and 64%, respectively, of C values. After 196 d of recovery, weights of the body, skeletal muscles and adipose tissues averaged 76, 84 and 51% of C values, respectively. Recovery of skeletal muscle paralleled the recovery of fiber cross-sectional area (84%) and DNA content (86%). Daily injections of 100 micrograms of growth hormone from 120 to 148 d produced no additional recovery. This study establishes that growth retardation of skeletal muscle is associated with reductions in the development of cross-sectional area and DNA content of muscle fibers.

Animals↗
PubMed1995

Expression of zfh-4, a new member of the zinc finger-homeodomain family, in developing brain and muscle.

We have identified zfh-4, a new member of a recently recognized zinc finger-homeodomain (zfh) family of putative transcription factors. Zfh-4 expression is prominent in developing muscle and brain. In both tissues, zfh-4 RNA levels are highest embryonically, then decrease gradually to barely detectable levels in adults. In myogenic cell lines, far more zfh-4 is expressed in proliferating myoblasts than in myotubes, suggesting a cellular basis for the developmental regulation observed in vivo. In contrast, zfh-4 RNA in brain is more abundant in postmitotic cells of the marginal zone than in proliferating cells of the ventricular zone. Within the brain, zfh-4 RNA is regionally localized: expression is highest in midbrain, readily detectable in hindbrain, and very low in cerebral cortex. Its patterns of expression, and its homology to known DNA binding proteins, support the idea that zfh-4 may be a regulator of gene expression in developing brain and muscle.

Amino Acid Sequence↗
PubMed2001

Sequential docking, molecular differentiation, and positioning of T-Tubule/SR junctions in developing mouse skeletal muscle.

Skeletal muscle Ca(2+) release units (CRUs) are junctions of the surface membrane/T-tubule system and the sarcoplasmic reticulum (SR) that function in excitation-contraction coupling. They contain high concentrations of dihydropyridine receptors (DHPRs) in the T-tubules and of ryanodine receptors (RyR) in the SR and they are positioned at specific locations in the sarcomere. In order to characterize the sequence of developmental steps leading to the specific molecular and structural organization of CRUs, we applied a range of imaging techniques that allowed us to follow the differentiation of the membrane compartments and the expression of junctional proteins in developing mouse diaphragm muscle. We find that docking of the two membrane systems precedes the incorporation of the RyRs into the junctions, and that T-tubule/SR junctions are formed and positioned at the I-A interface at a stage when the orientation of T-tubule is predominantly longitudinal. Thus, the sequence of developmental events is first the docking of T-tubules and SR, secondly the incorporation of RyR in the junctions, thirdly the positioning of the junctions in the sarcomere, and only much later the transverse orientation of the T-tubules. These sequential stages suggests an order of inductive processes for the molecular differentiation and structural organization of the CRUs in skeletal muscle development.

Animals↗
PubMed2002

Differential expression of two MyoD genes in fast and slow muscles of gilthead seabream ( Sparus aurata).

Members of the myogenic regulatory gene family, including MyoD, Myf5, Myogenin and MRF4, are specifically expressed in myoblast and skeletal muscle cells and play important roles in regulating skeletal muscle development and growth. They are capable of converting a variety of non-muscle cells into myoblasts and myotubes. To better understand their roles in the development of fish muscles, we have isolated the MyoD genomic genes from gilthead seabream (Sparus aurata), analyzed the genomic structures, patterns of expression and the regulation of muscle-specific expression. We have demonstrated that seabream contain two distinct non-allelic MyoDgenes, MyoD1 and MyoD2. Sequence analysis revealed that these two MyoD genes shared a similar gene structure. Expression studies demonstrated that they exhibited overlapping but distinct patterns of expression in seabream embryos and adult slow and fast muscles. MyoD1 was expressed in adaxial cells that give rise to slow muscles, and lateral somitic cells that give rise to fast muscles. Similarly, MyoD2 was initially expressed in both slow and fast muscle precursors. However, MyoD2 expression gradually disappeared in the adaxial cells of 10- to 15-somite-stage embryos, whereas its expression in fast muscle precursor cells was maintained. In adult skeletal muscles, MyoD1 was expressed in both slow and fast muscles, whereas MyoD2 was specifically expressed in fast muscles. Treating seabream embryos with forskolin, a protein kinase A activator, inhibited MyoD1 expression in adaxial cells, while expression in fast muscle precursors was not affected. Promoter analysis demonstrated that both MyoD1 and MyoD2 promoters could drive green fluorescence protein expression in muscle cells of zebrafish embryos. Together, these data suggest that the two non-allelic MyoD genes are functional in seabream and their expression is regulated differently in fast and slow muscles. Hedgehog signaling is required for induction of MyoDexpression in adaxial cells.

Amino Acid Sequence↗
PubMed1989

Expression of nerve-muscle topography during development.

Previous studies have indicated that in 2 muscles of the adult rat, the anterior serratus and the diaphragm, the rostrocaudal axis of the motoneuron pool projects topographically onto the rostrocaudal axis of the muscle. In the present work we have asked whether this orderly topography emerges as a function of postnatal synaptic rearrangement or whether this pattern is already established at birth. The anterior serratus muscle was studied over the period ranging from embryonic day 17 through postnatal day 30. Using 2 criteria of topography, average segmental innervation and average target field of cervical roots C6 and C7, we found that a topographic distribution of the motoneuron pool is already present prior to birth and maintained throughout the postnatal period. Moreover, both C6 and C7 form an orderly map over the surface of the serratus in the embryo, and the topography is sharpened during postnatal periods. The diaphragm also is topographically innervated at birth and undergoes a comparable sharpening of the projection map postnatally. We conclude that the topographic projection of motoneurons is established prior to birth in these muscles, and postnatal synaptic rearrangement serves to sharpen the topographic map toward the adult pattern. These results also suggest that the pursuit of basic mechanisms underlying topography should be directed toward initial embryonic nerve-muscle contacts.

Animals↗
PubMed1983

Extrasynaptic accumulations of acetylcholinesterase in the rat sternocleidomastoid muscle after neonatal denervation. Light and electron microscopic localization and molecular forms.

Denervated neonatal rat sternocleidomastoid muscle has decreased levels of total AChE when compared to control muscle. Denervated versus control values of total muscle AChE present a three-phase curve in function of time after denervation. There is a rapid initial fall 0-3 days after denervation, an increase during about 2 weeks, then again a decrease in total AChE. Thus, there is a transitory net accumulation of AChE after the initial fall of activity in denervated developing muscle. Extrasynaptic areas of high AChE activity develop between 1 and 2 weeks after denervation and remain visible up to 1 month after denervation before vanishing. An electron microscope study shows that these accumulations are internal to the muscle fiber, close to a limited number of muscle nuclei and associated to the sarcoplasmic reticulum and nuclear envelope, but not to the T-tubule system. As found in adult rat muscle, the initial fall in AChE affects first the 16 S AChE form, and soon after, the 4 S and 10 S AChE forms. A main difference with adult muscle is the sudden increase and predominance over other forms of 10 S AChE 2 weeks after denervation at birth. Later, the decrease in AChE affects 16 S and 4 S AChE before 10 S AChE. The regions rich in extrasynaptic sites of AChE accumulation possess a very high proportion of 10 S AChE. Thus, the mechanisms of biosynthesis, intracellular transport and/or secretion of AChE may be very different in young, developing muscle compared to adult muscle.

Acetylcholinesterase↗
PubMed2006

Effect of myostatin on turkey myogenic satellite cells and embryonic myoblasts.

Myostatin (GDF-8) inhibits the activation, proliferation, and differentiation of myogenic satellite cells. The relative importance of this growth factor is demonstrated in myostatin-null mice and cattle possessing defective myostatin genes. These defects result in greatly enhanced musculature. In the present study, we examined the effect of myostatin on turkey myogenic satellite cells and embryonic myoblasts. Compared with controls (P<0.05), proliferation of both turkey embryonic myoblasts and satellite cells was inhibited between 26 and 45% in serum-free medium containing 20 ng/mL myostatin. While individual turkey satellite cell clones differed in their responsiveness to myostatin, there were no significant differences in the responsiveness of fast and slow growing cells as groups (P>0.05). A slow growing clone that exhibited the greatest response to myostatin also exhibited the greatest depression of differentiation with this growth factor (P<0.05). All other turkey satellite cell clones exhibited similar responses to the differentiation depressing effects of myostatin (P>0.05). However, myostatin had no effect on differentiation of turkey embryonic myoblasts (P>0.05). When exposed to myostatin, 4 of 6 proliferating clones and all differentiating clones increased their expression of decorin, a growth inhibitor (P<0.05). The present study demonstrates that myostatin inhibits the proliferation and differentiation of satellite cells and suggests a role for decorin in myostatin action in muscle development.

Animals↗
PubMed1996

Expression and epitopic conservation of calponin in different smooth muscles and during development.

Calponin is a thin filament associated protein found in smooth muscle as a potential modulator of contraction. Five mouse monoclonal antibodies (mAbs CP1, CP3, CP4, CP7, and CP8) were prepared against chicken gizzard alpha-calponin. The CP1 epitopic structure is conserved in smooth muscles across vertebrate phyla and is highly sensitive to CNBr cleavage in contrast with the chicken-specific CP4 and the avian-mammalian-specific CP8 epitopes that are resistant to CNBr fragmentation. Using this panel of mAbs against multiple epitopes, only alpha-calponin was detected in adult chicken smooth muscles and throughout development of the gizzard. Western blotting showed that the calponin content varied among different smooth muscle tissues and correlated with that of h-caldesmon. In contrast with the constitutive expression of calponin in phasic smooth muscle of the digestive tract, very low levels of calponin were detected in adult avian tracheas and no calponin expression was detected in embryonic and young chick tracheas. These results provide information on the structural conservation of calponins and suggest a relationship between calponin expression and smooth muscle functional states.

Animals↗