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PubMed1995

Mutations in a novel gene, myoblast city, provide evidence in support of the founder cell hypothesis for Drosophila muscle development.

We have used mutations in the newly identified gene myoblast city to investigate the founder cell hypothesis of muscle development in Drosophila melanogaster. In embryos mutant for myoblast city the fusion of myoblasts into multinucleate muscles is virtually abolished. Nevertheless, a subset of the myoblasts develop specific muscle-like characteristics, including gene expression appropriate to particular muscles, migration to the appropriate part of the segment, correct position and orientation, and contact by motor neurons. We suggest that this subset of myoblasts represents the proposed muscle founder cells and we draw an analogy between these founder cells and the muscle pioneers described for grasshopper muscle development.

Animals↗
PubMed1995

Inactivation of Myf-6 and Myf-5 genes in mice leads to alterations in skeletal muscle development.

Myf-6, alternatively called MRF4 or herculin, is a member of a group of muscle-specific transcription factors which also comprises Myf-5, myogenin and MyoD. All family members show distinct expression patterns during skeletal muscle development and can convert a variety of cell lines to myocytes. We disrupted the Myf-6 gene in mice to investigate its functional role in the network of regulatory factors controlling myogenesis. Homozygous mice carrying the disrupted Myf-6 gene show pronounced down-regulation of Myf-5 transcription for reasons presently unknown. Consequently, these mice represent a double knock-out model for Myf-6 and Myf-5. The mutants resemble most of the Myf-5 phenotype with aberrant and delayed early myotome formation and lack of distal rib structures. In addition, we find a reduction in the size of axial muscles in the back. Apart from changes in the pattern of some contractile protein isoforms, the existing myofibers appear fairly normal. This suggests that Myf-6 has no major role in the maturation of myotubes, as previously proposed. Our results provide evidence that skeletal myogenesis can proceed in the absence of two myogenic factors, Myf-5 and Myf-6, therefore they must exert largely non-redundant functions in vivo.

Animals↗
PubMed1988

Myosin ATPase activity during avian cardiac and skeletal muscle development.

The myosin ATPase activity and myosin light chain composition in developing chick heart and skeletal muscles were studied and compared. Embryonic myosin was purified and characterized from day 7 to day 19 of embryogenesis. Embryonic cardiac myosin generally showed the same Ca2+-activated myosin ATPase activity level as the adult value. In comparison, pooled pectoralis and hindlimb skeletal muscles from day 10 through day 19 showed myosin ATPase activities that were all significantly less than the adult counterpart. The myosin light chain pattern of embryonic cardiac myosin remained relatively constant like the myosin ATPase activity, whereas developmental changes were observed in skeletal myosin light chains.

Animals↗
PubMed1993

GAP43 identifies developing muscle cells in human embryos.

GAP43 has long been regarded as a neurone specific molecule present intraneuronally in both the central and peripheral nervous system, especially during development and regeneration. GAP43 has, however, recently been demonstrated in developing muscle cells of the chicken. In the prsent investigation, we have used immunohistochemistry to investigate whether GAP43 is also expressed in developing human muscle cell. Using specific monoclonal antibodies as markers for developing muscle cells (desmin) and axon terminals (synaptophysin), our results show that GAP43 is expressed in aneural, human embryonic muscle cells.

Antibodies, Monoclonal↗
PubMed1990

Migration of myoblasts across basal lamina during skeletal muscle development.

Basal lamina is a sheet of extracellular matrix that separates cells into topologically distinct groups during morphogenesis and is thought to form a barrier to cell migration. We have examined whether, during normal muscle development, myoblasts--mononucleate muscle precursor cells--can cross the basal lamina that surrounds each multinucleate muscle fibre. We marked myoblasts in vivo by injecting replication-defective retroviral vectors encoding LacZ into muscle tissue and analysed the fate of their progeny by the expression of beta-galactosidase. A dual labelling method with broad application to retroviral lineage-marking studies was developed to ensure that most clusters of labelled cells were clones derived from a single precursor cell. Most of the myoblasts that were infected at a late stage of rat hindlimb development, when each fibre with its satellite myoblasts is individually encased in a basal lamina sheath, gave rise to clones that contributed to several labelled fibres. Our results show that myoblasts from healthy fibres migrate across basal lamina during normal development and could contribute to the repair of fibres damaged by injury or disease.

Animals↗
PubMed1979

Contractile protein isozymes in muscle development: identification of an embryonic form of myosin heavy chain.

The nature of the myosin heavy chain in embryonic muscle tissue, cultured muscle cells, and several adult muscles was investigated. After denaturation with sodium dodecyl sulfate, purified rat myosins were subjected to partial proteolytic cleavage or immunological analysis using microcomplement fixation. Three types of myosin heavy chains could be demonstrated by both approaches. Whereas adult muscles contain fast- or slow-type myosin heavy chains, embryonic tissue and cultured muscle cells harbor a distinct embryonic form. The existence of this distinct form further characterizes the isozymic transitions of contractile proteins during muscle development.

Aging↗
PubMed1978

Regulation of skeletal muscle development by the central nervous system in the fetal pig.

The effect of upper motor neuron regulation on skeletal muscle development was studied in the fetal pig. A region of the spinal cord at the level of the upper cervical vertebrae was destroyed by cauterization at 45 days of gestation in four pig fetuses. Five fetuses with intact spinal cords served as controls. Innervation and enzyme activities in the longissimus muscle, the ultrastructure and quantitation of satellite cells in the sartorius muscle, and plasma composition were evaluated at 110 days of gestation. The terminal innervation ratios were similar (P greater than 0.05) for muscles from control and cauterized fetuses. Endplate morphology was also similar. Therefore, innervation of newly formed primary fibers is not controlled by upper motor neurons after 45 days of gestation. Mean values for body weight, percentage of muscle dry weight, percentage of myofibers with myonuclei and plasma levels of protein, glucose, triglycerides, lactate, and creatine phosphokinase activity were similar (P greater than 0.05) between the two groups of fetuses. All but one muscle fiber examined was of the secondary fiber type. These observations suggest that the physiological maturity of the muscle was not appreciably altered even though glucose-6-phosphate dehydrogenase activity was higher (P greater than 0.05) and total phosphorylase activity was lower (P greater than 0.05) in the spinal cauterized fetuses than in the control group. The percentage of satellite cells was lower when based on the number of myofibers observed (P greater than 0.005) or on the number of nuclei contained within the basal lamina (P greater than 0.001) in the muscle of the spinal cauterized fetuses than in the control fetuses. The cytoplasm of satellite cells from the muscles of control fetuses was rich in organelles indicative of metabolic and mitotic activity whereas a paucity of such organelles was observed in the satellite cells of cauterized fetuses. Since the percentage of myofibers that had myonuclei was similar (P greater than 0.05) for the control and cauterized fetuses, it appeared that the myonuclear population was maintained by direct incorporation of the parent satellite cell.

Animals↗
PubMed1997

Mice lacking the ski proto-oncogene have defects in neurulation, craniofacial, patterning, and skeletal muscle development.

The c-ski proto-oncogene has been implicated in the control of cell growth and skeletal muscle differentiation. To determine its normal functions in vivo, we have disrupted the mouse c-ski gene. Our results show a novel role for ski in the morphogenesis of craniofacial structures and the central nervous system, and confirm its proposed function as a player in skeletal muscle development. Homozygous mutant mice show perinatal lethality resulting from exencephaly, a defect caused by failed closure of the cranial neural tube during neurulation. The timing of the neural tube defect in ski -/- embryos coincides with excessive apoptosis in the cranial neuroepithelium, as well as in the cranial mesenchyme. Homozygous ski mutants also exhibit a dramatic reduction in skeletal muscle mass, consistent with a defect in expansion of a myogenic precursor population. Nestin is an intermediate filament expressed in highly proliferative neuroepithelial stem cells and in myogenic precursors. Interestingly, we find decreased nestin expression in both the cranial neural tube and the somites of ski -/- embryos, compared with their normal littermates, but no reduction of nestin in the caudal neural tube. These results are consistent with a model in which ski activities are required for the successful expansion of a subset of precursors in the neuroepithelial or skeletal muscle lineages.

Animals↗
PubMed1985

Muscle development in the grasshopper embryo. II. Syncytial origin of the extensor tibiae muscle pioneers.

The extensor tibiae muscle (ETi) in the metathoracic leg of the grasshopper, which powers the jump, is among the most studied insect muscles. In contrast to many insect muscles which are simple (consisting of only a single bundle of muscle fibers), the ETi is a complex muscle which consists of an array of bundles of muscle fibers, each with a separate site of insertion on the body wall ectoderm and on the ETi apodeme ectoderm. Here we describe the embryonic development of this complex muscle. The ETi muscle develops from a single muscle pioneer (MP) which connects the initial invagination of the ETi apodeme to the wall of the femur. This MP then dramatically expands around the developing apodeme to form a large horseshoe-shaped, multinucleate cell, called the supramuscle pioneer (supra-MP); the number of nuclei in the supra-MP increases by cell fusion rather than by nuclear division. The arms of the supra-MP grow steadily longer and their outer edges begin to appear scalloped, certain areas remaining tightly apposed to the ectoderm of the wall of the leg while adjacent areas lose their adhesion and are pulled away. By about 50% of embryonic development the ETi supra-MP consists of a periodic series of bridges (cytoplasmic extensions) connecting the leg wall ectoderm with the apodeme, and linked into a giant syncytium near their inner, apodeme surface by a thin layer of cytoplasm containing hundreds of nuclei. Each bridge is surrounded by a cluster of many smaller mesoderm cells. Next the syncytium begins to divide such that by 60% the periodic bridges of the supra-MP have lost syncytial contact with each other and now themselves form an array of smaller, individual, multinucleate MPs connecting the body wall to the apodeme, each surrounded by a mass of undifferentiated mesoderm cells. This initial cycle of fusion and division is followed by a second similar cycle in which the individual mesoderm cells surrounding each MP fuse with the MP. At the same time, the MP divides into the initial bundle of smaller muscle fibers. Coincident with this division into muscle fibers is the further development of thick and thin filaments and the T-tubule system.

Animals↗
PubMed1990

Biogenesis of transverse tubules: immunocytochemical localization of a transverse tubular protein (TS28) and a sarcolemmal protein (SL50) in rabbit skeletal muscle developing in situ.

To study the biogenesis of transverse tubules, the temporal appearance and distribution of TS28 (a specific marker of transverse tubules absent from the sarcolemma in adult skeletal muscle; 28,000 Mr) and SL50 (specifically associated with the sarcolemma and absent from the region of the transverse tubules in adult rabbit skeletal muscle) (Jorgensen, A.O., W. Arnold, A. C.-Y. Shen, S. Yuan, M. Gaver, and K.P. Campbell. 1990. J. Cell Biol. 110:1173-1185) were determined in rabbit skeletal muscle developing in situ (day 17 of gestation to day 15 newborn) by indirect immunofluorescence labeling. The results presented show that the temporal appearance and subcellular distribution of TS28 is distinct from that of SL50 at the developmental stages examined. TS28 was first detected in some, but not all, multinucleated myotubes on day 17 of gestation. At this stage of development, SL50 and the Ca2(+)-ATPase of the sarcoplasmic reticulum were already present in all myotubes. TS28 first appeared in discrete foci mostly confined to the cell periphery of the myotubes. At subsequent stages of development (days 19-24 of gestation), TS28 was also found in shoft finger-like structures extending obliquely and transversely from the cell periphery towards the center of the myotubes. 1-2 d after birth, TS28 was observed in an anastomosing network composed of transversely oriented chickenwire-like networks extending throughout the cytoplasm and interconnected by longitudinally oriented fiber-like structures. As development proceeded, the transversely oriented network became increasingly dominant. By day 10 of postnatal development, the longitudinally oriented component of the tubular network was not regularly observed. At none of the developmental stages examined was TS28 observed to be uniformly distributed at the cell periphery. SL50, like TS28, first appeared in discrete foci at the cell periphery. However, shortly after its first appearance it appeared to be distributed along the entire cell periphery. Although the intensity of SL50 labeling increased with development, it remained confined to the sarcolemma and was absent from the interior regions of the myofibers, where transverse tubules were present at all subsequent developmental stages examined. Immunoblotting of cell extracts from skeletal muscle tissue at various stages of development showed that SL50 was first detected on day 24 of gestation, while TS28 was not detected until days 1-2 after birth. Comparison of these results with previous ultrastructural studies of the formation of transverse tubules supports the idea that the temporal appearance and subcellular distribution of TS28 correspond very closely to that of the distribution of forming transverse tubules in rabbit skeletal muscle developing in situ.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1993

Myosin light chain kinase expression during smooth muscle development.

The expression of smooth muscle myosin light chain kinase (MLCK) was investigated during chicken gizzard development. The molecular weight and the antigenic properties of MLCK did not change during development. The use of anion exchange high performance liquid chromatography (HPLC) enabled us to distinguish between MLCKs from post-hatched and adult chickens. A partial amino acid sequence determination of 4-day-old gizzard MLCK failed to disclose differences in the primary sequences of the two proteins. The results suggest that MLCK has the same primary sequence in all stages of gizzard development, although charge variants due to post-translational modifications may exist.

Amino Acid Sequence↗
PubMed1998

Patterns of superficial fibre formation in the European pearlfish (Rutilus frisii meidingeri) provide a general template for slow muscle development in teleost fish.

The debate about the pattern of muscle formation in teleost fish has recently been heightened in the literature. Here we examine superficial muscle development in the pearlfish, a cyprinid endemic to a small area of Central Europe, and uninfluenced by economic interest and breeding. Using light and electron microscopy, histochemistry and immunohistochemistry techniques, we report that: (1) Superficial fibre precursors originate close to the notochord, are part of the same cell population as the so-called muscle pioneer cells, and are transferred laterally to end up at the surface of the myotome. (2) Superficial fibre maturation is exceptionally rapid. Structural and enzymatic functionality is attained at a time when prospective deep fibres have not passed beyond the early myotube state. This strong contrast weakens as the embryo develops. (3) Apart from the muscle pioneers, the superficial fibres appear to be capable of functioning before they receive any direct innervation, implying that signals are transferred to these fibres via cell-to-cell junctions. We suggest that the capability of rapid superficial fibre maturation is a rather general feature among teleosts and may aid pre-hatch survival under a variable environment. Our results indicate that muscle formation in teleost fish may follow a common basic pattern that is open to considerable ontogenetic and phylogenetic modification in response to habitat conditions.

Animals↗
PubMed1976

Insulin action on glucose transport and calcium fluxes in developing muscle cells in vitro.

The glucose transport system of developing muscle cells in vitro is described. Uptake experiments showed stereospecificity but no saturation or competition. Km-values for early myoblasts could not be determined; with progressive development, the absolute amount of uptake increases and becomes insulin sensitive. Km-values of about 13 mM basal and 32 mM for insulin stimulation were determined and discussed with respect to the glucose transport mechanism. Basal and insulin-dependent transport were shown to be dependent on the presence of calcium in the medium. Moreover, the ionophore A 23187 could be shown to mimic the insulin effect on glucose uptake. 45Ca saturation and desaturation experiments showed that insulin enhances the "mitochondrial" calcium pool by 35% and increases the apparent "cytoplasmic" efflux rate constant by 50%. We propose that insulin increases the free cytoplasmic calcium concentration, which may be the intracellular signal for the stimulation of glucose transport.

Animals↗
PubMed1995

Synapse-associated expression of an acetylcholine receptor-inducing protein, ARIA/heregulin, and its putative receptors, ErbB2 and ErbB3, in developing mammalian muscle.

Developing motor axons induce synaptic specializations in muscle fibers, including preferential transcription of acetylcholine receptor (AChR) subunit genes by subsynaptic nuclei. One candidate nerve-derived signaling molecule is AChR-inducing activity (ARIA)/heregulin, a ligand of the erbB family of receptor tyrosine kinases. Here, we asked whether ARIA and erbB kinases are expressed in patterns compatible with their proposed signaling roles. In developing muscle, ARIA was present not only at synaptic sites, but also in extrasynaptic regions of the muscle fiber. ARIA was synthesized, rather than merely taken up, by muscle cells, as indicated by the presence of ARIA mRNA in muscle and of ARIA protein in a clonal muscle cell line. ARIA-responsive myotubes expressed both erbB2 and erbB3, but little EGFR/erbB1 or erbB4. In adults, erbB2 and erbB3 were localized to the postsynaptic membrane. ErbB3 was restricted to the postsynaptic membrane perinatally, at a time when ARIA was still broadly distributed. Thus, our data are consistent with a model in which ARIA interacts with erbB kinases on the muscle cell surface to provide a local signal that induces synaptic expression of AChR genes. However, much of the ARIA is produced by muscle, not nerve, and the spatially restricted response may result from the localization of erbB kinases as well as of ARIA. Finally, we show that erbB3 is not concentrated at synaptic sites in mutant mice that lack rapsyn, a cytoskeletal protein required for AChR clustering, suggesting that pathways for synaptic AChR expression and clustering interact.

Aging↗
PubMed1987

Evidence for sequential expression of multiple AMP deaminase isoforms during skeletal muscle development.

AMP deaminase (myoadenylate deaminase; EC 3.5.4.6) is an integral part of the myofibril in skeletal muscle, and this enzyme plays an important role in energy metabolism in this tissue. We report here the identification of three AMP deaminase isoforms during skeletal muscle development in the rat. An embryonic isoform is expressed in the developing hindlimb of the rat between 7 and 14 days of gestation. This isoform is not unique to skeletal muscle or the embryo as it is also expressed in many nonmuscle tissues of the perinatal and adult rat. A perinatal isoform of AMP deaminase that is restricted to skeletal muscle is produced 4-6 days before birth and persists for 2-3 weeks of postnatal life. An adult, skeletal muscle-specific isoform of AMP deaminase appears at birth and reaches maximal levels after 3 weeks of postnatal development. We conclude from these studies there is a developmentally controlled program that leads to the sequential expression of AMP deaminase isoforms during the transition from embryonic to adult skeletal muscle.

AMP Deaminase↗
PubMed1993

Histochemical and contractile property changes during human muscle development.

When the histochemical and contractile properties of infant muscles change postnatally, and what influence muscle function has on these changes, were the focus of this study. Contractile properties were measured in the plantaflexor (PF) and dorsiflexors (DF) of 19 newborns and 36 infants aged 5-16 months. Infants were tested between one and four times at monthly intervals. Measurements included maximal twitch tension (Pt), time to peak tension (TPT), and half-relaxation times (1/2RT). TPT was similar in PF (77 ms) and DF (73 ms) at birth, remained unchanged in DF, and slowed in PF to 110-120 ms between 9 and 12 months. Type I distributions were determined at autopsy in fetal through to adult muscles. Completion of differentiation occurred in soleus at about the age that contractile properties slowed and infants started to use these muscles more. A trend of higher percentages of type I distributions was also noted in children than either newborns or adults in other muscles. The implications of these findings and the clinical use of these methods for evaluating peripheral neuromuscular function is discussed.

Adolescent↗
PubMed1992

Formation of highly organized skeletal muscle fibers in vitro. Comparison with muscle development in vivo.

Two methods were developed in which long-term cultures of quail skeletal muscle were established so that all of the muscle fibers develop in a highly oriented manner. The muscle fibers became spontaneously and vigorously contractile and established strong connections with the extracellular matrix at their ends that closely duplicate the structure of the myotendinous junction. A continuous basal lamina was formed around each muscle fiber that contained type IV collagen, laminin and heparan sulfate proteoglycan. With one of the methods, an extensive extracellular matrix developed around each muscle fiber that was highly organized with the formation of a distinctive epimysium, perimysium and endomysium. Analysis of the cultures by both methods for different isoforms of myosin showed expression of an adult form of myosin by some of the muscle cells. The results therefore demonstrate that muscle development in the present culture systems proceeds extensively for several weeks. It will now be possible to investigate directly the structure of the connections between muscle fibers and the extracellular matrix.

Animals↗
PubMed1996

Pax3 modulates expression of the c-Met receptor during limb muscle development.

Pax3 is a transcription factor whose expression has been used as a marker of myogenic precursor cells arising in the lateral somite destined to migrate to and populate the limb musculature. Accruing evidence indicates that the embryologic origins of axial and appendicular muscles are distinct, and limb muscle abnormalities in both mice and humans harboring Pax3 mutations support this distinction. The mechanisms by which Pax3 affects limb muscle development are unknown. The tyrosine kinase receptor for hepatocyte growth factor/scatter factor encoded by the c-met protooncogene is also expressed in limb muscle progenitors and, like Pax-3, is required in the mouse for limb muscle development. Here, we show that c-met expression is markedly reduced in the lateral dermomyotome of Splotch embryos lacking Pax3. We show that Pax3 can stimulate c-met expression in cultured cells, and we identify a potential Pax3 binding site in the human c-MET promoter that may contribute to direct transcriptional regulation. In addition, we have found that several cell lines derived from patients with rhabdomyosarcomas caused by a t(2;13) chromosomal translocation activating PAX3 express c-MET, whereas those rhabdomyosarcoma cell lines examined without the translocation do not. These results are consistent with a model in which Pax3 modulates c-met expression in the lateral dermomyotome, a function that is required for the appropriate migration of these myogenic precursors to the limb where the ligand for c-met (hepatocyte growth factor/scatter factor) is expressed at high levels.

Animals↗