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PubMed1993

Ultrastructure of developing flight muscle in Drosophila. II. Formation of the myotendon junction.

Using ultra-thin section electron microscopy, the development of the myotendon junction (MTJ) of Drosophila indirect flight muscle (IFM) is described for the first time. The MTJ is a cell-cell junction between the IFM and epithelial tendon cells. The terminal Z-band of each myofibril forms a uniform junction with a tendon cell; each junction shows a precise sequence of folding and elaboration in which microtubule arrays in both cell types play a prominent role. Upon IFM/tendon cell contact (by approximately 32 hr pupation), numerous flat, focal dense plaques form between muscle and tendon cell membranes. In the muscle, transient arrays of microtubules, which will form "sleeves" around the developing myofibrils, delineate the perimeter of these focal plaques. Each of the dense plaques enlarges and develops into the modified terminal Z-band (MT-Z) of a myofibril, linking the thick and thin filaments of the highly ordered terminal sarcomere to the membrane via a dense feltwork. As these plaques develop into the MT-Z, the perimeter of each plaque advances, leaving the central region deeply indented. Between 50-75 hr pupation, secondary folds appear in each MTJ, and tendon cell microtubules that will form the tendon elements attach to specific dense sites on the secondary folds of the junctional membrane opposite the MT-Z. By 100 hr pupation, each MTJ develops numerous sharp folds, thereby tightly interdigitating the muscle and tendon cell. Amorphous density associated with the junctional membranes assumes a crystalline array that includes the membrane cytoskeletons of both cells and the extracellular matrix. At the end of pupation (approximately 112 hr), the final link between tendon cell and cuticle is formed as the tiny, dense-tipped microvilli in contact with the cuticle are replaced by extracellular tonofibrils, dense shafts that fill deep pits in the tendon cell and extend deeply into the cuticle. The tendon cell microtubules become bundled and decorated by fine "feather" filaments and the free ends of these microtubule bundles become linked to the membrane surrounding the pits.

Animals↗
PubMed2001

Evolutionary history of vertebrate appendicular muscle.

The evolutionary history of muscle development in the paired fins of teleost fish and the limbs of tetrapod vertebrates is still, to a large extent, uncertain. There has been a consensus, however, that in the vertebrate clade the ancestral mechanism of fin and limb muscle development involves the extension of epithelial tissues from the somite into the fin/limb bud. This mechanism has been documented in chondrichthyan, dipnoan, chondrostean and teleost fishes. It has also been assumed that in amniotes, in contrast, individual progenitor cells of muscles migrate from the somites into the limb buds. Neyt et al. now present the exciting finding that in zebrafishes this presumably derived mechanism involving individual cell migration, is present. They conclude, based on data on sharks, zebrafishes, chickens, quails and mice that the derived mechanism was present in the sarcopterygians. This conclusion, however, may be premature in the light of further data available in the literature, which show a highly mosaic distribution of this character in the vertebrate clade. Furthermore, a developmental mode exists that is intermediate between the supposed ancestral and derived modes in teleosts, reptiles and possibly amphibians.

Animals↗
PubMed2002

Localization of the novel Xin protein to the adherens junction complex in cardiac and skeletal muscle during development.

Previously, we demonstrated that chick embryos treated with antisense oligonucleotides against a striated muscle-specific Xin exhibit abnormal cardiac morphogenesis (Wang et al. [1999] Development 126:1281-1294); therefore, we surmised a role for Xin in cardiac development. Herein, we examine the developmental expression of Xin through immunofluorescent staining of whole-mount mouse embryos and frozen heart sections. Xin expression is first observed within the heart tube of embryonic day 8.0 (E8.0) mice, exhibiting a peripheral localization within the cardiomyocytes. Colocalization of Xin with both beta-catenin and N-cadherin is observed throughout embryogenesis and into adulthood. Additionally, Xin is found associated with beta-catenin within the N-cadherin complex in embryonic chick hearts by coimmunoprecipitation. Xin is detected earlier than vinculin in the developing heart and colocalizes with vinculin at the intercalated disc but not at the sarcolemma within embryonic and postnatal hearts. At E10.0, Xin is also detected in the developing somites and later in the myotendon junction of skeletal muscle but not within the costameric regions of muscle. In cultured C2C12 myotubes, the Xin protein is found in many speckled and filamentous structures, coincident with tropomyosin in the stress fibers. Additionally, Xin is enriched in the regions of cell-cell contacts. These data demonstrate that Xin is one of the components at the adherens junction of cardiac muscle, and its counterpart in skeletal muscle, the myotendon junction. Furthermore, temporal and spatial expressions of Xin in relation to intercalated disc proteins and thin filament proteins suggest roles for Xin in the formation of cell-cell contacts and possibly in myofibrillogenesis.

Animals↗
PubMed1990

Irreversible desensitization of ATP responses in developing chick skeletal muscle.

1. In developing chick skeletal muscle, extracellular adenosine 5'-triphosphate (ATP) elicits an early excitatory conductance increase followed by a late potassium conductance increase. Both of these responses desensitize profoundly. Intracellular recordings and whole-cell voltage-clamp recordings were made in order to examine the time course and mechanism of desensitization and the recovery from desensitization. 2. Most of the loss of responsiveness to ATP occurred during the first minute of exposure to ATP. For the excitatory conductance, the loss of responsiveness to ATP resulted in part from long-lasting activation of the ATP-sensitive channels and in part from entrance into an inactive (non-conducting) state. In contrast, desensitization of the potassium conductance was entirely the result of a relatively fast transition to an inactive state. 3. Recovery from desensitization took many hours for both responses and was quite sensitive to temperature. 4. Recovery from desensitization for both responses was prevented by preincubation with the glycosylation inhibitor, tunicamycin. Several lines of evidence suggest that tunicamycin treatment blocked the delivery of new ATP receptors to the cell surface. 5. The recovery of the early response to ATP following exposure to two non-competitive inhibitors of the ATP response was also examined. These two compounds are thought to covalently modify the receptor. After exposure to either of these inhibitors, responsiveness to ATP returned over a time course that was similar to the time course of recovery from desensitization. 6. These results indicate that, following activation, ATP receptors do not become available for reactivation, and that recovery from desensitization is due to the insertion of newly synthesized receptors into the plasma membrane.

Action Potentials↗
PubMed2004

A glutamate receptor-interacting protein homolog organizes muscle guidance in Drosophila.

During Drosophila embryogenesis, developing muscles extend growth-cone-like structures to navigate toward specific epidermal attachment sites. Here, we show that the homolog of Glutamate Receptor-Interacting Proteins (DGrip) acts as a key component of proper muscle guidance. Mutations in dgrip impair patterning of ventral longitudinal muscles (VLMs), whereas lateral transverse muscles (LTMs) that attach to intrasegmental attachment sites develop normally. Myoblast fusion, stabilization of muscle contacts, and general muscle function are not impaired in the absence of DGrip. Instead, the proper formation of cellular extensions during guidance fails in dgrip mutant VLMs. DGrip protein concentrates at the ends of VLMs while these muscles guide toward segment border attachment sites. Conversely, LTMs overexpressing DGrip form ectopic cellular extensions that can cause attachment of these muscles to other muscles at segment borders. Our data suggest that DGrip participates in the reception of an attractive signal that emanates from the epidermal attachment sites to direct the motility of developing muscles. This dgrip phenotype should be valuable to study mechanistic principles of Grip function.

Animals↗
PubMed1986

mRNA levels of cathepsins B and D during myogenesis.

Muscle development is characterized by the fusion of myoblasts to form myotubes and the co-ordinate expression of muscle-specific proteins such as actin, myosin and creatine phosphokinase. Our laboratory has been involved in the study of the role of lysosomal proteinases, namely, cathepsins B, H and L and the endogenous cysteine proteinase inhibitor, cystatin, during muscle differentiation in vitro. Specific activities of the cysteine proteinase in chicken primary cultures and a number of rat myogenic lines increased with the degree of myotube formation. This has suggested that lysosomal proteinases play an important role in myogenesis. We have measured the mRNA levels of two of the lysosomal enzymes, cathepsins B and D. This is advantageous because the presence of the endogenous inhibitor, cystatin, masks the levels of the specific activities of the cysteine proteinases present in the cell. RNA was extracted from developing muscle at three stages of development: proliferating myoblasts, confluent cells, and myotubes. Hybridization of RNA extracted from the L6 myogenic cell line with cathepsin B cDNA showed an increase in the level of cathepsin B mRNA. However, in the L8 rat myogenic line the level decreased after fusion. Cathepsin D mRNA levels remained constant throughout differentiation of the L8 cells. This paper also reports on the characterization of lysosomal proteinases of a newly obtained mouse myogenic line, C2.

Animals↗
PubMed2000

Total-body skeletal muscle mass: development and cross-validation of anthropometric prediction models.

BACKGROUND: Skeletal muscle (SM) is a large body compartment of biological importance, but it remains difficult to quantify SM with affordable and practical methods that can be applied in clinical and field settings. OBJECTIVE: The objective of this study was to develop and cross-validate anthropometric SM mass prediction models in healthy adults. DESIGN: SM mass, measured by using whole-body multislice magnetic resonance imaging, was set as the dependent variable in prediction models. Independent variables were organized into 2 separate formulas. One formula included mainly limb circumferences and skinfold thicknesses [model 1: height (in m) and skinfold-corrected upperarm, thigh, and calf girths (CAG, CTG, and CCG, respectively; in cm)]. The other formula included mainly body weight (in kg) and height (model 2). The models were developed and cross-validated in nonobese adults [body mass index (in kg/m(2)) < 30]. RESULTS: Two SM (in kg) models for nonobese subjects (n = 244) were developed as follows: SM = Ht x (0.00744 x CAG(2) + 0.00088 x CTG(2) + 0.00441 x CCG(2)) + 2.4 x sex - 0.048 x age + race + 7.8, where R:(2) = 0.91, P: < 0.0001, and SEE = 2.2 kg; sex = 0 for female and 1 for male, race = -2.0 for Asian, 1.1 for African American, and 0 for white and Hispanic, and SM = 0.244 x BW + 7.80 x Ht + 6.6 x sex - 0.098 x age + race - 3.3, where R:(2) = 0.86, P: < 0.0001, and SEE = 2.8 kg; sex = 0 for female and 1 for male, race = -1.2 for Asian, 1.4 for African American, and 0 for white and Hispanic. CONCLUSION: These 2 anthropometric prediction models, the first developed in vivo by using state-of-the-art body-composition methods, are likely to prove useful in clinical evaluations and field studies of SM mass in nonobese adults.

Adult↗
PubMed1995

An immunocytochemical marker for early type I muscle fibers in the developing rat hindlimb.

Muscle fibers develop sequentially from several generations of myotubes that express specific isoforms of myosin heavy chain (MHC). We observed that the chicken-derived monoclonal antibody (mAb) S46 binds to myotubes of the fetal rat hindlimb in a specific temporal and spatial pattern. To determine the type and fate of the S46-reactive myotubes, we immunoreacted sections of fetal, neonatal and postnatal hindlimb muscles to this antibody. The mAb S46 bound to a subpopulation of primary myotubes in the tibialis anterior, and to all primary and slow/fast secondary myotubes in the soleus muscle. The S46-reactive primary myotubes represented the oldest set of myotubes in the muscles. Reactivity to S46 was present from the earliest stages of muscle development, peaked in the late fetal period, and dissipated in the first postnatal week, suggesting that mAb S46 binds to a developmental form of slow myosin. The regional distribution of myotubes that bound S46 in fetal muscles was identical to the distribution of type I (slow-twitch) fibers in the adult, indicating that S46-reactive myotubes ultimately develop into type I extrafusal fibers. Thus, mAb S46 can be used as a marker for prospective type I extrafusal fibers in the rat hindlimb.

Animals↗
PubMed2005

The effect of early nutrition on satellite cell dynamics in the young turkey.

Early posthatch satellite cell mitotic activity is an important aspect of muscle development. An understanding of the interplay between nutrition and satellite cell mitotic activity will lead to more efficient meat production. The objective of this study was to test the influence of the leucine metabolite, beta-hydroxy beta-methylbutyrate (HMB), and feed deprivation on muscle development in the early posthatch poult. Male Nicholas poults were placed on 1 of 4 treatments: immediately fed a starter diet with 0.1% HMB (IF-HMB), immediately fed a starter diet containing 0.1% Solka-Floc for a control (IF-No HMB), feed and water withheld for 48 h immediately posthatch and then fed the HMB diet (WF-HMB), and feed and water withheld for 48 h immediately posthatch and then fed the control starter diet (WF-No HMB). 5-bromo-2'-deoxyuridine (BrdU) was injected intra-abdominally into all poults to label mitotically active satellite cells. The pectoralis thoracicus was harvested 2 h after the BrdU injection. Immunohistochemistry for BrdU, Pax7, and laminin along with computer-based image analysis was used to study muscle development. IF-HMB poults had higher body weights (P < 0.01) at 48 h and 1 wk of age and had higher satellite cell mitotic activity at 48 h of age (P < 0.01) compared with the IF-No HMB and WF poults. Therefore, dietary supplementation of HMB may have an anabolic effect on early posthatch muscle.

Animal Feed↗
PubMed1999

Development of muscle strength in relation to training level and testosterone in young male soccer players.

Isometric and functional strength of ninety-eight 11-yr-old male soccer players at an elite (E) and nonelite (NE) level were determined (3-4 times) through a 2-yr period, and the changes were related to growth and maturation. The initial isometric strength for extension with dominant leg [1,502 +/- 35 (E) vs. 1,309 +/- 39 (NE) N], extension with nondominant leg (1,438 +/- 37 vs. 1,267 +/- 45 N), extension with both legs (2,113 +/- 76 vs. 1,915 +/- 72 N), back muscles (487 +/- 11 vs. 414 +/- 10 N), abdominal muscles (320 +/- 9 vs. 294 +/- 8 N), and handgrip (304 +/- 10 vs. 259 +/- 8 N) increased by 15-40% during the period. Broad jump increased (P < 0. 05) by 15 (E) and 10% (NE). The E players had higher (P < 0.05) initial isometric strength and broad jump performance compared with NE players, and differences were maintained throughout the period (multiple ANOVA for repeated measures) also when adjustment was made for age, dimensions, testosterone, and insulin-like growth factor I (generalized estimating equations analyses). The development of strength for both E and NE players together was significantly (P < 0. 001) related to changes in serum testosterone concentrations. The present data indicate that testosterone is important for development of strength in young boys and that, independent of serum testosterone concentration, E players have developed greater muscle strength compared with NE players.

Adolescent↗
PubMed2001

[Effect of endostatin gene transfer mediated by electric pulses into skeletal muscles on development of atherosclerotic plaques in mice].

OBJECTIVE: To investigate the effect of endostatin gene transfer mediated by electric pulses into skeletal muscles of mice upon the develpment of atherosclerotic plaques. METHODS: Eukaryotic expression plasmid of mouse endostatin was injected into the muscles of 2 groups of ApoE-deficient mice, group A at the age of 24 weeks, and group B at the age of 36 weeks (named therapy group as a whole). Gene transfer was mediated by electric pulses for ten times. Empty plasmid was used to mice at the same ages as controls. Twenty weeks later, blood-lipid was tested, and the aortas of the experimental animals were taken out to examine the areas of atherosclerotic plaques and count the endothelial cells and microvessels in the plaques. RESULTS: In the 24-week-aged group, the stenosis rate of aorta 16% +/- 4% before the experiment. Twenty weeks later, the stenosis rate was 56% +/- 14% among the control mice, and was 34% +/- 8% among the treated ones with an improvement rate of 54%. In the 36-week-aged group, the stenosis rate of aorta was 30% +/- 6% before the experiment. Twenty weeks after the begining of experiment, the stenosis rate was 64% +/- 12% among the control mice, and was 49% +/- 10% among the treated ones with an improvement rate of 44%. Twenty weeks after the begining of experiment, the endothelial cell count and microvessel appearance rate were less among the therapy group than among the controls. There was no significant difference in blood-lipid between the therapy group and the control group. CONCLUSION: Endostatin gene transfer into skeletal muscle effectively inhibits the development of atherosclerotic plaques.

Animals↗
PubMed1997

The Caenorhabditis elegans NK-2 homeobox gene ceh-22 activates pharyngeal muscle gene expression in combination with pha-1 and is required for normal pharyngeal development.

Pharyngeal muscle development in the nematode Caenorhabditis elegans appears to share similarities with cardiac muscle development in other species. We have previously described CEH-22, an NK-2 class homeodomain transcription factor similar to Drosophila tinman and vertebrate Nkx2-5, which is expressed exclusively in the pharyngeal muscles. In vitro, CEH-22 binds the enhancer from myo-2, a pharyngeal muscle-specific myosin heavy chain gene. In this paper, we examine the role CEH-22 plays in pharyngeal muscle development and gene activation by (a) ectopically expressing ceh-22 in transgenic C. elegans and (b) examining the phenotype of a ceh-22 loss-of-function mutant. These experiments indicate that CEH-22 is an activator of myo-2 expression and that it is required for normal pharyngeal muscle development. However, ceh-22 is necessary for neither formation of the pharyngeal muscles, nor for myo-2 expression. Our data suggest parallel and potentially compensating pathways contribute to pharyngeal muscle differentiation. We also examine the relationship between ceh-22 and the pharyngeal organ-specific differentiation gene pha-1. Mutations in ceh-22 and pha-1 have strongly synergistic effects on pharyngeal muscle gene expression; in addition, a pha-1 mutation enhances the lethal phenotype caused by a mutation in ceh-22. Wild-type pha-1 is not required for the onset of ceh-22 expression but it appears necessary for maintained expression of ceh-22.

Animals↗
PubMed2003

Control of myoblast fusion by a guanine nucleotide exchange factor, loner, and its effector ARF6.

Myoblast fusion is essential for the formation and regeneration of skeletal muscle. In a genetic screen for regulators of muscle development in Drosophila, we discovered a gene encoding a guanine nucleotide exchange factor, called loner, which is required for myoblast fusion. Loner localizes to subcellular sites of fusion and acts downstream of cell surface fusion receptors by recruiting the small GTPase ARF6 and stimulating guanine nucleotide exchange. Accordingly, a dominant-negative ARF6 disrupts myoblast fusion in Drosophila embryos and in mammalian myoblasts in culture, mimicking the fusion defects caused by loss of Loner. Loner and ARF6, which also control the proper membrane localization of another small GTPase, Rac, are key components of a cellular apparatus required for myoblast fusion and muscle development. In muscle cells, this fusigenic mechanism is coupled to fusion receptors; in other fusion-competent cell types it may be triggered by different upstream signals.

ADP-Ribosylation Factor 6↗
PubMed1995

Myofibrillogenesis in rodent skeletal muscle in vitro: two pathways involving thick filament aggregates.

Thick filament aggregates play an important role in myofibrillogenesis in rodent skeletal muscle in vitro. This ultrastructural study describes these aggregates, shows their involvement in the process of myofibril formation, and correlates their appearance and function with current models of myofibrillogenesis. Initially, following myoblast fusion in normal mouse skeletal muscle in vitro, abundant stress fiber-like structures (SFLS) are found near the periphery of early myotubes. These undergo internal rearrangements, forming subcortical sarcomeres and early myofibrils. However, additional thick filaments are synthesized, and some join appositionally to the nascent myofibrils, increasing their diameter. More interiorly, this thick filament synthesis accelerates, with filaments aligning into aggregates resembling discrete A-bands, usually with M-lines and M-regions. The ends of these 'A-band' aggregates are infiltrated with ribosomes and capped by flocculent material. Ultimately, aggregates are incorporated into preexisting myofibrils or associate end-to-end to form new, parallel myofibrils, the flocculent material forming putative I-bands with diminished Z-lines and few thin filaments. As differentiation continues, Z-lines and thin filaments appear, forming true myofibrils. Dysgenic mouse skeletal muscle develops similarly, but when this non-contractile cell matures (i.e., generates action potentials), filaments and their organization break down. Cloned myogenic rat L5/A10 cells also follow this developmental pattern, but in mature, contracting myotubes, Z-lines remain irregular and thin filaments are reduced. In all three types of muscle developing in vitro, thick filament aggregates are a common and predominant feature and as such appear to constitute an additional or alternate pathway to previously described models of myofibrillogenesis.

Animals↗
PubMed1986

Presynaptic terminals persist following degeneration of "flight" muscle during development of a flightless grasshopper.

We have studied the development of a neuromuscular system for which mature function has been lost through evolution in the grasshopper, Barytettix psolus (Cohn and Cantrall, 1974). Barytettix is flightless throughout life and has only vestigial wings that are incapable of active movement. Adult Barytettix lack muscles homologous to the indirect flight muscles of locusts and grasshoppers that fly, while other thoracic muscles are similar. We have found, using light and electron microscopic examination of tissues from various developmental stages, that the metathoracic dorsal longitudinal muscle is present and is innervated during nymphal life but is absent in adults. Yet its nerve persists and, in the adult, contains axonal presynaptic specializations opposite inappropriate targets such as glial processes and basal lamina. Our findings indicate that selective muscle death during development is one mechanism underlying the reduction of the flight system of Barytettix through evolution. The finding that presynaptic terminals persist in the absence of the muscle indicates that the muscle and its innervation follow programs of development that are at least partially independent and reinforces the concept that in insects motorneurons, and perhaps neurons in general, are not dependent upon trophic influences from their targets for survival and maintenance of their differentiated phenotype.

Animals↗
PubMed1990

Impairment of developing fast muscles after nerve injury in the rat depends upon the period of denervation.

After injury to the peripheral nerve in rat pups at 5 days of age the development of the fast muscles tibialis anterior and extensor digitorum longus is impaired. Whether the length of time during which the muscles are denervated affects the degree of impairment was studied here. In one group of animals the peroneal nerve was crushed near to the muscles in one leg and further away from the muscles in the other leg. In another group of animals the sciatic nerve was crushed in one leg at 5 days and in some of these animals the nerve was crushed again 5-7 days later. The recovery of TA and EDL was measured by recording the weight and tension developed once reinnervation was complete. When the nerve was crushed close to the muscles, the muscles recovered significantly better than when the site of injury was further away, while delaying reinnervation by crushing the sciatic nerve a second time, impaired recovery of the muscles. It is concluded that the permanent impairment of fast muscles seen after neonatal nerve injury depends upon the length of time that the muscles are separated from their motoneurones.

Animals↗