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PubMedDate not supplied

Duchenne dystrophic muscle develops lesions in long-term coculture with mouse spinal cord.

When strips of human skeletal muscle from biopsies of normal children and donors with Duchenne muscular dystrophy (DMD) are explanted in organotypic coculture with fetal mouse spinal cord, many regenerating muscle fibers develop, become innervated, and maintain a remarkable degree of mature structure and function for more than 3-6 months in vitro. Sequential light microscopy in correlation with electron-microscopic and electrophysiologic analyses showed that despite cross-species innervation, these human muscle fibers develop stable cross-striations, peripherally positioned myonuclei, and mature, functional motor endplates. Of special interest is the onset of significant progressive abnormalities, e.g., unusual focal myofibrillar lesions, in substantial numbers of innervated mature DMD muscle fibers after 2-4 months in culture. The focal myofibrillar lesions were not detected in normal muscle fibers maintained as long as 6 months in coculture, nor are they comparable to the generalized loss of cross-striations observed in muscle atrophy following in vitro denervation of mature DMD fibers.

Animals↗
PubMed1995

Role of methylation in maintenance of positionally restricted transgene expression in developing muscle.

In transgenic mouse embryos, expression of a muscle-specific reporter, consisting of a chloramphenicol acetyltransferase gene linked to regulatory sequences from the rat myosin light chain 1/3 locus (MLC-CAT), is graded in developing axial muscles along the rostrocaudal axis and in cell cultures derived from these muscles. Here we demonstrate that maintenance of positional differences in MLC-CAT transgene expression cannot be attributed to differences in the transcriptional competence of corresponding muscles. Rather, patterns of transgene expression are reflected in the extent of CpG demethylation of both MLC1 promoter and MLC enhancer sequences. Variations in reporter gene expression can be reconstituted by in vitro methylation of specific CpGs in transfected MLC-CAT DNA. As the MLC-CAT transgene is activated during embryogenesis, demethylation of the MLC1 promoter lags behind that of the downstream MLC enhancer, which appears to be the initial target for epigenetic modification. In developing somites, demethylation of the transgenic MLC enhancer is not graded and therefore does not reflect early regional differences in MLC-CAT transgene expression patterns. These studies implicate selective methylation in the maintenance rather than in the establishment of transcriptional differences in developing muscles.

Animals↗
PubMed2003

Heparan sulfate 6-o-sulfotransferase is essential for muscle development in zebrafish.

Heparan sulfate proteoglycans function in development and disease. They consist of a core protein with attached heparan sulfate chains that are altered by a series of carbohydrate-modifying enzymes and sulfotransferases. Here, we report on the identification and characterization of a gene encoding zebrafish heparan sulfate 6-O-sulfotransferase (hs6st) that shows high homology to other heparan sulfate 6-O-sulfotransferases. When expressed as a fusion protein in cultured cells, the protein shows specific 6-O-sulfotransferase activity and preferentially acts on the iduronosyl N-sulfoglycosamine. In the developing embryo, hs6st is expressed in the brain, the somites, and the fins; the same structures that were affected upon morpholino-mediated functional knockdown. Morpholino injections significantly inhibited 6-O- but not 2-O-sulfation as assessed by HPLC. Morphants display disturbed somite specification independent of the somite oscillator mechanism and have impaired muscle differentiation. In conclusion, our results show that transfer of sulfate to specific positions on glycosaminoglycans is essential for muscle development.

Amino Acid Sequence↗
PubMed1996

Mutations in the rotated abdomen locus affect muscle development and reveal an intrinsic asymmetry in Drosophila.

In bilateral animals, the left and right sides of the body usually present asymmetric structures, the genetic bases of whose generation are still largely unknown [CIBA Foundation (1991) Biological Asymmetry and Handedness, CIBA Foundation Symposium 162 (Wiley, New York), pp. 1-327]. In Drosophila melanogaster, mutations in the rotated abdomen (rt) locus cause a clockwise helical rotation of the body. Even null alleles are viable but exhibit defects in embryonic muscle development, rotation of the whole larval body, and helical staggering of cuticular patterns in abdominal segments of the adult. rotated abdomen is expressed in the embryonic mesoderm and midgut but not in the ectoderm; it encodes a putative integral membrane glycoprotein (homologous to key yeast mannosyltransferases). Mesodermal cells defective in O-glycosylation lead to an impaired larval muscular system. We propose that the staggering of the adult abdominal segments would be a consequence of the relaxation of intrinsic rotational torque of muscle architecture, preventing the colateral alignment of the segmental histoblast cells during their proliferation at metamorphosis.

Amino Acid Sequence↗
PubMed1983

Semitendinosis muscle development in several strains of fetal and perinatal pigs.

At 110 d of gestation, fetuses were removed from Ossabaw, Yorkshire and crossbred sows and from sows selected for high (obese) or for low (lean) backfat thickness. Ossabaw and obese fetuses were smaller than lean, Yorkshire and crossbred fetuses (595 +/- 32 and 863 +/- 44 g vs 1,030 +/- 77, 1,380 +/- 1,144 +/- 80 g; means +/- SE), respectively. Minimum fiber diameters in the semitendinosus muscle were larger in obese, lean and Ossabaw fetuses than in Yorkshire and crossbred fetuses (12.9 +/- .3, 12.5 +/- .2 and 11.8 +/- .2 micron vs 10.2 +/- .2 and 11.1 +/- .8 micron), respectively. Histochemical analysis for NADH-tetrazoleum reductase (NADH-TR) and esterase activities indicated no fiber type differentiation and no strain differences. Fiber type differentiation was obvious with acid ATPase histochemistry in muscles from all fetuses. The white portion of the semitendinosus from Ossabaw, obese and lean fetuses had many fibers that contained no histochemically detectable lipid (oil red O staining). The unstained fibers (oil red O) were always the most peripherally located fibers in a fasciculi. In some instances, 50% of the fibers in a fasciculi were not stained for lipid. All the fibers in the red portion of muscle from Ossabaw, obese and lean fetuses contained lipid. All the fibers in the red and white portions of muscles from crossbred and Yorkshire fetuses contained lipid. Muscles from young (1 to 2 d old) Ossabaw, Yorkshire and crossbred pigs were also histochemically analyzed. Analysis for NADH-TR, esterase and alkaline phosphatase (capillary staining) activities indicated no fiber type differentiation and no strain differences. As in the fetuses, the white portion of muscle from Ossabaw pigs had many fibers with no lipid (oil red O). Lipid was present in all fibers in the deep portions of muscle from Ossabaws and in all fibers in both portions of muscle from crossbred and Yorkshire pigs. These results indicate that when lipid staining is used as the criterion, fiber type differentiation is evident in muscle from fetuses and young pigs from strains not genetically selected for muscling (Ossabaw, obese and lean strains). Furthermore, fiber type differentiation is not evident in muscle from strains of pigs genetically selected for greater muscling (crossbred and Yorkshires).

Animals↗
PubMed1986

Steroid control of neuron and muscle development during the metamorphosis of an insect.

Insect metamorphosis is controlled by a small ensemble of developmental hormones including a class of steroids--the ecdysteroids. In the tobacco hornworm, Manduca sexta, the progression from the larval to pupal to adult stages is controlled by the relative blood titers of ecdysteroids and juvenile hormone (JH). The cellular events in the nervous and muscular systems which accompany metamorphosis resemble those of embryonic development, but they occur in an animal which is larger and experimentally more tractable than an embryo. In this paper we review the role of ecdysteroids in directing the metamorphosis of the nervous and muscular systems in Manduca, and how JH modifies the cellular responses to the steroids. In particular, we describe how these hormones control muscle degeneration, changes in the structure and function of identified neurons, and programmed neuron death. One general finding is that interactions between cells (e.g., neurons and their target muscles) are not involved in their hormonal responses, but rather the hormones act independently and in parallel at the different sites. Another key finding is that the critical periods and hormonal requirements for the commitment to a particular differentiative pathway, and the phenotypic expression of that pathway, can differ, and are therefore experimentally separable. Finally, we find that the significance of a hormonal signal (e.g., a rise in blood ecdysteroids) is interpreted differently depending upon the previous history of hormone exposure of a neuron or muscle. This progressive change in the interpretation of hormonal signals is a major mechanism by which a limited number of hormones can orchestrate a complicated phenomenon such as metamorphosis.

Aging↗
PubMed1998

Transcriptional control of muscle development by myocyte enhancer factor-2 (MEF2) proteins.

Metazoans contain multiple types of muscle cells that share several common properties, including contractility, excitability, and expression of overlapping sets of muscle structural genes that mediate these functions. Recent biochemical and genetic studies have demonstrated that members of the myocyte enhancer factor-2 (MEF2) family of MADS (MCM1, agamous, deficiens, serum response factor)-box transcription factors play multiple roles in muscle cells to control myogenesis and morphogenesis. Like other MADS-box proteins, MEF2 proteins act combinatorially through protein-protein interactions with other transcription factors to control specific sets of target genes. Genetic studies in Drosophila have also begun to reveal the upstream elements of myogenic regulatory hierarchies that control MEF2 expression during development of skeletal, cardiac, and visceral muscle lineages. Paradoxically, MEF2 factors also regulate cell proliferation by functioning as endpoints for a variety of growth factor-regulated intracellular signaling pathways that are antagonistic to muscle differentiation. We discuss the diverse functions of this family of transcription factors, the ways in which they are regulated, and their mechanisms of action.

Animals↗
PubMedDate not supplied

Effects of chronic heat exposure and protein intake on growth performance, nitrogen retention and muscle development in broiler chickens.

The respective effects of ambient temperature, dietary crude protein and feed intake were investigated in finishing chickens and the consequence of protein supplementation under high temperature conditions was analysed in particular. Heat-related reduction in growth was associated with decreased nitrogen retention (-30 or -35% according to the diet), which could not be explained by the observed lower feed intake alone. Tissue samples performed in 5- to 6-week-old chicks showed varying effects of heat according to the muscles studied: at 32 degrees C, the proportion of Pectoralis major muscle (in percentage of body weight) appeared slightly reduced (reduction lower than 10%), whereas the proportion of two leg muscles were increased (+10 to +15% for the Sartorius muscle; +5% for the gastrocnemius muscle). At 32 degrees C, providing a high protein diet significantly (P < 0.05) increased weight gain and feed efficiency, and slightly improved whole body protein deposition.

Animal Nutritional Physiological Phenomena↗
PubMed2002

Muscle development and lineage-specific expression of CiMDF, the MyoD-family gene of Ciona intestinalis.

The expression pattern of CiMDF, the MyoD-family gene of Ciona intestinalis, was analyzed in unmanipulated and microsurgically derived partial embryos. CiMDF encodes two transcripts during development (coding for distinct proteins), the smaller of which, CiMDFa, was detected in maternal RNA. Zygotic activity of CiMDF initiated in cleaving embryos of 32-64 cells. Both CiMDFa and CiMDFb transcripts were detected at this time; however, CiMDFa accumulated more rapidly before declining in abundance such that, by the early tail-formation stage, CiMDFb was more prevalent. Microsurgical isolations of various lineage blastomeres from the eight-cell stage were used to analyze CiMDF expression in the two embryonic lineages that give rise to larval tail muscle-autonomously specified primary cells and conditionally specified secondary cells. CiMDFa and CiMDFb transcripts were detected in both lineages, suggesting that neither functioned in a lineage-specific manner. The data also demonstrated that CiMDF expression was autonomous in the primary lineage (i.e., cells derived from the B4.1 blastomeres) and correlated with histospecific differentiation of muscle. In the secondary lineage (i.e., cells derived from the A4.1 and b4.2 blastomeres), CiMDF expression was conditional and, as in the primary lineage, correlated with muscle differentiation. These experiments reveal similar patterns of CiMDF activity in the primary and secondary muscle lineages and imply a requirement for the expression of this gene in both lineages during larval tail muscle development.

Animals↗
PubMed1994

Differential expression of an endogenous mannose-binding protein R1 during muscle development and regeneration delineating its role in myoblast fusion.

The role of the endogenous brain carbohydrate-binding protein R1 in muscle cell development and regeneration was analysed both in vivo and in vitro. In vivo, R1 was developmentally regulated, with an embryonic 65,00 subunit and a neonatal 67,000 subunit, being replaced progressively by a 135,000 adult form. Lectin R1 was intracellularly localized at birth and in the prenatal period. During development and at the time of myoblast fusion, the antigen was progressively found at the surface, where it remained at low levels in the adult. In vitro, in pure myoblast cultures, only the embryonic form was present. The ultrastructural studies indicated that the lectin could participate in the membrane fusion process during myoblast fusion. The specific role in myoblast fusion, derived from the ultrastructural localization of R1, was evidenced by a strong inhibitory effect of anti-R1 Fab fragments (10-100 micrograms/ml), relative to control Fab fragments. In vivo, the embryonic subunit pattern and subcellular distribution of R1 reappeared in muscle cells after lesion of the adult muscle. This suggested that, as observed in vitro, R1 participated in vivo in the phenomenon of myoblast fusion. Similar modifications in subunit expression were observed in muscles after denervation (the embryonic form of lectin R1 reappearing after lesion), suggesting that R1 could be involved in the process of neuromuscular junction formation. Thus, it is proposed that the carbohydrate-binding protein R1 is an important recognition molecule for the formation of myotubes. Its potential involvement in a recognition process between axons and muscle cells during neuromuscular junction formation is discussed.

Animals↗
PubMed1996

The function of type IV collagen during Drosophila muscle development.

Type IV collagen forms a network that provides the major structural support for basement membranes. Basement membranes are specialized forms of extracellular matrix with important functions in development. One collagen gene (Dcg1) was characterized in Drosophila melanogaster and shown to encode a collagen chain related to vertebrate basement membrane type IV collagen chains. Therefore, to access the functional importance of type IV collagen during Drosophila myogenesis, we adopted two different approaches to decrease the Dcg1 gene expression in Drosophila embryos. We describe, here, that the decrease in Dcg1 gene expression causes, in particular, defective muscle attachments. These mutant phenotypes suggest that type IV collagen acts to stabilize cell-matrix interactions.

Animals↗
PubMed1999

Response of chick lines selected on carcass quality to dietary lysine supply: live performance and muscle development.

Broiler carcass quality can be improved by conventional selection techniques. In this regard, an experimental "quality" line (QL) was selected for high breast meat yield. We analyzed the effects of this selection on the dietary lysine requirement in chicks from 0 to 3 wk. Control (CL) and QL chicks were provided ad libitum access to isoenergetic diets containing 20% crude protein but differing in their lysine content (0.75, 0.88, 1.01, and 1.13%). Two-way ANOVA showed a significant effect (P < 0.01) of genotype on body weight, growth rate, feed intake, and weight of Pectoralis major and Gastrocnemius muscles. Conversely, the Sartorius muscle weight was not modified (P = 0.21) by genotype. Lysine deficiency markedly reduced body weight, growth rate, and feed intake, and increased feed conversion ratio (P < 0.001). Low dietary levels of lysine also depressed the weight of Gastrocnemius, Sartorius, and P. major (P < 0.001). The body or muscle weight response to diet lysine concentration depended on the line, with QL chicks appearing less sensitive to lysine deficiency. Consequently, their dietary requirements could be lower. Finally, when weight gain and P. major muscle protein deposition were plotted against lysine intake, QL chicks appeared to be more efficient than CL chicks. The underlying mechanisms responsible for this await clarification.

Animal Nutritional Physiological Phenomena↗
PubMed1988

Embryonic acetylcholine receptors guarantee spontaneous contractions in rat developing muscle.

Many proteins are expressed in distinct embryonic and adult forms. However, in most cases we do not know why the embryonic form of proteins is required. This question can be readily addressed for the acetylcholine receptor (AChR) because developmentally specified modifications of this ligand-gated ion channel can be directly related to changes in membrane currents. In developing rat soleus muscle, spontaneous transmitter release causes miniature end-plate currents (m.e.p.cs) to flow into the muscle cell. We show here that these m.e.p.cs in neonatal soleus trigger spontaneous contractions. By injecting m.e.p.cs into young fibres, we showed that only embryonic m.e.p.cs can trigger such contractions; adult m.e.p.cs do not last long enough. Developing muscle fibres must be active for synapse and muscle differentiation. Our experiments indicate that the embryonic form of the AChR is essential for spontaneous contractile activity and may therefore be required for normal neuromuscular development.

Action Potentials↗