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At least 451 records · Page 25Linked to original sources
PubMed1999

SF/HGF is a mediator between limb patterning and muscle development.

Scatter factor/hepatocyte growth factor (SF/HGF) is known to be involved in the detachment of myogenic precursor cells from the lateral dermomyotomes and their subsequent migration into the newly formed limb buds. As yet, however, nothing has been known about the role of the persistent expression of SF/HGF in the limb bud mesenchyme during later stages of limb bud development. To test for a potential role of SF/HGF in early limb muscle patterning, we examined the regulation of SF/HGF expression in the limb bud as well as the influence of SF/HGF on direction control of myogenic precursor cells in limb bud mesenchyme. We demonstrate that SF/HGF expression is controlled by signals involved in limb bud patterning. In the absence of an apical ectodermal ridge (AER), no expression of SF/HGF in the limb bud is observed. However, FGF-2 application can rescue SF/HGF expression. Excision of the zone of polarizing activity (ZPA) results in ectopic and enhanced SF/HGF expression in the posterior limb bud mesenchyme. We could identify BMP-2 as a potential inhibitor of SF/HGF expression in the posterior limb bud mesenchyme. We further demonstrate that ZPA excision results in a shift of Pax-3-positive cells towards the posterior limb bud mesenchyme, indicating a role of the ZPA in positioning of the premuscle masses. Moreover, we present evidence that, in the limb bud mesenchyme, SF/HGF increases the motility of myogenic precursor cells and has a role in maintaining their undifferentiated state during migration. We present a model for a crucial role of SF/HGF during migration and early patterning of muscle precursor cells in the vertebrate limb.

Animals↗
PubMed1997

Absence of oculomotor and trochlear motoneurons leads to altered extraocular muscle development in the Wnt-1 null mutant mouse.

Wnt-1 null mutant mice lack midbrain somatic motor nuclei. Primordial migration and spatial patterning of the extraocular muscles, however, was preserved, but myogenesis was disrupted in aneural muscles. Some muscles normally innervated by oculomotor and trochlear nuclei received aberrant innervation, which proved sufficient to maintain prenatal stages of myogenesis. The absence of motoneurons followed by innervation from inappropriate motoneuron pools is a viable candidate mechanism in ocular motility disorders, including Duane retraction syndrome and congenital fibrosis of extraocular muscle.

Alleles↗
PubMed1999

The alpha7beta1 integrin in muscle development and disease.

The alpha7beta1 integrin is a laminin receptor on the surface of skeletal myoblasts and myofibers. Alternative forms of both the alpha7 and beta1 chains are expressed in a developmentally regulated fashion during myogenesis. These different alpha7beta1 isoforms localize at specific sites on myofibers and appear to have distinct functions in skeletal muscle. These functions include the migration and proliferation of developing myoblasts, the formation and integrity of neuromuscular and myotendinous junctions, and the "gluing" together of muscle fibers that is essential to the generation of contractile force. The alpha7beta1 integrin appears to be both directly and indirectly causally related to several muscle diseases. Enhanced expression of alpha7beta1-mediated linkage of the extracellular matrix is seen in Duchenne muscular dystrophy and may compensate for the absence of the dystrophin-mediated linkage. Downregulation of expression of the integrin may contribute to the development of pathology in congenital laminin deficiencies. Mutations in the alpha7 integrin gene underlie additional congenital muscle diseases. The functional roles of this integrin in the formation and stability of the neuromuscular and myotendinous junctions and its localization between fibers suggest that altered expression or function of this integrin may have widespread involvement in other myopathies. The localization of the alpha7 gene at human chromosome 12q13 is a useful clue for focusing such studies.

Animals↗
PubMed2000

Utrophin may be a precursor of dystrophin during skeletal muscle development.

Expression patterns of utrophin were investigated and compared to those of dystrophin and associated proteins in skeletal muscle of rat embryos from E12 to E21 by immunohistochemistry. Utrophin was readily detected from E12 on, earlier than full-length dystrophin on E14. A shorter dystrophin isoform was observed from E12 to E16. The level of utrophin reached a maximum on E16-17 and then declined while that of dystrophin increased after E17. A complementary distribution of these two molecules was observed on E18. Beta-dystroglycan appeared as early as utrophin. Sarcoglycans, appearing from E14 on, were anchored first by utrophin and then by dystrophin. These results elucidate the chronological order of expression of the dytrophin/utrophin protein complex and indicate that this protein complex is originally stabilized by utrophin. This study supports our hypothesis that utrophin might be a developmental precursor of dystrophin.

Animals↗
PubMed1986

Transcriptional regulation of nicotinic acetylcholine receptor genes during muscle development.

The quantities of nicotinic acetylcholine receptors measured by alpha-bungarotoxin binding on the surface of mouse skeletal muscle C2 cells increase by approximately 10- to 100-fold during their terminal differentiation in culture. By northern blot analysis, we have determined that the steady-state levels of the AChR alpha and delta subunit mRNAs increase by approximately 15-fold during differentiation of C2 cells. To determine if the differences in message levels during myogenesis are due to changes in transcriptional rates of these genes, nuclear run-on experiments were done using nuclei from 3-day-old undifferentiated cells and 7-day-old differentiated cells. The rates of transcription for both the alpha and delta subunit genes changed from levels that could not be detected over background in nuclei from undifferentiated cells to levels that were at least 8-fold over background in differentiated nuclei. As internal controls, we measured the rates of transcription of mouse actin and histone genes. The signals obtained from both undifferentiated and differentiated nuclei were approximately 50-fold over background for both genes, indicating that the absence of detectable transcription of receptor subunit genes in undifferentiated C2 is specific.

Animals↗
PubMed1990

Histomorphometrical analysis of the influence of soft diet on masticatory muscle development in the muscular dystrophic mouse.

The known difference in the severity of dystrophy between the masseter and the digastric muscle of the mouse (dy/dy C57BL/J6) may be attributed to the differences in muscle work load. This possibility was tested by subjecting 3-week-old mice (normal and dystrophic) to a soft diet for 4 weeks. Microscopic examination of haematoxylin-eosin stained sections of these muscles showed that the fibre size dispersion (a measure of disease severity) decreased slightly but significantly in the masseters of mice on a soft diet. It was thus possible to improve the condition of dystrophic masticatory muscles by changing their function. Body weight curves measured during the experimental period suggest that the dystrophic mice may have been under weight because of malnutrition due to lack of sufficient masticatory power.

Animals↗
PubMed1990

[Changes in the muscle fiber conduction velocity (MFCV) due to the masticatory muscle development. 1. Preliminary study in adults].

The purpose of this study was to investigate the methods involved in observing the muscle fiber conduction velocity (MFCV) both in the masseter muscle and the m. biceps brachii in healthy persons. Three adults were the subjects in this study, none of whom had any gnathofacial dysfunction. The EMG activities were recorded from the m. biceps brachii with the arm bent at right angles and the masseter muscle in the intercuspal position, in both muscles during 50% of maximum voluntary isometric contraction on the habitual side. Three types of surface electrodes were used. Type 1. the disc type electrodes array arranged straight, Type 2. the disc type electrodes array arranged independently, Type 3. the strip type surface electrodes array arranged straight. The EMG activities preamplified at three conditions of time constant, e.g., 0.003, 0.01, 0.03 sec on m. biceps brachii were analyzed through a personal computer system and a FFT analyser. The conduction velocity was calculated by the cross-correlation method. The results obtained in this study were as follows: 1) No differences in the MFCV between the time constant were noticed. 2) The electrode array arranged straight was effective in the measurement of the MFCV in adults and in particular the strip type series electrodes array arranged straight was the most effective to measure the MFCV in the masseter muscle. 3) The average MFCV of the m. biceps brachii and the masseter muscle were 4.13 +/- 0.29 m/sec and 14.28 +/- 1.21 m/sec respectively.

Adult↗
PubMed1998

The open duration of fetal ACh receptor-channel changes during mouse muscle development.

1. We performed an RNase protection assay on cultured C2C12 mouse myotubes, demonstrating that the gamma subunit of the fetal muscle acetylcholine receptor (AChR) exists as two splice variants, which differ in the presence of the amino terminal exon 5. 2. We studied unitary ACh-evoked events in fibres acutely dissociated from the hindlimb flexor digitorum brevis muscle of BALB/C mice aged between embryonic day 16 (E16) and postnatal day 6 (P6). 3. At all ages, the channel conductance was about 30 pS, typical of the fetal form of the AChR. The mean open time increased significantly from 6 ms at E16 to 9 ms at E19, then decreased to about 5 ms during the first postnatal week. The lengthening of the open time was considerably delayed in hypothyroid mice. Data were recorded at 24-26 degrees C. 4. On the basis of previously reported experiments in heterologous expression systems, we suggest that the modulation of channel open time is related to the expression of the AChR incorporating the gammas subunit. These events might be coupled to the crucial modifications in muscle innervation that take place during the same developmental period.

Animals↗
PubMed1984

A single troponin T gene regulated by different programs in cardiac and skeletal muscle development.

A cloned complementary DNA derived from a messenger RNA transiently present at low abundance levels in early chick embryonic skeletal muscle hybridizes to a messenger RNA present at high abundance levels in cardiac muscle. Genomic DNA hybridization and nucleotide sequence identity of complementary DNA's from both heart and skeletal muscle demonstrate that the messenger RNA's from both sources are encoded by the same gene. The encoded polypeptide is a troponin T sequence which is probably a cardiac isoform. This single copy troponin T isogene is governed by different regulatory programs in heart and skeletal muscle differentiation.

Animals↗
PubMed2000

Caenorhabditis elegans twist plays an essential role in non-striated muscle development.

The basic helix-loop-helix (bHLH) transcription factor Twist plays a role in mesodermal development in both invertebrates and vertebrates. In an effort to understand the role of the unique Caenorhabditis elegans Twist homolog, hlh-8, we analyzed mesodermal development in animals with a deletion in the hlh-8 locus. This deletion was predicted to represent a null allele because the HLH domain is missing and the reading frame for the protein is disrupted. Animals lacking CeTwist function were constipated and egg-laying defective. Both of these defects were rescued in transgenic mutant animals expressing wild-type hlh-8. Observing a series of mesoderm-specific markers allowed us to characterize the loss of hlh-8 function more thoroughly. Our results demonstrate that CeTwist performs an essential role in the proper development of a subset of mesodermal tissues in C. elegans. We found that CeTwist was required for the formation of three out of the four non-striated enteric muscles born in the embryo. In contrast, CeTwist was not required for the formation of the embryonically derived striated muscles. Most of the post-embryonic mesoderm develops from a single lineage. CeTwist was necessary for appropriate patterning in this lineage and was required for expression of two downstream target genes, but was not required for the expression of myosin, a marker of differentiation. Our results suggest that mesodermal patterning by Twist is an evolutionarily conserved function.

Animals↗
PubMed2003

Effects of delayed feed intake on body, intestine, and muscle development in neonate broilers.

The short-term effects of delayed feeding (DF) for 2 d posthatching were measured in neonate chicks and compared to early feeding (EF). Chicks from 10 independent families were used in this study to determine whether genetic background control of growth may be influenced by EF and DF. Early feeding maintained significant interfamily body weight variations from hatch to 4 d of age, whereas there were no significant differences from 1 d of age when feeding was delayed to 48 h posthatching. These results suggest that posthatching feeding delay may distort genetic selection by masking the expression of genetic potential and disturbing the estimation of chick breeder value. In DF chicks, overall body growth was delayed until the beginning of feeding and body weight at 6 d of age was 25% lower than EF chicks. Availability of feed after the fasting period was not sufficient to compensate for the retardation of weight gain in either body weight or in intestine and breast muscle weight. However, initiation of intestine growth in DF chicks occurred from 1 d of age despite the lack of feeding, whereas feed intake was essential to enhance muscle growth. The potential for protein synthesis was lower in DF than in EF chicks during the first 2 d posthatching (P < 0.001) and then reached similar values after feed intake. These results confirm that initiation of growth in neonate chicks is improved by earlier feeding after hatching. Awareness of changes in overall body weight caused by posthatching food deprivation, especially in the intestine and muscle might help in the development of new diets which could minimize retardation of body weight gain in chicks.

Aging↗
PubMed1994

A screen for genetic loci required for body-wall muscle development during embryogenesis in Caenorhabditis elegans.

We have used available chromosomal deficiencies to screen for genetic loci whose zygotic expression is required for formation of body-wall muscle cells during embryogenesis in Caenorhabditis elegans. To test for muscle cell differentiation we have assayed for both contractile function and the expression of muscle-specific structural proteins. Monoclonal antibodies directed against two myosin heavy chain isoforms, the products of the unc-54 and myo-3 genes, were used to detect body-wall muscle differentiation. We have screened 77 deficiencies, covering approximately 72% of the genome. Deficiency homozygotes in most cases stain with antibodies to the body-wall muscle myosins and in many cases muscle contractile function is observed. We have identified two regions showing distinct defects in myosin heavy chain gene expression. Embryos homozygous for deficiencies removing the left tip of chromosome V fail to accumulate the myo-3 and unc-54 products, but express antigens characteristic of hypodermal, pharyngeal and neural development. Embryos lacking a large region on chromosome III accumulate the unc-54 product but not the myo-3 product. We conclude that there exist only a small number of loci whose zygotic expression is uniquely required for adoption of a muscle cell fate.

Animals↗
PubMed1990

Functional implications of the unusual spatial distribution of a minor alpha-tubulin isotype in Drosophila: a common thread among chordotonal ligaments, developing muscle, and testis cyst cells.

Three of the four alpha-tubulin genes in Drosophila melanogaster are temporally regulated. mRNA from one of these genes, alpha 85E-tubulin, first appears in 6- to 8-hr embryos and persists, with marked fluctuations, through the end of pupal development. In adults, alpha 85E mRNA has been unequivocally identified only in testes. In the present study, isotype-specific antibodies have been used to localize alpha 85E tubulin protein in whole tissues. The results demonstrate a spatially restricted expression pattern of the alpha 85E gene that includes tissues of both ectodermal and mesodermal origins. Specifically, embryonic accumulation of alpha 85E tubulin is limited to support cells of chordotonal organs and the developing musculature of the viscera and body wall. In late third instar larvae, chordotonal organs and a subset of larval nerves, but not muscle, stain with anti-alpha 85E. The timing of protein accumulation during pupal development suggests that alpha 85E tubulin is involved in the construction of the adult as well as the larval musculature. In testis, only the somatically derived cyst cells that surround developing spermatid bundles accumulate alpha 85E-tubulin. The cell types that express alpha 85E share a requirement for extensive cell shape changes during development, suggesting that this minor alpha-tubulin may have distinct functional properties.

Animals↗
PubMed1990

Acetylcholinesterase activity of developing muscles in the lower limb of the rat.

A cytochemical study of acetylcholinesterase was done in the lower limb of the prenatal rat and in the gastrocnemius muscle of the postnatal rat. Between 15 and 17 days of gestation, mesenchymal cells constituting the muscle primordia are characterized by the presence of enzyme activity in their rough endoplasmic cisterns and nuclear envelopes, while those involved in the formation of the neocapillary and cartilage do not show enzyme activity. This suggests that mesenchymal cells destined to myogenic cells actively produce acetylcholinesterase in a limited period, which may play a role in cellular aggregation and fusion during the muscular morphogenesis. Cytochemical findings as to extensive networks of secondary synaptic folds of the neuromuscular junctions and invaginations of the sarcolemma in the extrasynaptic regions are also illustrated in the differentiating gastrocnemius muscles.

Acetylcholinesterase↗
PubMed2005

Screening for the coccidiostats halofuginone and nicarbazin in egg and chicken muscle: development of an ELISA.

Nicarbazin and halofuginone have been widely used as coccidiostats for the prevention and treatment of coccidiosis in poultry. It has been shown that accidental cross-contamination of feed can lead to residues of these compounds in eggs and/or muscle. This paper describes a direct competitive assay for detecting halofuginone and nicarbazin, developed as qualitative screening assay. In an optimized competitive ELISA, antibodies showed 50% binding inhibition at approximately 0.08 ng ml(-1) for halofuginone and 2.5 ng ml(-1) for dinitrocarbanilide (marker residue for nicarbazin). Extraction from the matrix was carried out with acetonitrile followed by a wash with hexane. The assay's detection capability (CCbeta) for halofuginone was < 0.5 microg kg(-1) in egg and < 1 microg kg(-1) in muscle. For dinitrocarbanilide, the CCbeta was estimated at < 3 microg kg(-1) in egg and < 10 microg kg(-1) in chicken muscle.

Animals↗
PubMed1992

Activation of the gene encoding the glycolytic enzyme beta-enolase during early myogenesis precedes an increased expression during fetal muscle development.

We define the spatial and temporal patterns of expression of the gene encoding the glycolytic enzyme, beta-enolase, during mouse ontogenesis. Transcripts were detected by in situ hybridization using 35S labelled cRNA probes. The beta-enolase gene is expressed only in striated muscles. It is first detected in the embryo, in the cardiac tube and in newly formed myotomes. In the muscle masses of the limb, beta gene expression occurs at a low level in primary fibers, and subsequently greatly increases at a time which corresponds to the onset of innervation and secondary fiber formation. Later in development, it becomes undetectable in slow-twitch fibers. Our results demonstrate the multistep regulation of the beta-enolase gene. The regulation of this muscle-specific gene in somites is discussed in terms of the myogenic sequences of the MyoD family shown to be present when it is activated.

Animals↗