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PubMed1989

Physiological relevance of the changing subunit composition and regulatory properties of the 6-phosphofructo-1-kinase isozyme pools during heart and muscle development.

During postnatal development, the subunit compositions of the 6-phosphofructo-1-kinase isozyme pools of heart and skeletal muscle are known to change. The isozyme pools from fetal muscle were composed of the L-type (60%), and M-type (36%) and C-type (4%) subunits and the isozymes from fetal and early neonatal heart contain nearly equal amounts of all three subunits. During postnatal development of both tissues, the proportion of the M-type subunit increases until it is the only type present in adult muscle and the major subunit in adult heart (75%). The isozyme pool from fetal muscle exhibit a decreased affinity for fructose-6-P and a greater susceptibility to ATP inhibition compared to the M-rich isozymes which are subsequently present. The isozyme pools from fetal and early neonatal heart, if compared to the M-rich isozymes which are present later during heart development and to the fetal muscle isozymes, exhibited the least affinity for fructose-6-P and the greatest susceptibility to ATP inhibition. Comparison of the isozyme pools containing little or no C-type subunit with those from fetal and early neonatal heart clearly indicates that the presence of substantial levels of the C-type subunit imposed a decreased ability for fructose-2,6-P2 to both lower affinity for fructose-6-P and antagonize sensitivity to ATP inhibition. Although still not thoroughly appreciated, it appears that the changing nature of the isozyme pools in these tissues permits regulation of glucose metabolism in a manner which allows efficient utilization of nutritional opportunities and which adequately meets the energy requirements of each tissue at different stages of development.

Adenosine Triphosphate↗
PubMed2000

Muscle develops a specific form of small heat shock protein complex composed of MKBP/HSPB2 and HSPB3 during myogenic differentiation.

Previously, we identified a new mammalian sHSP, MKBP, as a myotonic dystrophy protein kinase-binding protein, and suggested its important role in muscle maintenance (Suzuki, A., Sugiyama, Y., Hayashi, Y., Nyu-i, N., Yoshida, M., Nonaka, I., Ishiura, S., Arahata, K., and Ohno, S. (1998) J. Cell Biol. 140, 1113-1124). In this paper, we develop the former work by performing extensive characterization of five of the six sHSPs so far identified, that is, HSP27, alphaB-crystallin, p20, MKBP/HSPB2, and HSPB3, omitting lens-specific alphaA-crystallin. Tissue distribution analysis revealed that although each sHSP shows differential constitutive expression in restricted tissues, tissues that express all five sHSPs are only muscle-related tissues. Especially, the expressions of HSPB3, identified for the first time as a 17-kDa protein in this paper, and MKBP/HSPB2 are distinctly specific to muscles. Moreover, these sHSPs form an oligomeric complex with an apparent molecular mass of 150 kDa that is completely independent of the oligomers formed by HSP27, alphaB-crystallin, and p20. The expressions of MKBP/HSPB2 and HSPB3 are induced during muscle differentiation under the control of MyoD, suggesting that the sHSP oligomer comprising MKBP/HSPB2 and HSPB3 represents an additional system closely related to muscle function. The functional divergence among sHSPs in different oligomers is also demonstrated in several ways: 1) an interaction with myotonic dystrophy protein kinase, which has been suggested to be important for the maintenance of myofibril integrity, was observed only for MKBP/HSPB2; 2) a myotube-specific association with actin bundles was observed for HSP27 and alphaB-crystallin, but not for MKBP/HSPB2; and 3) sHSPs whose mRNAs are induced by heat shock are alphaB-crystallin and HSP27. Taken together, the results suggest that muscle cells develop two kinds of stress response systems composed of diverged sHSP members, and that these systems work independently in muscle maintenance and differentiation.

Adult↗
PubMedDate not supplied

Genotype and sexual influences on growth and muscle development of chicken embryos.

The influence of sex and genotype on growth of chick embryos was studied using eggs from commercial broiler hens mated with broiler strain males (BrBr) or with bantam males (BaBr) and using eggs from bantam females mated to bantam males (BaBa) or to broiler strain males (BrBa). Male BrBr embryos were first significantly heavier than females at 9 days of incubation. The influence of sire's genotype was expressed between 6 and 16 days of incubation but not at 20 days. Dam's genotype, and the associated difference in egg weight, significantly affected embryo weight by 12 days of incubation and by 20 days it alone influenced embryo weight. Plasma insulin-like growth factor-I (IGF-I) levels of BrBr and BaBr embryos did not differ at 8, 10, 12, or 14 days of incubation, nor were there sex differences. There were no genotype differences in whole body protein concentration, DNA concentration or protein:DNA ratios at 4 or 8 days of incubation. At 12 days the pectoralis major DNA concentration of BaBa embryos was significantly higher than that of all other groups. Pectoralis muscle protein concentration of BrBa embryos was significantly lower than those of BaBr embryos at 12 days of incubation, but by 16 days it was highest. The protein:DNA ratios of embryos developing in bantam eggs were significantly lower than those in broiler eggs at 12 days. In summary, genotypic and sex differences in body weight and muscularity that develop after hatching appear to be predetermined by differences in embryonic growth patterns, but there is no clear relationship between embryonic growth, plasma IGF-I concentration or the concentration of DNA or protein in pectoralis muscle.

Age Factors↗
PubMed1975

Acetylcholine receptor turnover in membranes of developing muscle fibers.

[125I mono-iodo-alpha-bungarotoxin is used as a specific marker in a description of acetylcholine receptor metabolism. It is concluded that acetylcholine receptors in the surface membranes of chick and rat myotubes developing in cell cultures have a half-life of 22-24 h. Alpha-bungarotoxin (bound to a receptor which is removed from the membrane) is degraded to monoiodotyrosine which appears in the medium. Several observations are consistent with a model in which receptors or alpha-bungarotoxin-receptor complexes are internalized and then degraded: (a) the rate of appearance of iodotyrosine does not reach its maximal rate until 90 min after alpha-bungarotoxin is bound to the surface receptors; (b) 2,4-dinitrophenol, reduced temperature, and cell disruption all inhibit the degradation process. The degradation of surface receptors is not coupled to the process by which receptors are incorporated into the membrane. Evidence suggest that receptors are incorporated into the surface membrane from a presynthesized set of receptors containing about 10% as many alpha-bungarotoxin binding sites as does the surface. Additionally, a third set of acetylcholine receptors is described containing about 30% as amny binding sites as does the surface. These "hidden" recptors are not precursors yet are not readily accessible for binding of extracellular alpha-bungarotoxin. These findings are discussed in relation to both plasma membrane biosynthesis and control of chemosensitivity in developing and denervated skeletal muscle.

Animals↗
PubMed1992

Structural analysis of muscle development: transverse tubules, sarcoplasmic reticulum, and the triad.

Increased interest in the mechanism of excitation-contraction (E-C) coupling over the last few years has been accompanied by numerous investigations into the development of the underlying cellular structures. Areas of particular interest include: (1) the compartmentalization and specialization of an external and an internal membrane system, the T-tubules, and the sarcoplasmic reticulum, respectively; (2) interactions between the membrane proteins of both systems upon the formation of a junction, the triad; and (3) membrane-cytoskeletal interactions leading to the orderly arrangement of the triads with respect to the myofibrils. Structural studies using newly available specific molecular probes and a variety of in vivo and in vitro model systems have provided new insights into the cellular and molecular mechanisms involved in the development of the E-C coupling apparatus in skeletal muscle.

Animals↗
PubMed2003

Laminin alpha5 chain is required for intestinal smooth muscle development.

Laminins (comprised of alpha, beta, and gamma chains) are heterotrimeric glycoproteins integral to all basement membranes. The function of the laminin alpha5 chain in the developing intestine was defined by analysing laminin alpha5(-/-) mutants and by grafting experiments. We show that laminin alpha5 plays a major role in smooth muscle organisation and differentiation, as excessive folding of intestinal loops and delay in the expression of specific markers are observed in laminin alpha5(-/-) mice. In the subepithelial basement membrane, loss of alpha5 expression was paralleled by ectopic or accelerated deposition of laminin alpha2 and alpha4 chains; this may explain why no obvious defects were observed in the villous form and enterocytic differentiation. This compensation process is attributable to mesenchyme-derived molecules as assessed by chick/mouse alpha5(-/-) grafted associations. Lack of the laminin alpha5 chain was accompanied by a decrease in epithelial alpha3beta1 integrin receptor expression adjacent to the epithelial basement membrane and of Lutheran blood group glycoprotein in the smooth muscle cells, indicating that these receptors are likely mediating interactions with laminin alpha5-containing molecules. Taken together, the data indicate that the laminin alpha5 chain is essential for normal development of the intestinal smooth muscle and point to possible mesenchyme-derived compensation to promote normal intestinal morphogenesis when laminin alpha5 is absent.

Animals↗
PubMed1985

Control of peptide-chain initiation in rat skeletal muscle. Development of methods for preparation of native ribosomal subunits and analysis of the effect of insulin on formation of 40 S initiation complexes.

A method was developed for isolation of native ribosomal subunits from rat gastrocnemius muscle. Native 40 S subunits which were isolated by this method retained their associated nonribosomal proteins and consisted primarily of particles with equilibrium densities of 1.41 and 1.48 g/cm3. Based on the binding of radiolabeled Met-tRNAmeti, the 1.41 g/cm3 particle was identified as the 40 S initiation complex. Insulin deficiency in vivo resulting from either diabetes or fasting led to a 2-fold increase in 75 S monomers but had no effect on the numbers of native 40 and 60 S subunits or the relative distribution of the 1.41 and 1.48 g/cm3 particles. The rate of protein synthesis in perfused muscle preparations derived from insulin-deficient rats was reduced to about half the control value. Addition of insulin to the perfusate restored protein synthesis and 75 S monomers to control levels. The effect of insulin on protein synthesis was associated with a 1.5-fold increase in the amount of Met-tRNAmeti bound to the 1.41 g/cm3 particle. These findings identify formation of 40 S initiation complexes as a site of action of insulin on protein synthesis in skeletal muscle.

Animals↗
PubMed2002

Slow myosins in muscle development.

Myogenesis has been a system central to investigations on mechanisms of diversification within groups of differentiating cells. Diversity among cell types has been well described in striated muscle tissue at the protein and enzymatic-function levels for decades, but it is only in recent years that some understanding of the molecular mechanisms responsible for this diversity has begun to emerge. Study of the expression of the slow isoforms of the myosin heavy chain has contributed to our understanding of how cell diversity arises within skeletal and cardiac muscle. Slow MyHc isoforms are developmentally responsive to a number of cues provided by the nervous systems, the endocrine system and, later in development, to functional demands on these developing tissues. Perhaps most informative have been studies on the mechanism for regulation of slow MyHc expression in mammals and birds where studies on the calcineurin-NF-AT pathways and nuclear hormone action have been shown to control MyHC gene expression in skeletal muscle and in the developing heart. The mechanisms involved in cell diversification in myogenesis are undoubtedly more varied and complex than those currently offered to explain cell diversification, but these recent studies have broadened our understanding of the interplay between the nervous system, the endocrine system and cell lineages in controlling cell diversification. Greater focus on the first fibers and cardiomyocytes to form in the embryo are likely to bring additional insights into the mechanism crucial for establishing the patterns of diversity required for successful formation of embryonic tissues.

Animals↗
PubMed1983

Muscle development in large and small pig fetuses.

The largest and smallest littermates were chosen by weight from litters of 38 days' gestation to 1 day post partum. Complete frozen sections of the semitendinosus muscle were used to provide a qualitative and quantitative account of the development of the primary and secondary generations of muscle fibres. The results showed that the time of formation of primary and secondary fibres, and the numbers of primary fibres formed, were the same in both large and small littermates. The number of secondary fibres formed, however, was lower in the smaller fetuses and resulted in there being a 17% difference in total fibre number at birth. Primary fibres in small fetuses were smaller, due to the smaller central myofibril-free region. This small size may have restricted the available surface area for secondary fibre formation. Fibre hyperplasia was found to cease between 85 and 95 days' gestation, and so the fibre number difference is likely to be permanent.

Animals↗
PubMed1976

Formation of myoneural and myotendinous junctions in the chick embryo. Role of acetylcholinesterase-rich granules in the developing muscle fibers.

The mode of formation of the myoneural and myotendinous junctions was investigated in the thigh muscles of the chick embryo. Myotendinous junctions first appeared on day 11 of incubation, whereas myoneural junctions developed on day 12. Intracellular AChE activity in the muscles increased by the 12th day of incubation, and decreased rapidly after the formation of the myoneural junctions. Light and electron microscopically, AChE activity was demonstrated in the nuclear envelope, sarcoplasmic reticulum, Golgi complex, and in large granules which appeared to be derived from the Golgi complex. Large granules showing an intense AChE activity accumulated in the sarcoplasm at the poles of the muscle fiber before the formation of myotendinous junctions. After the translocation of this intracellular enzyme onto the sarcolemma, most likely the result of an exocytosis of the granules, the myotendinous junctions were formed. The AChE-rich granules present in the middle of myotubes developed into spindle- or comma-shaped cisternae which were located in the sarcoplasm just below the presumptive motor endplates. The present results suggest that the transport of AChE-rich granules to the sarcolamma is the first step in the formation of myoneural and myotendinous junctions.

Acetylcholinesterase↗
PubMed1981

Ultrastructural analysis of skeletal muscle development in the fetal pig.

Myogenesis was investigated at the ultrastructural level in the fetal pig at 35, 52, 65, 80, 95 and 110 days of gestation. At each stage of gestation, the predominant type II fiber type portion of the peroneus longus and sartorius muscles was examined. The sequence of events for normal myogenesis in the pig was generally similar to that reported for the skeletal muscle of other vertebrate species. In addition, the time interval for sequential development of myogenesis was similar between the two muscles. Centrioles were identified in primary fetal fibers and also in secondary fibers. No morphological evidence of mitotic activity was found in the myonuclei. The organization of myofibers into fasciculi was unrelated both temporally and spatially to capillary and neural development.

Animals↗
PubMed1998

Temporary exposure of ovine embryos to an advanced uterine environment does not affect fetal weight but alters fetal muscle development.

Embryo transfer techniques may result in fetuses that are heavier at birth and that have been described as highly muscled. The aim of this study was to investigate myogenesis in lambs derived from embryo transfer. Embryos were transferred at Day 3 (estrus = Day 0) to a 3 days-advanced uterine environment, maintained there for 3 days, recovered, and then returned to a synchronous (Day 6) uterus; these fetuses comprised the asynchronous group. Control animals were created by synchronous embryo recovery and single transfer at Day 3. Asynchronous transfer did not affect fetal weight or curved crown-rump length between 46 and 135 days of gestation. No differences were detected between groups at Days 110-135 with respect to muscle mass or protein, RNA, and DNA content. However, total muscle fiber number was significantly increased in plantaris muscles from the asynchronous groups at Day 110 and Day 125, suggestive of prolonged hyperplasia. In addition, the levels of Myf 5 protein and the secondary-to-primary fiber ratio were altered in plantaris muscle from the asynchronous group. The growth data are in contrast to previously reported findings. The results show that fetal myogenesis can be altered by very early events in embryogenesis and suggest that any inferences made solely on the basis of fetal or muscle weight may be fallacious.

Animals↗
PubMed2003

Effect of selection for growth rate and inheritance on posthatch muscle development in turkeys.

The inheritance of, and effect of selection for increased BW on, measurements of muscle fibers and extracellular space in turkeys were studied using a randombred control line (RBC2), a subline (F) of RBC2 selected long-term only for increased 16 wk BW, a commercial sire line (B), and reciprocal crosses of the F and B lines. Measures of additive genetic variation were obtained by comparing all of the pure lines or just the large-bodied F and B lines. Estimates of nonadditive genetic variation were obtained by contrasting the average of the reciprocal crosses with the average of the parental lines. A contrast of the reciprocal crosses provided estimates of sex linkage or maternal effects. Samples of pectoralis major muscle were obtained from three males and three females of each genetic group at 1, 4, 8, and 16 wk of age in a manner to avoid muscle contraction. After fixing and cross sectioning, the muscle samples were stained with hematoxylin and eosin to view muscle morphology. The stained sections were analyzed for muscle fiber width, muscle fiber bundle width (except at 16 wk of age), number of fibers within a 136-microm2 area, and extracellular matrix perimysial (PW) and endomysial (EW) width. Additive genetic variation, as measured by line differences, of measures of muscle fibers and extracellular matrix was a more important source of variation when the RBC2 line was included in the comparison. When all of the pure lines were compared, line differences were significant for fiber bundle width at 4 wk of age; individual fiber width and number of fibers in a given area at 4, 8, and 16 wk of age; PW at all ages; and EW at 1, 8, and 16 wk of age. With the possible exception of PW, nonadditive genetic variation was not an important source of variation for muscle measurements. For PW, the estimates of heterosis were -14.6, 26.4, 14.5, and 17.3% at 1, 4, 8, and 16 wk of age, respectively, but none of the values was significant (P > 0.05). Genetic increases in BW were associated with an increase in muscle fiber width, a smaller number of fibers in a given area, and less extracellular space at older ages. Apparent differences in growth patterns among the genetic groups may have been responsible for the different patterns of change in muscle measurements in the various genetic groups over ages.

Age Factors↗
PubMed1993

Regulation of fat and muscle development by transforming growth factor alpha in transgenic mice and in cultured cells.

Transgenic mice overexpressing transforming growth factor alpha (TGF-alpha) under control of the metallothionein promoter had, on average, 20% reductions in body and carcass weights compared to nontransgenic littermates. This loss resulted from significant decreases in the comparative weights of bone, muscle, and especially fat. Transgenic epididymal fat pads were reduced by 40-80%, and total body fat content by 50%, relative to control animals. Distal hindlimb muscle weights were 20% below normal, and other skeletal muscles were visibly smaller in size. Weight reductions were accompanied by decreases in the cellularity of transgenic fat pads and muscles and by decreases in the number and area of striated muscle fibers. These findings were not obviously attributable to differences in metabolic rates since transgenic and control mice displayed similar levels of energy expenditure per unit lean body mass. The effects of TGF-alpha on the development of these tissues could be mimicked in culture for fat but not muscle. Thus, TGF-alpha did not inhibit the differentiation of the mouse skeletal myoblast cell line C2C12 as evidenced by the expression of muscle-specific actin and fusion to form multinucleated myotubes. However, TGF-alpha repressed the differentiation of the preadipocyte cell line 3T3-F442A in a dose-dependent and reversible manner as judged by morphological conversion and diminished expression of mRNAs encoding the adipocyte-specific markers adipsin and glycerophosphate dehydrogenase. This repression, which occurred without marked stimulation of proliferation, was incomplete even in the presence of high concentrations of growth factor. Despite its effects on adipose development, introduction of the metallothionein-TGF-alpha transgene into the ob/ob genetic background did not suppress the marked obesity characteristic of this mutation. Finally, endogenous TGF-alpha epidermal growth factor receptor mRNAs were detected in normal adipose tissue, suggesting that regulation of adipogenesis by this growth factor may be physiological.

Adipose Tissue↗
PubMed1989

Histochemical studies of muscle development in decapitated and hypophysectomized pig fetuses: blood vessel development.

In Exp. 1, fetuses were decapitated in utero on d 45 of gestation and examined at 110 d of gestation; in Exp. 2, fetuses were hypophysectomized (hypox) in utero with a cauterizing needle at d 70 of gestation and examined at 110 d of gestation. Semitendinosus muscles were sampled and transverse cryostat sections were cut from the medial portion of the muscle. Quantitative analysis of lectin-stained sections showed that capillary:fiber ratios (C/F) were lower (P less than .01) for sections from decapitated and hypox fetuses than for sections from control fetuses. The superficial and deep aspects of muscle sections from control fetuses had markedly different C/F ratios (deep region, 24.1 +/- 2; superficial region, 11.2 +/- .5). Fetal decapitation and hypophysectomy abolished differences in C/F ratios between deep and superficial regions of muscle sections (hypox fetuses; deep region, 6.9 +/- 1; superficial region, 6.4 +/- .6). Capillaries in sections from control fetuses were reactive for several enzymes, whereas capillaries in sections from experimental fetuses (decapitated and hypox) were not reactive for these enzymes. The number of small arterioles was reduced in sections from experimental fetuses (decapitated and hypox) compared with sections from control fetuses. These studies demonstrate that lowering the levels of pituitary hormones in the fetus retards the development of blood vessels in muscle tissue both quantitatively and qualitatively.

Animals↗