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At least 199 records · Page 11Linked to original sources
PubMed1992

Inactivation of MyoD in mice leads to up-regulation of the myogenic HLH gene Myf-5 and results in apparently normal muscle development.

The myogenic basic HLH transcription factor family of genes, composed of MyoD, myogenin, Myf-5, and Myf-6, are thought to regulate skeletal muscle differentiation. To understand the role of MyoD in myogenesis, we have introduced a null mutation of MyoD into the germline of mice. Surprisingly, mice lacking MyoD are viable and fertile. Histological examination of skeletal muscle failed to reveal any morphological abnormalities in these mice. Furthermore, Northern analysis revealed normal levels of skeletal muscle-specific mRNAs. Significantly, Myf-5 mRNA levels are elevated in postnatal mutant mice. Normally, Myf-5 expression becomes markedly reduced at day 12 of gestation when MyoD mRNA first appears. This suggests that Myf-5 expression is repressed by MyoD. Our results indicate that MyoD is dispensable for skeletal muscle development in mice, revealing some degree of functional redundancy in the control of the skeletal myogenic developmental program.

Animals↗
PubMed1982

The pattern of muscle development in the chick leg.

The splitting pattern and the spatial arrangement of the musculature were studied in the chick tibiotarsal segment. All 15 muscles evolve from the two opposed premuscular masses which become dorsal and ventral to the chondrogenic core before day 5 of incubation. Binary and tertiary divisions and subdivisions of these muscle masses between day 5 and day 7.5 of incubation produce the muscular pattern characteristic of the hind limb zeugopod.

Animals↗
PubMed1997

Smooth muscle development in the obstructed fetal bladder.

OBJECTIVES: To evaluate changes in the smooth muscle and connective tissue development in the obstructed and normal fetal bladder. METHODS: The smooth muscle and connective tissue composition of 19 fetal urinary bladders, including those of 9 fetuses with anatomic obstruction and 10 controls free of urologic disease, were analyzed by light microscopy and computer-assisted color image analysis. RESULTS: The bladder wall thickness was markedly increased in obstructed fetuses throughout gestation as compared with that in controls. The disparity in bladder wall thickness increased rapidly during gestation. The percent area density of smooth muscle and connective tissue as well as the ratio of smooth muscle to connective tissue remained the same in the obstructed and normal control fetal bladders. CONCLUSIONS: Although bladder outlet obstruction is associated with a marked increase in bladder wall thickness, the percent of smooth muscle and connective tissue comprising the mural histology remains relatively constant as compared with that of normal fetal controls. This study suggests that bladder outlet obstruction in the fetus is not associated with excess collagen deposition but rather with an increased amount of bladder with normal cellular content and a concomitant increase in smooth muscle development.

Connective Tissue↗
PubMed1984

Cardiac muscle development in mice exposed to ethanol in utero.

The purpose of the present research was to determine the effect of in utero ethanol exposure on cardiac muscle development. Pregnant albino mice (Swiss strain) at 8 days of gestation were divided into three groups: a normal group fed Purina lab chow for rodents and water ad libitum; an ethanol group fed the liquid diet ENSURE with 20% of the calories derived from ethanol (12.6 +/- 1.2 gm/kg body weight per day); and an isocaloric group pairfed ENSURE with 20% of the calories derived from sucrose. These diets were continued until birth, at which time the litter size, crown to rump length, and weight were recorded. Randomly selected neonatal pups from each litter were decapitated and their hearts immediately processed for transmission electron microscopy. Litter size, crown to rump length, and body weight of the ethanol-treated mice at birth were significantly less than normal but not less than pairfed controls. Ultrastructural evaluation of cardiac muscle from mice treated in utero with ethanol in comparison to that from both normal and pair-fed control animals revealed various degrees of morphological alterations. The most pronounced alterations were in mitochondrial structure and included an increase in mitochondrial volume per cytoplasmic volume and a marked decrease in the amount of inner mitochondrial membrane. Myofibrillar abnormalities were also evident in the ethanol group but not in either control group. These abnormalities included a decrease in the myofibril volume per cytoplasmic volume and a disruption in myofibril organization particularly the Z-bands. The ultrastructural alterations in the cardiac muscle from the ethanol treated group were not a result of malnutrition or dehydration as the pairfed group did not exhibit these changes. It is apparent from this study that exposure of mice in utero to ethanol can cause ultrastructural abnormalities in cardiac muscle cells. Whether these changes result in heart pathophysiology and persist to adulthood are not known.

Animals↗
PubMed1994

[Expression and localization of dystrophin during human skeletal, cardiac and smooth muscle development].

Dystrophin, the Duchenne muscular Dystrophy gene product, is a large cytoskeletal protein associated with a complex of membrane proteins, the Dystrophin Glycoprotein Complex (DGC). Dystrophin is localized to the sarcolemmal membrane of all normal muscle types, but is absent from muscles of DMD patients. Using monoclonal antibodies raised against distinct regions of the dystrophin, we studied its expression and subcellular localization during human skeletal, cardiac and smooth muscle development. We have shown that the expression and the association of dystrophin with the plasma membrane take place earlier in cardiac and smooth muscles (8 weeks of gestation) than in skeletal muscles. In skeletal muscles, dystrophin is first observed in the cytoplasm, and is progressively localized to the plasma membrane from 10 weeks onwards. We obtained differences in staining when using antibodies against either the central part of the protein or the carboxy-terminal domain, and we suggested that isoforms of dystrophin, probably differing in their carboxy-terminal end and their capacity to associate with the plasma membrane were differentially expressed during development and in different tissue-types (7). These findings are discussed in the context of the pathology of Duchenne Muscular Dystrophy.

Dystrophin↗
PubMed1999

Synergistic regulation of vertebrate muscle development by Dach2, Eya2, and Six1, homologs of genes required for Drosophila eye formation.

We have identified a novel vertebrate homolog of the Drosophila gene dachshund, Dachshund2 (Dach2). Dach2 is expressed in the developing somite prior to any myogenic genes with an expression profile similar to Pax3, a gene previously shown to induce muscle differentiation. Pax3 and Dach2 participate in a positive regulatory feedback loop, analogous to a feedback loop that exists in Drosophila between the Pax gene eyeless (a Pax6 homolog) and the Drosophila dachshund gene. Although Dach2 alone is unable to induce myogenesis, Dach2 can synergize with Eya2 (a vertebrate homolog of the Drosophila gene eyes absent) to regulate myogenic differentiation. Moreover, Eya2 can also synergize with Six1 (a vertebrate homolog of the Drosophila gene sine oculis) to regulate myogenesis. This synergistic regulation of muscle development by Dach2 with Eya2 and Eya2 with Six1 parallels the synergistic regulation of Drosophila eye formation by dachshund with eyes absent and eyes absent with sine oculis. This synergistic regulation is explained by direct physical interactions between Dach2 and Eya2, and Eya2 and Six1 proteins, analogous to interactions observed between the Drosophila proteins. This study reveals a new layer of regulation in the process of myogenic specification in the somites. Moreover, we show that the Pax, Dach, Eya, and Six genetic network has been conserved across species. However, this genetic network has been used in a novel developmental context, myogenesis rather than eye development, and has been expanded to include gene family members that are not directly homologous, for example Pax3 instead of Pax6.

Amino Acid Sequence↗
PubMed1984

Appearance of high-molecular-weight acetylcholinesterase in aneural muscle developing in vivo.

Acetylcholinesterase was studied in the superior oblique muscle of the duck embryo during the course of in vivo development. Normally developing, paralyzed, and uninnervated muscles were studied using velocity sedimentation for separation of various forms and biochemical determination of enzyme activity, and light and electron microscopy for histochemical and cytochemical localization of enzyme. Results indicate that neither muscle activity nor contact by the motor neurons is essential for the appearance of high-molecular-weight form of acetylcholinesterase on muscle cells developing in vivo. Acetylcholinesterase activity per muscle was considerably lower in the paralyzed and aneural muscles than the normal muscle. The absolute loss of acetylcholinesterase parallels loss of muscle protein in paralyzed and aneural muscles and may be secondary. Paralysis or absence of innervation had no significant effect on the specific activity of acetylcholinesterase.

Acetylcholinesterase↗
PubMed1985

Heart C-protein is transiently expressed during skeletal muscle development in the embryo, but persists in cultured myogenic cells.

The expression of cardiac and white skeletal C-protein isoforms was analyzed in developing chicken embryos and in primary skeletal muscle cell cultures by immunoblot and immunofluorescence staining using polyclonal antibodies specific for both of the two different proteins. In the embryo, cardiac C-protein was detected in the developing heart from very early stages through adulthood. In skeletal muscle, cardiac C-protein is shown to be transiently expressed between Days 3 and 15 during development. In contrast, the expression of white skeletal C-protein is gradual and progressive starting approximately from Day 15 on in development. In primary cell cultures of skeletal muscle, however, cardiac C-protein remained expressed throughout prolonged culture time, this in conjunction with white skeletal C-protein. Thus the down regulation of cardiac C-protein and the transition from cardiac C-protein to adult skeletal (white) C-protein which was observed during skeletal muscle development in vivo, does not seem to go to completion in the in vitro system.

Animals↗
PubMed1994

Genes critical for muscle development and function in Caenorhabditis elegans identified through lethal mutations.

By taking advantage of a lethal phenotype characteristic of Caenorhabditis elegans embryos that fail to move, we have identified 13 genes required for muscle assembly and function and discovered a new lethal class of alleles for three previously known muscle-affecting genes. By staining mutant embryos for myosin and actin we have recognized five distinct classes of genes: mutations in four genes disrupt the assembly of thick and thin filaments into the myofilament lattice as well as the polarized location of these components to the sarcolemma. Mutations in another three genes also disrupt thick and thin filament assembly, but allow proper polarization of lattice components based on the myosin heavy chain isoform that we analyzed. Another two classes of genes are defined by mutations with principal effects on thick or thin filament assembly into the lattice, but not both. The final class includes three genes in which mutations cause relatively minor defects in lattice assembly. Failure of certain mutants to stain with antibodies to specific muscle cell antigens suggest that two genes associated with severe disruptions of myofilament lattice assembly may code for components of the basement membrane and the sarcolemma that are concentrated where dense bodies (Z-line analogs) and M-lines attach to the cell membrane. Similar evidence suggests that one of the genes associated with mild effects on lattice assembly may code for tropomyosin. Many of the newly identified genes are likely to play critical roles in muscle development and function.

Actins↗
PubMed1996

Hypothyroidism alters diaphragm muscle development.

The impact of hypothyroidism (Hyp) on myosin heavy chain (MHC) isoform expression, maximum specific force (P0), fatigability, and maximum unloaded shortening velocity (V0) was determined in the rat diaphragm muscle (Dia) at 0, 7, 14, 21, and 28 days of age. Hyp was induced by treating pregnant rats with 6-n-propyl-2-thiouracil (0.05% in drinking water) beginning at gestational day 10 and was confirmed by reduced plasma levels of 3,5,3'-triiodothyronine and thyroxine. MHC isoforms were separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and analyzed by densitometry. Isometric P0 and fatigue resistance of the Dia were measured in vitro at 26 degrees C, and V0 was determined at 15 degrees C with the slack test. Compared with control muscles, expression of MHC-slow was higher and expression of adult fast MHC isoforms was lower in Hyp Dia at all ages. The neonatal isoform of MHC continued to be expressed in the Hyp Dia until day 28. At each age, P0 and fatigability were reduced and V0 was slower in the Hyp Dia. We conclude that Hyp-induced alterations in MHC isoform expression do not fully predict the changes in Dia contractile properties.

Aging↗
PubMed1995

Molecular analysis of smooth muscle development in the mouse.

Little is currently known regarding the ontogeny of smooth muscle tissues during normal mammalian development. The alpha-smooth muscle and gamma-smooth muscle isoactins have been shown to be excellent molecular markers of smooth muscle cell phenotype. This study characterizes both the temporal and spatial patterns of alpha-smooth muscle and gamma-smooth muscle isoactin expression in the developing mouse. In situ analysis was performed on serial sections of whole mouse embryos on embryonic day 9, 11, 13, 15, and 17 using alpha-smooth muscle and gamma-smooth muscle isoactin-specific riboprobes. Distinct temporal and spatial patterns of alpha-smooth muscle and gamma-smooth muscle isoactin gene expression were observed in the developing gastrointestinal tract, urogenital tract, respiratory tract, and vascular system. Independent expression of the alpha-smooth muscle isoactin was observed during the early stages of skeletal, cardiac, and smooth muscle myogenesis as well as in a novel subset of distinct organs including the postnatal component of the hindgut, allantois, and primitive placenta. The results of this study indicate that distinct cellular phenotypes are involved in smooth muscle myogenesis and suggest that organ-specific mechanisms might exist for the initiation of smooth muscle development in vivo. In addition, the pattern of independent alpha-smooth muscle isoactin expression observed in this study provides novel information regarding the early stages of hindgut and placental development, and suggests that a common functional phenotype may be associated with the early stages of skeletal, cardiac, and smooth muscle myogenesis.

Actins↗