Developmental regulation of creatine kinase gene expression by myogenic factors in embryonic mouse and chick skeletal muscle

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 1017-1029 ◽  
Author(s):  
G.E. Lyons ◽  
S. Muhlebach ◽  
A. Moser ◽  
R. Masood ◽  
B.M. Paterson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Striated Muscle ◽  
Myogenic Differentiation ◽  
Developmental Regulation ◽  
Specific Gene ◽  
Kinase Gene ◽  
Embryonic Mouse ◽  
Myogenic Factors

The B isoform of creatine kinase (BCK), which is expressed at a high level in embryonic neural tissues, is also expressed abundantly in developing striated muscle and is an early marker for skeletal myogenesis. Using isoform-specific 35S-labeled antisense cRNA probes for in situ hybridization, we have detected BCK mRNAs in embryonic mouse and chick myotomes, the first skeletal muscle masses to form in developing embryos. These transcripts are detectable as soon as myotomes are morphologically distinguishable. BCK is expressed at high levels in both skeletal and cardiac muscle in mouse and chick embryos. In the mouse, BCK transcript levels fall of rapidly in striated muscle shortly after the onset of MCK gene expression. The M isoform of creatine kinase (MCK), the striated muscle-specific isoform, is expressed later than BCK. In the mouse, BCK transcripts are expressed in myotomes at 8.5 days post coitum (p.c.), but MCK transcripts are not detected before 13 days p.c. In the chick, BCK mRNAs are present at Hamburger-Hamilton stage 13, but MCK mRNAs are not detected before stage 19. We have compared the patterns of expression of the CK genes with those of myogenic differentiation factor genes, which are thought to regulate skeletal muscle-specific gene expression. In the chick, both CMD1, first detected at stage 13, and myogenin, first detected at stage 15, are present prior to MCK, which begins to be expressed at stage 19. Unlike the mouse embryo, CMD1, the chick homologue of MyoD1, is expressed before chick myogenin. In the mouse, myogenin, first detected at 8.5 days p.c., is expressed at the same time as BCK in myotomes. Both myogenin and MyoD1, which begins to be detected two days later than myogenin, are expressed at least two days before MCK. It has been proposed that the myogenic factors, MyoD1 and myogenin, directly regulate MCK gene expression in the mouse by binding to its enhancer. However, our results show that MCK transcripts are not detected until well after MyoD1 and myogenin mRNAs are expressed, suggesting that these factors by themselves are not sufficient to initiate MCK gene expression.

M-creatine kinase gene expression in mechanically overloaded skeletal muscle of transgenic mice

1995 ◽  
Vol 269 (3) ◽  
pp. C665-C674 ◽  
Author(s):  
R. W. Tsika ◽  
S. D. Hauschka ◽  
L. Gao
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Creatine Kinase ◽  
Kinase Gene ◽  
Mouse Muscle ◽  
Average Decrease ◽  
Mechanical Overload ◽  
Mouse Lines ◽  
Specific Mrna

The molecular pathways and regulatory molecules that underlie changes in gene transcription during mechanical overload of skeletal muscle remain obscure. To better understand this process, we have examined mouse muscle creatine kinase (MCK) gene expression in mechanically overloaded plantaris (OP) muscle of transgenic and nontransgenic mice. Northern blot analysis revealed that endogenous MCK-specific mRNA transcripts were decreased 150% in the OP muscles after 6 wk. To identify the MCK gene regions involved in the response to mechanical overload, three different mouse MCKCAT transgenes were studied by measuring chloramphenicol acetyltransferase (CAT assays) activity in OP and sham-operated (control plantaris) muscles. Mouse lines carrying (+enh206)117MCKCAT and -1256MCKCAT transgenes exhibited 30 and 40% lower CAT levels, whereas two mouse lines carrying -3300MCKCAT transgenes exhibited average decreases of 430%. Nearly identical results, including measurements of exogenous CAT mRNA, were obtained 2 days postoverload. Six weeks or 2 days of mechanical overload led to an average decrease in MM-CK isoprotein of 140%. These data provide evidence that mechanical overload induces changes in MCK gene expression that appear to be regulated by at least two portions of the MCK gene: the 206 base pair 5' enhancer and the -3,300 to -1,257 region.

scholarly journals Functional Promiscuity of Gene Regulation by Serpentine Receptors in Dictyostelium discoideum

1998 ◽  
Vol 18 (10) ◽  
pp. 5744-5749 ◽  
Author(s):  
Irene Verkerke-Van Wijk ◽  
Ji-Yun Kim ◽  
Raymond Brandt ◽  
Peter N. Devreotes ◽  
Pauline Schaap
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Dictyostelium Discoideum ◽  
Developmental Regulation ◽  
Mutant Cell ◽  
Gene Induction ◽  
Specific Gene ◽  
Wild Type ◽  
Animal Development ◽  
Camp Stimulation

ABSTRACT Serpentine receptors such as smoothened and frizzled play important roles in cell fate determination during animal development. InDictyostelium discoideum, four serpentine cyclic AMP (cAMP) receptors (cARs) regulate expression of multiple classes of developmental genes. To understand their function, it is essential to know whether each cAR is coupled to a specific gene regulatory pathway or whether specificity results from the different developmental regulation of individual cARs. To distinguish between these possibilities, we measured gene induction in car1 car3 double mutant cell lines that express equal levels of either cAR1, cAR2, or cAR3 under a constitutive promoter. We found that all cARs efficiently mediate both aggregative gene induction by cAMP pulses and induction of postaggregative and prespore genes by persistent cAMP stimulation. Two exceptions to this functional promiscuity were observed. (i) Only cAR1 can mediate adenosine inhibition of cAMP-induced prespore gene expression, a phenomenon that was found earlier in wild-type cells. cAR1’s mediation of adenosine inhibition suggests that cAR1 normally mediates prespore gene induction. (ii) Only cAR2 allows entry into the prestalk pathway. Prestalk gene expression is induced by differentiation-inducing factor (DIF) but only after cells have been prestimulated with cAMP. We found that DIF-induced prestalk gene expression is 10 times higher in constitutive cAR2 expressors than in constitutive cAR1 or cAR3 expressors (which still have endogenous cAR2), suggesting that cAR2 mediates induction of DIF competence. Since in wild-type slugs cAR2 is expressed only in anterior cells, this could explain the so far puzzling observations that prestalk cells differentiate at the anterior region but that DIF levels are actually higher at the posterior region. After the initial induction of DIF competence, cAMP becomes a repressor of prestalk gene expression. This function can again be mediated by cAR1, cAR2, and cAR3.

A ras-dependent pathway abolishes activity of a muscle-specific enhancer upstream from the muscle creatine kinase gene

1989 ◽  
Vol 9 (2) ◽  
pp. 594-601
Author(s):  
E A Sternberg ◽  
G Spizz ◽  
M E Perry ◽  
E N Olson
Keyword(s):  
Creatine Kinase ◽  
Growth Factors ◽  
Myogenic Differentiation ◽  
Regulatory Elements ◽  
Negative Control ◽  
Proximal Promoter ◽  
Muscle Creatine Kinase ◽  
Kinase Gene ◽  
Muscle Creatine ◽  
Ras Oncogenes

Differentiation of skeletal myoblasts is accompanied by induction of a series of tissue-specific genes whose products are required for the specialized functions of the mature muscle fiber. The program for myogenic differentiation is subject to negative control by several peptide growth factors and by the products of mutationally activated ras oncogenes, which persistently activate intracellular cascades normally triggered by specific growth factors. Previously, we reported that induction of the muscle creatine kinase (mck) gene during myogenesis was dependent on a distal upstream enhancer that cooperated with a proximal promoter to direct high levels of expression in developing muscle cells (E. A. Sternberg, G. Spizz, W. M. Perry, D. Vizard, T. Weil, and E. N. Olson, Mol. Cell. Biol. 8:2896-2909). To investigate the mechanisms whereby ras blocks the induction of muscle-specific genes, we have examined the ability of mck 5' regulatory elements to direct expression of the linked reporter gene for chloramphenicol acetyltransferase (cat) in C2 myoblasts bearing mutant N-ras and H-ras oncogenes. In this paper we report that expression of activated ras alleles abolishes activity of the mck upstream enhancer but does not affect the activity of the mck promoter. The ability of ras to repress the expression of mck-cat fusion genes that have been transfected either transiently or stably into myoblasts suggests that ras may exert its effects on muscle-specific genes through mechanisms independent of chromatin configurations or DNA methylation. These results also suggest that ras blocks establishment of the myogenic phenotype by preventing the accumulation of regulatory factors required for transcriptional induction of muscle-specific genes.

scholarly journals New Role for Serum Response Factor in Postnatal Skeletal Muscle Growth and Regeneration via the Interleukin 4 and Insulin-Like Growth Factor 1 Pathways

2006 ◽  
Vol 26 (17) ◽  
pp. 6664-6674 ◽  
Author(s):  
Claude Charvet ◽  
Christophe Houbron ◽  
Ara Parlakian ◽  
Julien Giordani ◽  
Charlotte Lahoute ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Factor ◽  
Serum Response Factor ◽  
Muscle Growth ◽  
Interleukin 4 ◽  
Specific Gene ◽  
Response Factor ◽  
Insulin Like Growth Factor ◽  
Serum Response

ABSTRACT Serum response factor (SRF) is a crucial transcriptional factor for muscle-specific gene expression. We investigated SRF function in adult skeletal muscles, using mice with a postmitotic myofiber-targeted disruption of the SRF gene. Mutant mice displayed severe skeletal muscle mass reductions due to a postnatal muscle growth defect resulting in highly hypotrophic adult myofibers. SRF-depleted myofibers also failed to regenerate following injury. Muscles lacking SRF had very low levels of muscle creatine kinase and skeletal alpha-actin (SKA) transcripts and displayed other alterations to the gene expression program, indicating an overall immaturity of mutant muscles. This loss of SKA expression, together with a decrease in beta-tropomyosin expression, contributed to myofiber growth defects, as suggested by the extensive sarcomere disorganization found in mutant muscles. However, we observed a downregulation of interleukin 4 (IL-4) and insulin-like growth factor 1 (IGF-1) expression in mutant myofibers which could also account for their defective growth and regeneration. Indeed, our demonstration of SRF binding to interleukin 4 and IGF-1 promoters in vivo suggests a new crucial role for SRF in pathways involved in muscle growth and regeneration.

Genotypes Of The Skeletal Muscle Creatine Kinase Gene And Exertional Rhabdomyolyis

2009 ◽  
Vol 41 ◽  
pp. 164
Author(s):  
Yuval Heled ◽  
Patricia A. Deuster ◽  
Sheila Muldoon ◽  
Carmen Sesvold-Contreras ◽  
Kimbra Kenny ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Creatine Kinase ◽  
Kinase Gene ◽  
Muscle Creatine

scholarly journals Different regulatory sequences control creatine kinase-M gene expression in directly injected skeletal and cardiac muscle.

1993 ◽  
Vol 13 (2) ◽  
pp. 1264-1272 ◽  
Author(s):  
C K Vincent ◽  
A Gualberto ◽  
C V Patel ◽  
K Walsh
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Cardiac Muscle ◽  
Serum Response Factor ◽  
Sequence Motif ◽  
Regulatory Sequences ◽  
Response Factor ◽  
Specific Expression ◽  
Serum Response

Regulatory sequences of the M isozyme of the creatine kinase (MCK) gene have been extensively mapped in skeletal muscle, but little is known about the sequences that control cardiac-specific expression. The promoter and enhancer sequences required for MCK gene expression were assayed by the direct injection of plasmid DNA constructs into adult rat cardiac and skeletal muscle. A 700-nucleotide fragment containing the enhancer and promoter of the rabbit MCK gene activated the expression of a downstream reporter gene in both muscle tissues. Deletion of the enhancer significantly decreased expression in skeletal muscle but had no detectable effect on expression in cardiac muscle. Further deletions revealed a CArG sequence motif at position -179 within the promoter that was essential for cardiac-specific expression. The CArG element of the MCK promoter bound to the recombinant serum response factor and YY1, transcription factors which control expression from structurally similar elements in the skeletal actin and c-fos promoters. MCK-CArG-binding activities that were similar or identical to serum response factor and YY1 were also detected in extracts from adult cardiac muscle. These data suggest that the MCK gene is controlled by different regulatory programs in adult cardiac and skeletal muscle.

Conserved and muscle-group-specific gene expression patterns shape postnatal development of the novel extraocular muscle phenotype

2004 ◽  
Vol 18 (2) ◽  
pp. 184-195 ◽  
Author(s):  
Georgiana Cheng ◽  
Anita P. Merriam ◽  
Bendi Gong ◽  
Patrick Leahy ◽  
Sangeeta Khanna ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
System Development ◽  
Expression Patterns ◽  
Neuromuscular Diseases ◽  
Local Environment ◽  
Oculomotor System ◽  
Muscle Group ◽  
Specific Gene ◽  
Extrinsic Factors

Current models in skeletal muscle biology do not fully account for the breadth, causes, and consequences of phenotypic variation among skeletal muscle groups. The muscle allotype concept arose to explain frank differences between limb, masticatory, and extraocular (EOM) muscles, but there is little understanding of the developmental regulation of the skeletal muscle phenotypic range. Here, we used morphological and DNA microarray analyses to generate a comprehensive temporal profile for rat EOM development. Based upon coordinate regulation of morphologic/gene expression traits with key events in visual, vestibular, and oculomotor system development, we propose a model that the EOM phenotype is a consequence of extrinsic factors that are unique to its local environment and sensory-motor control system, acting upon a novel myoblast lineage. We identified a broad spectrum of differences between the postnatal transcriptional patterns of EOM and limb muscle allotypes, including numerous transcripts not traditionally associated with muscle fiber/group differences. Several transcription factors were differentially regulated and may be responsible for signaling muscle allotype specificity. Significant differences in cellular energetic mechanisms defined the EOM and limb allotypes. The allotypes were divergent in many other functional transcript classes that remain to be further explored. Taken together, we suggest that the EOM allotype is the consequence of tissue-specific mechanisms that direct expression of a limited number of EOM-specific transcripts and broader, incremental differences in transcripts that are conserved by the two allotypes. This represents an important first step in dissecting allotype-specific regulatory mechanisms that may, in turn, explain differential muscle group sensitivity to a variety of metabolic and neuromuscular diseases.

scholarly journals Multiscale 3D Genome Reorganization during Skeletal Muscle Stem Cell Lineage Progression and Muscle Aging

2021 ◽  
Author(s):  
Huating WANG ◽  
Yu Zhao ◽  
Yingzhe Ding ◽  
Liangqiang He ◽  
Yuying Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Stem Cell ◽  
Stem Cell Differentiation ◽  
Regulatory Elements ◽  
Specific Gene ◽  
Muscle Stem Cell ◽  
3D Genome ◽  
Chromatin Looping ◽  
Early Activation

Abstract 3D genome rewiring is known to influence spatiotemporal expression of lineage-specific genes and cell fate transition during stem cell differentiation and aging processes. Yet it is unknown how 3D architecture remodels and orchestrates transcriptional changes during skeletal muscle stem cell (also called satellite cell, SC) activation, proliferation and differentiation course. Here, using in situ Hi-C we comprehensively map the 3D genome topology reorganization at multiscale levels during mouse SC lineage progression and integrate with transcriptional and chromatin signatures to elucidate how 3D genome rewiring dictates gene expression program. Specifically, rewiring at compartment level is most pronounced when SC becomes activated. Striking loss in TAD border insulation and chromatin looping also occurs during early activation process. Meanwhile, TADs can also form TAD clusters and super-enhancer containing TAD clusters orchestrate stage-specific gene expression during SC early activation. Furthermore, we elucidate 3D chromatin regulation of key transcription factor, PAX7 and identify cis-regulatory elements that are crucial for local chromatin architecture and Pax7 expression. Lastly, 3D genome remodeling is profiled in SCs isolated from naturally aging mice, unveiling that geriatric SCs display a prominent gain in long-range contacts and loss of TAD border insulation. Genome compartmentalization and chromatin looping are evidently altered in aged SC while geriatric SC display a more prominent loss in strength of TAD borders. Together, our results implicate 3D chromatin extensively reorganizes at multiple architectural levels and underpin the transcriptome remodeling during SC lineage development and SC aging.

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