M-CAT binding factor, a novel trans-acting factor governing muscle-specific transcription.

Mar, J H; Ordahl, Charles P.

doi:10.1128/mcb.10.8.4271

Cited by 171 publications

(113 citation statements)

References 55 publications

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“…However, not all muscle genes contain functional E boxes in their regulatory promoter regions, and myogenic bHLH proteins can also activate transcription of muscle-specific genes that lack E boxes in their control regions (3). As expected, from these data, other muscle-specific transcription factors have been described to function as intermediates in the activation of gene expression during myogenesis, such as the M-CAT binding factor (11), and the myocyte enhancer factor 2 (MEF2) (12,13).…”

mentioning

confidence: 79%

Myogenesis and MyoD Down-regulate Sp1

Viñals

Fandos

Santalucı́a

et al. 1997

Journal of Biological Chemistry

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Muscle cell differentiation caused a reduction of glucose transport, GLUT1 glucose transporter expression, and GLUT1 mRNA levels. A fragment of 2.1 kilobases of the rat GLUT1 gene linked to chloramphenicol acetyltransferase drove transcriptional activity in myoblasts, and differentiation caused a decrease in transcription. Transient transfection of 5 and 3 deletion constructs showed that the fragment ؊99/؊33 of the GLUT1 gene drives transcriptional activity of the GLUT1 gene and participates in the reduced transcription after muscle differentiation. Electrophoretic mobility shift assays showed the binding of Sp1 protein to the fragment ؊102/ ؊37 in the myoblast state but not in myotubes, and Sp1 was found to transactivate the GLUT1 promoter. Western blot analysis indicated that Sp1 was drastically down-regulated during myogenesis. Furthermore, the forced over-expression of MyoD in C3H10T1/2 cells mimicked the effects observed during myogenesis, Sp1 down-regulation and reduced transcriptional activity of the GLUT1 gene promoter.In all, these data suggest a regulatory model in which MyoD activation during myogenesis causes the down-regulation of Sp1, which contributes to the repression of GLUT1 gene transcription and, therefore, leads to the reduction in GLUT1 expression and glucose transport.

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mentioning

confidence: 79%

Myogenesis and MyoD Down-regulate Sp1

Viñals

Fandos

Santalucı́a

et al. 1997

Journal of Biological Chemistry

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“…Differentiation of cardiac muscle progenitor cells involves the selective activation of the GATA4 and Nkx2.5 transcription factors in pluripotent mesoderm (18 -20). However, because mutation of TEF-1 binding sequences in the promoters of cardiac-specific genes causes a loss of tissue specificity (2), and because ablation of TEF-1 expression causes abnormal cardiac development and an embryonic lethal phenotype (21), these studies support a role for TEF-1 factors in cardiac development. In the adult, cardiac myocytes respond to growth-promoting stimuli by undergoing hypertrophy, rather than cell division.…”

mentioning

confidence: 86%

“…Cardiac troponin T is expressed in fetal skeletal muscle and in cardiac muscle. Mutation analysis of the cardiac troponin T promoter showed that the MCAT element (originally defined as a muscle-specific cytidine-adenosine-thymidine sequence, 5Ј-CATTCCT-3Ј) is required for high levels of promoter activity in cardiac and skeletal muscle cells (1,2). Similar MCAT elements have been characterized in a large number of skeletal and cardiac muscle-specific promoters (3).…”

mentioning

confidence: 93%

Vgl-4, a Novel Member of the Vestigial-like Family of Transcription Cofactors, Regulates α1-Adrenergic Activation of Gene Expression in Cardiac Myocytes

Chen

Mullett

Stewart

2004

Journal of Biological Chemistry

100

104

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Cardiac and skeletal muscle genes are regulated by the transcriptional enhancer factor (TEF-1) family of transcription factors. In skeletal muscle, TEF-1 factors interact with a skeletal muscle-specific cofactor called Vestigial-like 2 (Vgl-2) that is related to the Drosophila protein Vestigial. Here, we characterize Vgl-4, the only member of the Vestigial-like family expressed in the heart. Unlike other members of the Vgl family that have a single TEF-1 interaction domain called the tondu (TDU) motif, Vgl-4 has two TDU motifs in its carboxyl-terminal domain. Like other Vgl factors, Vgl-4 physically interacts with TEF-1 in an immunoprecipitation assay. Vgl-4 functionally interacts with TEF-1 and also with myocyte enhancer factor 2 in a mammalian two-hybrid assay. Overexpression of Vgl-4 in cardiac myocytes interfered with the basal expression and ␣ 1 -adrenergic receptor-dependent activation of a TEF-1-dependent skeletal ␣-actin promoter. In cardiac myocytes cultured in serum and in serum-free medium, a myc-tagged Vgl-4 protein was located in the nucleus and cytoplasm but was exported from the nucleus when cells were treated with ␣ 1 -adrenergic receptor agonist. A chimeric nuclear-retained Vgl-4 protein inhibited ␣ 1 -adrenergic receptor-dependent activation. In contrast, deletion of the TDU motifs of Vgl-4 prevented Vgl-4 nuclear localization, relieved Vgl-4 interference of basal activity, and enhanced ␣ 1 -adrenergic up-regulation of the skeletal ␣-actin promoter. Nuclear export of Vgl-4 is dependent on the nuclear exportin CRM-1. These results suggest that Vgl-4 modulates the activity of TEF-1 factors and counteracts ␣ 1 -adrenergic activation of gene expression in cardiac myocytes.

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“…Nuclear extracts were prepared from tissue culture cells as described previously (28). Breast muscle from 13-day chicken embryos was dissected, and nuclei isolated were as described by Mar and Ordahl (46). Extracts Nucleotide sequence accession number.…”

Section: Materuils and Methodsmentioning

confidence: 99%

Analysis of the myogenin promoter reveals an indirect pathway for positive autoregulation mediated by the muscle-specific enhancer factor MEF-2.

Edmondson¹,

Cheng²,

Cserjesi³

et al. 1992

Mol. Cell. Biol.

291

253

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Transcriptional cascades that specify cell fate have been well described in invertebrates. In mammalian development, however, gene hierarchies involved in determination of cell lineage are not understood. With the recent cloning of the MyoD family of myogenic regulatory factors, a model system has become available with which to study the dynamics of muscle determination in mammalian development. Myogenin, along with other members of the MyoD gene family, possesses the apparent ability to redirect nonmuscle cells into the myogenic lineage. This ability appears to be due to the direct activation of an array of subordinate or downstream genes which are responsible for formation and function of the muscle contractile apparatus. Myogenin-directed transcription has been shown to occur through interaction with a DNA consensus sequence known as an E box (CANNTG) present in the control regions of numerous downstream genes. In addition to activating the transcription of subordinate genes, members of the MyoD family positively regulate their own expression and cross-activate one another's expression. These autoregulatory interactions have been suggested as a mechanism for induction and maintenance of the myogenic phenotype, but the molecular details of the autoregulatory circuits are undefined. Here we show that the myogenin promoter contains a binding site for the myocytespecific enhancer-binding factor, MEF-2, which can function as an intermediary of myogenin autoactivation. Since MEF-2 can be induced by myogenin, these results suggest that myogenin and MEF-2 participate in a transcriptional cascade in which MEF-2, once induced by myogenin, acts to amplify and maintain the myogenic phenotype by acting as a positive regulator of myogenin expression.The formation of skeletal muscle during vertebrate development involves the induction of mesoderm from primary ectoderm and the subsequent generation of proliferating myoblasts that ultimately terminally differentiate in response to environmental cues. The recent discovery of a family of related muscle-specific factors that can convert fibroblasts to myoblasts has contributed to rapid progress toward understanding the molecular events that underlie the establishment of the skeletal muscle phenotype (for reviews, see references 55 and 69). Members of this muscle regulatory gene family include MyoD (21), myogenin (25, 77), myf5 (9), and MRF4/herculin/myf6 (8,48,61), each of which can activate myogenesis when introduced into a wide range of nonmuscle cell types.

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M-CAT binding factor, a novel trans-acting factor governing muscle-specific transcription.

Abstract: The cardiac troponin T (cTNT) promoter contains a highly muscle specific distal promoter element capable of conferring muscle-specific transcription from a heterologous TATA box-transcription initiation site.

Cited by 171 publications

References 55 publications

Myogenesis and MyoD Down-regulate Sp1

Myogenesis and MyoD Down-regulate Sp1

Vgl-4, a Novel Member of the Vestigial-like Family of Transcription Cofactors, Regulates α1-Adrenergic Activation of Gene Expression in Cardiac Myocytes

Analysis of the myogenin promoter reveals an indirect pathway for positive autoregulation mediated by the muscle-specific enhancer factor MEF-2.

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