scholarly journals Molecular cloning of up-regulated cytoskeletal genes from regenerating skeletal muscle: potential role of myocyte enhancer factor 2 proteins in the activation of muscle-regeneration-associated genes

1997 ◽  
Vol 325 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Waleed M. AKKILA ◽  
Rebecca L. CHAMBERS ◽  
Olga I. ORNATSKY ◽  
John C. McDERMOTT
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Regulatory Protein ◽  
Cdna Clones ◽  
Myocyte Enhancer Factor 2 ◽  
Consensus Binding Site ◽  
Mobility Shift ◽  
Adult Skeletal Muscle ◽  
Myocyte Enhancer Factor ◽  
Enhancer Factor

A subtractive hybridization and cloning strategy was used to identify genes that are up-regulated in regenerating compared with normal skeletal muscle. The gastrocnemius muscle of CD1 mice was injected with a myotoxic agent (BaCl2). A cDNA library was constructed from the regenerating muscle, and was screened with subtracted probes enriched in genes up-regulated during regeneration. Cofilin and vimentin cDNA clones were isolated. Both cofilin and vimentin were demonstrated to be overexpressed in regenerating compared with non-regenerating muscle (17-fold and 19-fold induction respectively). Cofilin and vimentin mRNAs also exhibited an increased expression in C2C12 myoblasts and a decreased expression in differentiated myotubes. Analysis of the regeneration-induced vimentin enhancer/promoter region revealed a consensus binding site for the myocyte enhancer factor 2 (MEF2) transcription factors. Electrophoretic mobility-shift assays and in vivo reporter assays revealed that MEF2 DNA-binding activity and transcriptional activation are increased in regenerating skeletal muscle, indicating that they may play a role in the activation of muscle genes during regeneration. These data suggest that both cofilin (an actin-regulatory protein) and vimentin (an intermediate filament) may be key components of the cytoskeletal reorganization that mediates muscle cell development and adult skeletal-muscle repair.

scholarly journals Direct Interaction between Myocyte Enhancer Factor 2 (MEF2) and Protein Phosphatase 1α Represses MEF2-Dependent Gene Expression

2009 ◽  
Vol 29 (12) ◽  
pp. 3355-3366 ◽  
Author(s):  
R. L. S. Perry ◽  
C. Yang ◽  
N. Soora ◽  
J. Salma ◽  
M. Marback ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Protein Interactions ◽  
Protein Phosphatase ◽  
Hippocampal Neurons ◽  
Neuronal Cell ◽  
Direct Interaction ◽  
Myocyte Enhancer Factor 2 ◽  
Myocyte Enhancer Factor ◽  
Enhancer Factor

ABSTRACT The myocyte enhancer factor 2 (MEF2) transcription factors play important roles in neuronal, cardiac, and skeletal muscle tissues. MEF2 serves as a nuclear sensor, integrating signals from several signaling cascades through protein-protein interactions with kinases, chromatin remodeling factors, and other transcriptional regulators. Here, we report a novel interaction between the catalytic subunit of protein phosphatase 1α (PP1α) and MEF2. Interaction occurs within the nucleus, and binding of PP1α to MEF2 potently represses MEF2-dependent transcription. The interaction utilizes uncharacterized domains in both PP1α and MEF2, and PP1α phosphatase activity is not obligatory for MEF2 repression. Moreover, a MEF2-PP1α regulatory complex leads to nuclear retention and recruitment of histone deacetylase 4 to MEF2 transcription complexes. PP1α-mediated repression of MEF2 overrides the positive influence of calcineurin signaling, suggesting PP1α exerts a dominant level of control over MEF2 function. Indeed, PP1α-mediated repression of MEF2 function interferes with the prosurvival effect of MEF2 in primary hippocampal neurons. The PP1α-MEF2 interaction constitutes a potent locus of control for MEF2-dependent gene expression, having potentially important implications for neuronal cell survival, cardiac remodeling in disease, and terminal differentiation of vascular, cardiac, and skeletal muscle.

Invited Review: Regulation of skeletal muscle GLUT-4 expression by exercise

2002 ◽  
Vol 93 (2) ◽  
pp. 782-787 ◽  
Author(s):  
G. Lynis Dohm
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Control ◽  
Therapeutic Strategies ◽  
Glucose Disposal ◽  
Research Needs ◽  
Maximal Rate ◽  
Myocyte Enhancer Factor 2 ◽  
Glut 4 ◽  
Myocyte Enhancer Factor ◽  
Enhancer Factor

The amount of GLUT-4 protein is a primary factor in determining the maximal rate of glucose transport into skeletal muscle. Therefore, it is important that we understand how exercise regulates GLUT-4 expression so that therapeutic strategies can be designed to increase muscle glucose disposal as a treatment for diabetes. Muscle contraction increases the rates of GLUT-4 transcription and translation. Transcriptional control likely requires at least two DNA binding proteins, myocyte enhancer factor-2 and GLUT-4 enhancer factor, which bind to the promoter. Increased GLUT-4 expression may be mediated by the enzyme AMP-activated kinase, which is activated during exercise and has been demonstrated to increase GLUT-4 transcription. Further research needs to be done to investigate whether AMP-activated kinase activates myocyte enhancer factor-2 and GLUT-4 enhancer factor to increase transcription of the GLUT-4 gene.

scholarly journals AVP Induces Myogenesis through the Transcriptional Activation of the Myocyte Enhancer Factor 2

2002 ◽  
Vol 16 (6) ◽  
pp. 1407-1416 ◽  
Author(s):  
Bianca Maria Scicchitano ◽  
Lucia Spath ◽  
Antonio Musarò ◽  
Mario Molinaro ◽  
Sergio Adamo ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Myocyte Enhancer Factor 2 ◽  
Myocyte Enhancer Factor ◽  
Enhancer Factor
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