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Published on: April 29, 2011
Myocardin and ternary complex factors compete for SRF to control smooth muscle gene expression
Zhigao Wang1, Da-Zhi Wang, Dirk Hockemeyer
1Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, Texas 75390-9148, USA.
Nature
|March 12, 2004
Summary
Smooth muscle cells
Area of Science:
- Molecular Biology
- Cellular Biology
- Gene Regulation
Background:
- Smooth muscle cells exhibit phenotypic plasticity, switching between differentiated and proliferative states.
- Transcriptional mechanisms governing this plasticity are not fully understood.
- Serum response factor (SRF) plays a key role in regulating smooth muscle gene expression.
Purpose of the Study:
- To elucidate the transcriptional mechanisms controlling smooth muscle cell phenotypic plasticity.
- To investigate the roles of myocardin and ternary complex factors (TCFs) in SRF-mediated gene regulation.
- To determine how growth signals influence smooth muscle gene expression.
Main Methods:
- Investigated the interaction between SRF, myocardin, and TCFs (specifically Elk-1).
- Analyzed the effects of growth signals on smooth muscle gene expression.
- Utilized a mutant smooth muscle promoter to assess TCF function in vivo.
Main Results:
- Growth signals induce Elk-1 to displace myocardin from SRF, repressing smooth muscle genes.
- Myocardin and Elk-1 compete for the same binding site on SRF.
- TCFs are crucial for suppressing smooth muscle gene expression in vivo, as shown by ectopic transcription in the embryonic heart.
Conclusions:
- Growth and developmental signals dynamically regulate smooth muscle gene expression.
- The balance of SRF association with antagonistic cofactors (myocardin and Elk-1) dictates smooth muscle cell phenotype.
- TCFs act as key myogenic repressors in smooth muscle development and plasticity.
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