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First published online 26 January 2005
doi: 10.1242/dev.01684
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1 Department of Cell Biology and Anatomy, University of Arizona Health Sciences
Center, 1501 N. Campbell Avenue, PO Box 245044, Tucson, AZ, 85724, USA
2 Carolina Cardiovascular Biology Center, Department of Cell and Developmental
Biology, University of North Carolina, Chapel Hill, NC 27599-7126, USA
3 Department of Molecular Biology, University of Texas Southwestern Medical
Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA
Author for correspondence (e-mail:
pkrieg{at}email.arizona.edu)
Accepted 14 December 2004
Myocardin is a cardiac- and smooth muscle-specific cofactor for the ubiquitous transcription factor serum response factor (SRF). Using gain-of-function approaches in the Xenopus embryo, we show that myocardin is sufficient to activate transcription of a wide range of cardiac and smooth muscle differentiation markers in non-muscle cell types. We also demonstrate that, for the myosin light chain 2 gene (MLC2), myocardin cooperates with the zinc-finger transcription factor Gata4 to activate expression. Inhibition of myocardin activity in Xenopus embryos using morpholino knockdown methods results in inhibition of cardiac development and the absence of expression of cardiac differentiation markers and severe disruption of cardiac morphological processes. We conclude that myocardin is an essential component of the regulatory pathway for myocardial differentiation.
Key words: Tbx5, Gata4, Nkx2-5, Smooth muscle, Transgenesis
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