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Program of Developmental Neurobiology, Institute of Molecular Medicine and Genetics and Department of Neurology, Medical College of Georgia, Augusta, Georgia 30912,1 Department of Physiology, Chronic Inflammatory Disease Research Center, BK21 Neuroscience Graduate Program, Ajou University School of Medicine, Suwon 443-749, Republic of Korea2
Received 12 September 2007/ Returned for modification 6 November 2007/ Accepted 17 February 2008
Wnt regulation of muscle development is thought to be mediated by the β-catenin-TCF/LEF-dependent canonical pathway. Here we demonstrate that β-catenin, not TCF/LEF, is required for muscle differentiation. We showed that β-catenin interacts directly with MyoD, a basic helix-loop-helix transcription factor essential for muscle differentiation and enhances its binding to E box elements and transcriptional activity. MyoD-mediated transactivation is inhibited in muscle cells when β-catenin is deficient or the interaction between MyoD and β-catenin is disrupted. These results demonstrate that β-catenin is necessary for MyoD function, identifying MyoD as an effector in the Wnt canonical pathway.
Published ahead of print on 3 March 2008.
Supplemental material for this article may be found at http://mcb.asm.org/.
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