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β-Catenin Interacts with MyoD and Regulates Its Transcription Activity ^,

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.

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