Beta-catenin interacts with MyoD and regulates its transcription activity

Mol Cell Biol. 2008 May;28(9):2941-51. doi: 10.1128/MCB.01682-07. Epub 2008 Mar 3.

Abstract

Wnt regulation of muscle development is thought to be mediated by the beta-catenin-TCF/LEF-dependent canonical pathway. Here we demonstrate that beta-catenin, not TCF/LEF, is required for muscle differentiation. We showed that beta-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 beta-catenin is deficient or the interaction between MyoD and beta-catenin is disrupted. These results demonstrate that beta-catenin is necessary for MyoD function, identifying MyoD as an effector in the Wnt canonical pathway.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Line
  • Gene Expression Regulation, Developmental
  • Mice
  • Muscle, Skeletal / cytology
  • Myoblasts / cytology
  • Myoblasts / metabolism
  • Myogenic Regulatory Factors / genetics
  • Myogenic Regulatory Factors / physiology*
  • Protein Binding
  • Signal Transduction
  • TCF Transcription Factors / metabolism
  • Transcriptional Activation
  • Wnt Proteins / physiology
  • beta Catenin / physiology*

Substances

  • Mdfi protein, mouse
  • Myogenic Regulatory Factors
  • TCF Transcription Factors
  • Wnt Proteins
  • beta Catenin