Curbing the nuclear activities of beta-catenin. Control over Wnt target gene expression

EMBO Rep. 2000 Jul;1(1):24-8. doi: 10.1093/embo-reports/kvd012.


Wnt molecules control numerous developmental processes by altering specific gene expression patterns, and deregulation of Wnt signaling can lead to cancer. Many Wnt factors employ beta-catenin as a nuclear effector. Upon Wnt stimulation, beta-catenin heterodimerizes with T-cell factor (TCF) DNA-binding proteins to form a transcriptional activator complex. As the activating subunit of this complex, beta-catenin performs dual tasks: it alleviates repression of target gene promoters and subsequently it activates them. Beta-catenin orchestrates these effects by recruiting chromatin modifying cofactors and contacting components of the basal transcription machinery. Although beta-catenin and TCFs are universal activators in Wnt signaling, their target genes display distinct temporal and spatial expression patterns. Apparently, post-translational modifications modulate the interactions between TCFs and beta-catenin or DNA, and certain transcription factors can sequester beta-catenin from TCFs while others synergize with beta-catenin-TCF complexes in a promoter-specific manner. These mechanisms provide points of intersection with other signaling pathways, and contribute to the complexity and specificity of Wnt target gene regulation.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Nucleus / metabolism*
  • Cytoskeletal Proteins / metabolism*
  • DNA-Binding Proteins / metabolism
  • Gene Expression Regulation
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism
  • Signal Transduction
  • Trans-Activators*
  • Transcription Factors / metabolism*
  • Wnt Proteins
  • Zebrafish Proteins*
  • beta Catenin


  • Cytoskeletal Proteins
  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • Trans-Activators
  • Transcription Factors
  • Wnt Proteins
  • Zebrafish Proteins
  • beta Catenin