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ZIRC
ZFIN ID: ZDB-PUB-080326-27
Nuclear Dvl, c-Jun, beta-catenin, and TCF form a complex leading to stabilization of beta-catenin-TCF interaction
Gan, X.Q., Wang, J.Y., Xi, Y., Wu, Z.L., Li, Y.P., and Li, L.
Date: 2008
Source: The Journal of cell biology 180(6): 1087-1100 (Journal)
Registered Authors: Li, Lin
Keywords: none
MeSH Terms:
  • Adaptor Proteins, Signal Transducing/genetics
  • Adaptor Proteins, Signal Transducing/metabolism*
  • Animals
  • Cell Line
  • Cell Line, Tumor
  • Cell Nucleus/genetics
  • Cell Nucleus/metabolism*
  • Down-Regulation/genetics
  • Gene Expression Regulation/genetics
  • Humans
  • Macromolecular Substances/metabolism
  • Phosphoproteins/genetics
  • Phosphoproteins/metabolism*
  • Promoter Regions, Genetic/genetics
  • Proto-Oncogene Proteins c-jun/genetics
  • Proto-Oncogene Proteins c-jun/metabolism*
  • Regulatory Elements, Transcriptional/genetics
  • Signal Transduction/genetics
  • TCF Transcription Factors/genetics
  • TCF Transcription Factors/metabolism*
  • Transcription Factor 7-Like 2 Protein
  • Transcription, Genetic/genetics
  • Wnt Proteins/genetics*
  • Wnt Proteins/metabolism
  • Zebrafish
  • beta Catenin/genetics
  • beta Catenin/metabolism*
PubMed: 18347071 Full text @ J. Cell Biol.
FIGURES
ABSTRACT
In canonical Wnt signaling, Dishevelled (Dvl) is a critical cytoplasmic regulator that releases beta-catenin from degradation. Here, we find that Dvl and c-Jun form a complex with beta-catenin-T-cell factor 4 (TCF-4) on the promoter of Wnt target genes and regulate gene transcription. The complex forms via two interactions of nuclear Dvl with c-Jun and beta-catenin, respectively, both of which bind to TCF. Disrupting the interaction of Dvl with either c-Jun or beta-catenin suppresses canonical Wnt signaling-stimulated transcription, and the reduction of Dvl diminished beta-catenin-TCF-4 association on Wnt target gene promoters in vivo. Expression of a TCF-Dvl fusion protein largely rescued the c-Jun knockdown Wnt signaling deficiency in mammalian cells and zebrafish. Thus, we confirm that c-Jun functions in canonical Wnt signaling and show that c-Jun functions as a scaffold in the bet Expression of a TCF-Dvl fusion protein largely rescued the c-Jun knockdown Wnt signaling deficiency in mammalian cells and zebrafish. Thus, we cona-catenin-TCFs transcription complex bridging Dvl to TCF. Our results reveal a mechanism by which nuclear Dvl cooperates with c-Jun to regulate gene transcription stimulated by the canonical Wnt signaling pathway.
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