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  • The EMBO Journal (2000) 19, 6121 - 6130
  • doi:10.1093/emboj/19.22.6121

Pontin52 and Reptin52 function as antagonistic regulators of bold beta-catenin signalling activity

Andreas Bauer1,2,5, Sophie Chauvet3,5, Otmar Huber4,5, Fabrice Usseglio3,5, Ute Rothbächer3, Denise Aragnol3, Rolf Kemler1 and Jacques Pradel3

  1. Max-Planck Institute of Immunobiology, Department of Molecular Embryology, Stübeweg 51 , D-79108 Freiburg Germany
  2. Present address: CellZome GmbH, Meyerhofstrasse 1, 69123 Heidelberg, Germany
  3. Laboratoire de Génétique et Physiologie du Développement, Institut de Biologie du Développement de Marseille, CNRS/INSERM/Université de la Méditerranée, Parc Scientifique de Luminy, Case 907, 13288 Marseille Cedex 9, France
  4. Institute of Clinical Chemistry and Pathobiochemistry, University Hospital Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
  5. A.Bauer, S.Chauvet, O.Huber and F.Usseglio contributed equally to this work

Correspondence to:

Jacques Pradel, E-mail: pradel@lgpd.univ-mrs.fr

Received 29 August 2000; Accepted 27 September 2000; Revised 27 September 2000

In Wnt-stimulated cells, beta-catenin becomes stabilized in the cytoplasm, enters the nucleus and interacts with HMG box transcription factors of the lymphoid-enhancing factor-1 (LEF-1)/T-cell factor (TCF) family, thereby stimulating the transcription of specific target genes. We recently identified Pontin52 as a nuclear protein interacting with beta-catenin and the TATA-box binding protein (TBP), suggesting its involvement in regulating beta-catenin-mediated transactivation. Here, we report the identification of Reptin52 as an interacting partner of Pontin52. Highly homologous to Pontin52, Reptin52 likewise binds beta-catenin and TBP. Using reporter gene assays, we show that the two proteins antagonistically influence the transactivation potential of the beta-catenin–TCF complex. Furthermore, we demonstrate the evolutionary conservation of this mechanism in Drosophila. dpontin and dreptin are essential genes that act antagonistically in the control of Wingless signalling in vivo. These results indicate that the opposite action of Pontin52 and Reptin52 on beta-catenin-mediated transactivation constitutes an additional mechanism for the control of the canonical Wingless/Wnt pathway.

  • Keywords:

    • beta-catenin,
    • chromatin,
    • Tip49,
    • transcriptional regulation,
    • Wg,
    • Wnt signalling