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Pontin52 and Reptin52 function as antagonistic regulators of β‐catenin signalling activity
Author(s) -
Bauer Andreas,
Chauvet Sophie,
Huber Otmar,
Usseglio Fabrice,
Rothbächer Ute,
Aragnol Denise,
Kemler Rolf,
Pradel Jacques
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.22.6121
Subject(s) - biology , function (biology) , signalling , beta catenin , beta (programming language) , microbiology and biotechnology , signal transduction , computational biology , wnt signaling pathway , computer science , programming language
In Wnt‐stimulated cells, β‐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 β‐catenin and the TATA‐box binding protein (TBP), suggesting its involvement in regulating β‐catenin‐mediated transactivation. Here, we report the identification of Reptin52 as an interacting partner of Pontin52. Highly homologous to Pontin52, Reptin52 likewise binds β‐catenin and TBP. Using reporter gene assays, we show that the two proteins antagonistically influence the transactivation potential of the β‐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 β‐catenin‐mediated transactivation constitutes an additional mechanism for the control of the canonical Wingless/Wnt pathway.