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Molecular and Cellular Biology, December 2004, p. 10689-10702, Vol. 24, No. 24
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.24.10689-10702.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Interaction and Functional Cooperation between the LIM Protein FHL2, CBP/p300, and ß-Catenin

Charlotte Labalette, Claire-Angélique Renard, Christine Neuveut, Marie-Annick Buendia,* and Yu Wei*

Unité d'Oncogenèse et Virologie Moléculaire, INSERM U.579, Institut Pasteur, Paris, France

Received 23 December 2003/ Returned for modification 9 February 2004/ Accepted 13 September 2004

Transcriptional activation of gene expression by Wnt signaling is driven by the association of ß-catenin with TCF/LEF factors and the recruitment of transcriptional coactivators. It has been shown that the LIM protein FHL2 and the acetyltransferase CBP/p300 individually stimulate ß-catenin transactivating activity and that ß-catenin is acetylated by p300. Here, we report that FHL2 and CBP/p300 synergistically enhanced ß-catenin/TCF-mediated transcription from Wnt-responsive promoters and that the acetyltransferase activity of CBP/p300 was involved in the cooperation. CBP/p300 interacted directly with FHL2, predominantly through the CH3 domain but not the histone acetyltransferase domain, and different regions of CBP/p300 were involved in FHL2 and ß-catenin binding. We provided evidence for the formation of a ternary complex by FHL2, CBP/p300, and ß-catenin and for colocalization of the three proteins in the nucleus. In murine FHL2–/– embryo fibroblasts, the transactivation activity of ß-catenin/TCF was markedly reduced, and this defect could be restored by exogenous expression of FHL2. However, CBP/p300 were still able to coactivate the ß-catenin/TCF complex in FHL2–/– cells, suggesting that FHL2 is dispensable for the coactivator function of CBP/p300 on ß-catenin. Furthermore, we found that FHL2 significantly increased acetylation of ß-catenin by p300 in vivo. Finally, we showed that FHL2, CBP/p300, and ß-catenin could synergistically activate androgen receptor-mediated transcription, indicating that the synergistic coactivator function is not restricted to TCF/LEF.

* Corresponding author. Mailing address: Unité d'Oncogenèse et Virologie Moléculaire, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 33-145 68 88 51. Fax: 33-145 68 89 43. E-mail for Yu Wei: ywei{at}pasteur.fr. E-mail for Marie-Annick Buendia: mbuendia{at}pasteur.fr.

Molecular and Cellular Biology, December 2004, p. 10689-10702, Vol. 24, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.24.10689-10702.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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