TY - JOUR
T1 - Cooperativity in transactivation between retinoic acid receptor and TFIID requires an activity analogous to E1A
AU - Berkenstam, Anders
AU - del Mar Vivanco Ruiz, Maria
AU - Barettino, Domingo
AU - Horikoshi, Masami
AU - Stunnenberg, Hendrik G.
N1 - Funding Information:
We wish to thank Rolf de Groot for RAC65 cells, Timothy Hoey and Robert Weinzierl in Robert Tjian’s laboratory for Drosophila TFIID cDNA and TFIID monoclonal antibodies, Satoshi Hasegawa and Bob Roeder for providing hTFllD N-terminal deletions, and Peter Hirsch-mann and Vera Sonntag-Buck for excellent technical assistance. We also thank Peter Becker, lain Mattaj, Lennart Philipson, Hans Schdler, Francis Stewart, and members of the Stunnenberg laboratory for comments on the manuscript. A. 8. is supported by a postdoctoral fellowship from the Swedish Natural Science Research Council and D. B. by a European Community postdoctoral fellowship. M. H. is an Alexandrine and Alexander L. Sinsheimer Scholar. This work is supported by National Institutes of Health grants to M. H. and Robert G. Roeder.
PY - 1992/5/1
Y1 - 1992/5/1
N2 - In embryonal carcinoma (EC) cells retinoic acid (RA) strongly induces transcription from the RA receptor β2 (RARβ2) promoter through an RA response element (RARE) located in close proximity to the TATA box. Here we demonstrate that recombinant human TATA box-binding protein, hTFIID, and RAR functionally cooperate in transactivation of the RARβ2 promoter in EC cells in a strictly RA-dependent manner. We demonstrate that the core domain of hTFIID is sufficient to mediate RAR-dependent transcription and that Drosophila, but not yeast, TFIID can substitute for hTFIID. In COS cells ectopic expression of the E1A protein is a prerequisite for hTFIID and RAR to cooperate in transactivation. We propose a model for transcriptional regulation of the RARβ2 promoter in EC cells in which RAR, following activation by RA, functionally interacts with hTFIID via an E1A-like activity present in EC cells.
AB - In embryonal carcinoma (EC) cells retinoic acid (RA) strongly induces transcription from the RA receptor β2 (RARβ2) promoter through an RA response element (RARE) located in close proximity to the TATA box. Here we demonstrate that recombinant human TATA box-binding protein, hTFIID, and RAR functionally cooperate in transactivation of the RARβ2 promoter in EC cells in a strictly RA-dependent manner. We demonstrate that the core domain of hTFIID is sufficient to mediate RAR-dependent transcription and that Drosophila, but not yeast, TFIID can substitute for hTFIID. In COS cells ectopic expression of the E1A protein is a prerequisite for hTFIID and RAR to cooperate in transactivation. We propose a model for transcriptional regulation of the RARβ2 promoter in EC cells in which RAR, following activation by RA, functionally interacts with hTFIID via an E1A-like activity present in EC cells.
UR - https://www.scopus.com/pages/publications/0026632817
U2 - 10.1016/0092-8674(92)90443-G
DO - 10.1016/0092-8674(92)90443-G
M3 - Article
C2 - 1316240
AN - SCOPUS:0026632817
SN - 0092-8674
VL - 69
SP - 401
EP - 412
JO - Cell
JF - Cell
IS - 3
ER -