Open AccessSynergism between a half‐site and an imperfect estrogen‐responsive element, and cooperation with COUP‐TFI are required for estrogen receptor (ER) to achieve a maximal estrogen‐stimulation of rainbow trout ER gene
Author(s) -
Petit Fabrice G.,
Métivier , Raphaël,
Valotaire , Yves,
Pakdel Farzad
Publication year - 1999
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1046/j.1432-1327.1999.00072.x
Subject(s) - hormone response element , enhancer , estrogen receptor , promoter , transactivation , biology , transcriptional regulation , estrogen , microbiology and biotechnology , transcription factor , gene , gene expression , genetics , cancer , breast cancer
In all oviparous, liver represents one of the main E 2 ‐target tissues where estrogen receptor (ER) constitutes the key mediator of estrogen action. The rainbow trout estrogen receptor (rtER) gene expression is markedly up‐regulated by estrogens and the sequences responsible for this autoregulation have been located in a 0.2 kb upstream transcription start site within – 40/– 248 enhancer region. Absence of interference with steroid hormone receptors and tissue‐specific factors and a conserved basal transcriptional machinery between yeast and higher eukaryotes, make yeast a simple assay system that will enable determination of important cis ‐acting regulatory sequences within rtER gene promoter and identification of transcription factors implicated in the regulation of this gene. Deletion analysis allowed to show a synergistic effect between an imperfect estrogen‐responsive element (ERE) and a consensus half‐ERE to achieve a high hormone‐dependent transcriptional activation of the rtER gene promoter in the presence of stably expressed rtER. As in mammalian cells, here we observed a positive regulation of the rtER gene promoter by the chicken ovalbumin upstream promoter‐transcription factor I (COUP‐TFI) through enhancing autoregulation. Using a point mutation COUP‐TFI mutant unable to bind DNA demonstrates that enhancement of rtER gene autoregulation requires the interaction of COUP‐TFI to the DNA. Moreover, this enhancement of transcriptional activation by COUP‐TFI requires specifically the AF‐1 transactivation function of ER and can be observed in the presence of E 2 or 4‐hydroxytamoxifen but not ICI 164384. Thus, this paper describes the reconstitution of a hormone‐responsive transcription unit in yeast in which the regulation of rtER gene promoter could be enhanced by the participation of cis ‐elements and/or trans ‐acting factors, such as ER itself or COUP‐TF.