Springer Online Journal Archives 1860-2000
Abstract Rainbow trout estrogen receptor (rtER) concentration was highly induced in the liver after in vivo estradiol (E2) treatment or in vitro, in hepatocyte aggregate culture. Determination of transcription rate and mRNA half-life demonstrated that E2-induction of hepatic rtER level is caused essentially by an increase in the transcriptional and post-transcriptional activity of rtER gene. However, the expression of rtER gene in the liver seems to be down-regulated by glucocorticoids. We have used transient transfection assays with reporter plasmids linked to 5′ flanking regions of the rtER gene promoter, to identify cis-elements responsible for E2 inducibility. Deletion analysis localized a functional estrogen-responsive-element (ERE), near the transcription start site, with one mutation on the first base compared to the consensus sequence. This element and 200 bp fragment of the rtER promoter encompassing the ERE appear to be the major cis-acting element involved in the regulation of the gene. Data obtained from transfection experiments and footprinting analysis, suggested that the receptor is one of the major trans-factors implicated in the regulation of its own gene. However, interaction of ER with other transcription factors is required for maximal E2-stimulation.
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