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Regulation of the Intronic Promoter of Rat Estrogen Receptor Gene, Responsible for Truncated Estrogen Receptor Product-1 Expression

Université de Rennes I, Interactions Cellulaires et Moléculaires, Equipe Information et Programmation Cellulaires, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 6026, Campus de Beaulieu, 35042 Rennes Cedex, France

Address all correspondence and requests for reprints to: Dr. M.-L. Thieulant, Equipe Information et Programmation Cellulaires, Unité Mixte de Recherche 6026, Bat 13, Campus de Beaulieu, 35042 Rennes Cedex, France. E-mail: Marie-Lise.Thieulant{at}univ-rennes1.fr.

We have characterized the intronic promoter of the rat estrogen receptor (ER) gene, responsible for the lactotrope-specific truncated ER product (TERP)-1 isoform expression. Transcriptional regulation was investigated by transient transfections using 5'-deletion constructs. TERP promoter constructs were highly active in MMQ cells, a pure lactotrope cell line, whereas a low basal activity was detected in T3–1 gonadotrope cells or in COS-7 monkey kidney cells. Serial deletion analysis revealed that 1) a minimal -693-bp region encompassing the TATA box is sufficient to allow lactotrope-specific expression; 2) the promoter contains strong positive cis-acting elements both in the distal and proximal regions, and 3) the region spanning the -1698/-1194 region includes repressor elements. Transient transfection studies, EMSAs, and gel shifts demonstrated that estrogen activates the TERP promoter via an estrogen-responsive element (ERE1) located within the proximal region. Mutation of ERE1 site completely abolishes the estradiol-dependent transcription, indicating that ERE1 site is sufficient to confer estrogen responsiveness to TERP promoter. In addition, ER action was synergized by transfection of the pituitary-specific factor Pit-1. EMSAs showed that a single Pit-1 DNA binding element in the vicinity of the TATA box is sufficient to confer response by the TERP promoter. In conclusion, we demonstrated, for the first time, that TERP promoter regulation involves ERE and Pit-1 cis-elements and corresponding trans-acting factors, which could play a role in the physiological changes that occur in TERP-1 transcription in lactotrope cells.

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