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Transcriptional Regulation of the Gonadotropin-Releasing Hormone Receptor Gene Is Mediated in Part by a Putative Repressor Element and by the Cyclic Adenosine 3',5'-Monophosphate Response Element¹

Oregon Regional Primate Research Center (G.M.N., P.M.C), Beaverton, Oregon 97006; and the Department of Physiology and Pharmacology, (P.M.C.), Oregon Health Sciences University, Portland, Oregon 97201

Address all correspondence and requests for reprints to: Dr. P. Michael Conn, 505 NW 185th Avenue, Beaverton, Oregon 97006. E-mail: connm{at}ohsu.edu

The levels of the GnRH receptor (GnRHR) and its messenger RNA depend on the pattern of administration of GnRH. In this study, internal deletion mutants in a luciferase reporter gene vector (GnRHR-pXP2) containing a 1226-bp promoter fragment of mouse GnRHR gene were used to examine the regulation of GnRHR gene transcription in GGH₃ cells. Our results indicate that the mouse GnRHR promoter contains one putative repressor element located at position -343/-335. When this sequence was deleted, the GnRHR promoter activity was significantly increased in both basal and GnRH agonist (Buserelin)-, phorbol ester-, and forskolin-stimulated cells. Gel mobility shift assay showed that the sequence -343/-335 is capable of binding GGH₃ nuclear proteins. With deletion of the cAMP response element (-107/-100), basal and Buserelin-stimulated transcription was decreased. The same response was observed after stimulation with forskolin. Stimulation with (Bu)₂cAMP did not alter transcription above basal levels. The stimulation with phorbol ester resulted in an attenuated increase in transcriptional activity, suggesting that this sequence of the GnRHR promoter is a cAMP response element. These results suggest that the transcriptional activity of the GnRHR gene is mediated in part by a putative repressor element and by the cAMP response element.

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