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Submitted on September 1, 2005
Accepted on October 19, 2005
Center for Animal Biotechnology and Genomics, Department of Animal Science, and Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843 USA
* To whom correspondence should be addressed. E-mail: fbazer{at}cvm.tamu.edu.
Establishment of pregnancy in ruminants results from paracrine signaling by interferon 
(IFNT) from the conceptus to uterine endometrial luminal (LE) epithelia that prevents release of luteolytic prostaglandin F2alpha (PGF) pulses. In cyclic and pregnant ewes, progesterone down-regulates progesterone receptor (PGR) gene expression in LE. In cyclic ewes, loss of PGR allows for increases in estrogen receptor 
(ESR1) and then oxytocin receptor (OXTR) gene expression followed by oxytocin-induced PGF pulses. In pregnant ewes, IFNT inhibits transcription of the ESR1 gene, which presumably inhibits OXTR gene transcription. Alternatively, IFNT may directly inhibit OXTR gene transcription. The 5' promoter/enhancer region of the ovine OXTR gene was cloned and found to contain predicted binding sites for AP-1, SP1 and PGR, but not for ESR1. Deletion analysis showed that the basal promoter activity was dependent on the region from -144 to -4 bp that contained only SP1 sites. IFNT did not affect activity of the OXTR promoter. In cells transfected with ESR1, estradiol-17beta and ICI 182,780 increased promoter activity due to GC-rich SP1 binding sites at positions -104 and -64. Mutation analyses showed that the proximal SP1 sites mediated ESR1 action as well as basal activity of the promoter. In response to progesterone, PGR-B also increased OXTR promoter activity. SP1 protein was constitutively expressed and abundant in the LE of the ovine uterus. These results support the hypothesis that the antiluteolytic effects of IFNT are mediated by direct inhibition or silencing of ESR1 gene transcription, thereby precluding ESR1/SP1 from stimulating OXTR gene transcription.
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