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Biology of Reproduction 65, 1038-1049 (2001)
© 2001 Society for the Study of Reproduction, Inc.

Regular Article

Interferon Regulatory Factor-Two Restricts Expression of Interferon-Stimulated Genes to the Endometrial Stroma and Glandular Epithelium of the Ovine Uterus1

Youngsok Choi4,a, Greg A. Johnson3,4,a, Robert C. Burghardtb, Luc R. Berghmanc, Margaret M. Joyce3,a, Kristin M. Taylora, M. David Stewarta, Fuller W. Bazer2,a, and Thomas E. Spencera

a Center for Animal Biotechnology and Genomics, Department of Animal Science, b Department of Veterinary Anatomy and Public Health, and c Departments of Poultry Science and Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843

ABSTRACT

Interferon tau (IFN{tau}) is the signal for maternal recognition of pregnancy in ruminants. The positive effects of IFN{tau} on IFN-stimulated gene (ISG) expression are mediated by ISG factor 3 (ISGF3), which is composed of signal transducer and activator of transcription (Stat) 1, Stat 2, and IFN regulatory factor-9 (IRF-9), and by gamma-activated factor (GAF), which is a Stat 1 homodimer. Induction of ISGs, such as ISG17 and 2',5'-oligoadenylate synthetase, by IFN{tau} during pregnancy is limited to the endometrial stroma (S) and glandular epithelium (GE) of the ovine uterus. The IRF-2, a potent transcriptional repressor of ISG expression, is expressed in the luminal epithelium (LE). This study determined effects of the estrous cycle, pregnancy, and IFN{tau} on expression of Stat 1, Stat 2, IRF-9, IRF-1, and IRF-2 genes in the ovine endometrium. In cyclic ewes, Stat 1, Stat 2, IRF-1, and IRF-9 mRNA and protein were detected at low levels in the S and GE. During pregnancy, expression of these genes increased only in the S and GE. Expression of IRF-2 was detected only in the LE and superficial GE (sGE) of both cyclic and pregnant ewes. In cyclic ewes, intrauterine administration of IFN{tau} stimulated Stat 1, Stat 2, IRF-9, and IRF-1 expression in the endometrium. Ovine IRF-2 repressed transcriptional activity driven by IFN-stimulated response elements that bind ISGF3, but not by gamma-activation sequences that bind GAF. These results suggest that IRF-2 in the LE and sGE restricts IFN{tau} induction of ISGs to the S and GE. In the S and GE, IFN{tau} hyperactivation of ISG expression likely involves formation and actions of the transcription factors ISGF3 and, perhaps, IRF-1.

FOOTNOTES

First decision: 1 May 2001.

1 Supported by NIH grant HD32534 (to F.W.B. and T.E.S.) and, in part, by NIH grants HD08501 (to G.A.J.) and P30 ES09106.

2 Correspondence: Fuller W. Bazer, Center for Animal Biotechnology and Genomics, 442D Kleberg Center, 2471 TAMU, Texas A&M University, College Station, TX 77843-2471. FAX: 979 862 2662; fbazer{at}cvm.tamu.edu

3 Current address: Animal and Veterinary Science Department, Center for Reproductive Biology, University of Idaho, Moscow, ID 83844-2330.

4 These authors contributed equally to this work and should be considered first coauthors.




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