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Endocrinology Vol. 142, No. 5 1786-1794
Copyright © 2001 by The Endocrine Society

ARTICLES

Interferon-{tau} (IFN{tau}) Regulation of IFN-Stimulated Gene Expression in Cell Lines Lacking Specific IFN-Signaling Components1

M. David Stewart2, Greg A. Johnson2, Fuller W. Bazer and Thomas E. Spencer

Center for Animal Biotechnology and Genomics, Department of Animal Science, Texas A&M University, College Station, Texas 77843-2471

Address all correspondence and requests for reprints to: Thomas E. Spencer, Center for Animal Biotechnology and Genomics, 442 Kleberg Center, 2471 TAMU, Texas A&M University, College Station, Texas 77843-2471. E-mail: tspencer{at}ansc.tamu.edu

Interferon-{tau} (IFN{tau}) is a unique type I IFN secreted by the ruminant conceptus that acts in a paracrine manner on the endometrial epithelium to signal pregnancy recognition. In the ovine endometrium, IFN{tau} suppresses estrogen receptor {alpha} and oxytocin receptor gene expression, but increases or induces expression of IFN-simulated genes (ISGs), including signal transducer and activator of transcription-1 (STAT1), STAT2, ISG factor-3{gamma} (ISGF3{gamma})/p48/IFN regulatory factor-9, and 2',5'-oligoadenylate synthetase (OAS). Human fibroblast cell lines lacking specific IFN signaling components were employed to determine the roles of STAT1, STAT2, and ISGF3{gamma} in the effects of IFN{tau} on ISG protein expression. Results indicated that STAT1{alpha} or STAT1ß is required for IFN{tau} effects on STAT2, ISGF3{gamma}, and OAS (40/46, 69/71, and 100 kDa). STAT2 is required for effects on STAT1, ISGF3{gamma}, and all OAS forms. ISGF3{gamma} is required for effects of IFN{tau} on STAT2 and 40/46- and 69/71-kDa OAS and plays a role in the effects of IFN{tau} on 100-kDa OAS and STAT1. Mutation of Tyr701, but not Ser727, of STAT1 abolished the effects of IFN{tau} on ISG expression. Mutation of the SH2 domain of STAT1 abolished the effects of IFN{tau} on all ISGs and reduced increases in 100-kDa OAS. These data illustrate the importance of transcription factors composed of STAT1, STAT2, and ISGF3{gamma} in the signaling pathway mediating the effects of IFN{tau} on ISG expression.




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