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Biology of Reproduction 67, 972-980 (2002)
© 2002 Society for the Study of Reproduction, Inc.

Regular Article

An Activator Protein-1 Complex Mediates Epidermal Growth Factor Regulation of Equine Glycoprotein {alpha} Subunit Expression in Trophoblast Cells1

Theingi M. Thwaya, and Michael W. Wolfe2,a

a Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160-7401

Equids and primates are the only species known to express the placental hormone chorionic gonadotropin (CG). CG is a member of the heterodimeric glycoprotein family and is composed of an {alpha} subunit linked to a hormone-specific ß subunit. Previously, we have reported that epidermal growth factor (EGF) regulates the equine glycoprotein hormone {alpha} subunit promoter through a protein kinase C (PKC)/mitogen-activated protein kinase (MAPK) signal transduction pathway in trophoblasts. The current study investigates the regulatory element/factors involved in the induction of equine glycoprotein {alpha} subunit gene expression by EGF. Using 5' deletion mutagenesis, we have delineated the primary EGF/PKC responsive region of the equine {alpha} subunit gene to be located between -2039 to -2032 base pairs upstream of the transcriptional start site. The sequence within this region contains an activator protein 1 (AP-1)-like response element (TGAATCA) and is similar to a consensus AP-1 (TGAC/GTCA) response element. This element appeared to preferentially interact with a c-fos/JunD heterodimer. Stimulation by EGF induced the binding of c-fos and JunD to this element and subsequently elevated promoter activity. In conclusion, an EGF/PKC/MAPK signal transduction pathway regulates equine glycoprotein {alpha} subunit gene expression through a distinct regulatory element(s) that lies between -2039 to -2032 of the equine glycoprotein {alpha} subunit promoter in trophoblasts and involves an AP-1 complex.

First decision: 26 November 2001.

1 This research was supported in part by grant R29 DK50668 from the National Institutes of Health to M.W.W. and was supported by NICHD/NIH through cooperative agreement U54 HD 33994 as part of the Specialized Cooperative Center Program in Reproductive Research. T.M.T. is supported in part by a fellowship from Biomedical Research Program at University of Kansas Medical Center.

2 Correspondence: Michael Wolfe, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160-7401. FAX: 913 588 7430; mwolfe2{at}kumc.edu






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