The chicken vitellogenin II gene is flanked by a GATA factor-dependent estrogen response unit

• Published in: Molecular endocrinology (Baltimore, Md.) Md.), 1996-08, Vol.10 (8), p.937-944
• Main Authors: Davis, D L, Burch, J B
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Chickens - genetics; Chloramphenicol O-Acetyltransferase - genetics; DNA-Binding Proteins - genetics; DNA-Binding Proteins - pharmacology; Erythroid-Specific DNA-Binding Factors; Estrogens - pharmacology; GATA6 Transcription Factor; Gene Expression; Mutagenesis, Site-Directed; Recombinant Fusion Proteins; Trans-Activators - pharmacology; Transcription Factors - genetics; Transcription Factors - pharmacology; Transfection; Vitellogenins - genetics
• ISSN: 0888-8809
• DOI: 10.1210/me.10.8.937

The chicken vitellogenin II (VTGII) gene is flanked by an imperfect estrogen response element (ERE) at -350 and a perfect ERE at -620. In the present study we show that this imperfect ERE lies within an estrogen response unit (ERU) that requires a GATA factor and the estrogen receptor to function as an estrogen-dependent enhancer. We infer that GATA-6 contributes to the estrogen-dependent and liver-specific regulation of the endogenous VTGII gene since this is the predominant GATA factor expressed in adult liver. Our analysis of the VTGII ERU revealed four salient points. First, this ERU is comprised of an ERE and a bank of functionally redundant GATA-binding sites. Second, the GATA-6 transactivation domain is necessary (and sufficient, when tethered near the ERE) to render this ERU functional. Third, ERU enhancer activity is dependent on GATA 6, regardless of whether the resident ERE is imperfect or perfect. Fourth, in contrast to a report that the estrogen receptor antagonizes the activity of another GATA factor (GATA-1), we show that these two factors can function in a synergistic manner within the context of the VTGII ERU.