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Vol. 273, Issue 2, 1175-1183, January 9, 1998

Antiprogestins Mediate Differential Effects on Glucocorticoid Receptor Remodeling of Chromatin Structure

Christy J. Fryer, Steven K. Nordeen^¶, and Trevor K. Archer

From the Departments of  Ob/Gyn, Biochemistry and Oncology, The University of Western Ontario, London Regional Cancer Centre, London, Ontario N6A 4L6, Canada and the ^¶ Department of Pathology, The University of Colorado Health Sciences Center, Denver, Colorado 80262

We examined the mechanism(s) by which the progesterone receptor (PR) is able to inhibit glucocorticoid receptor (GR) activation from the mouse mammary tumor virus (MMTV) promoter in vivo. Using specific hormone antagonists, we demonstrate that the PR complexed with an type II antiprogestin blocks glucocorticoid-induced activation of the MMTV promoter. However, when complexed with a type I antiprogestin the PR is unable to block glucocorticoid-induced activation. PR repression of GR activity results from the inhibition of the ability of the GR to remodel chromatin such that the antiprogestin-occupied/PR prevents the glucocorticoid induced assembly of a preinitiation complex at MMTV promoter. These experiments suggest that the specific chromatin organization of the MMTV promoter provides a mechanism for regulating cross-talk between the GR and PR in vivo.

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