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Originally published In Press as doi:10.1074/jbc.M006757200 on October 3, 2000

J. Biol. Chem., Vol. 275, Issue 52, 41512-41520, December 29, 2000
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G Protein beta gamma Subunits Inhibit Nongenomic Progesterone-induced Signaling and Maturation in Xenopus laevis Oocytes
EVIDENCE FOR A RELEASE OF INHIBITION MECHANISM FOR CELL CYCLE PROGRESSION*

Lindsey B. Lutz, Bonnie Kim, David Jahani, and Stephen R. HammesDagger

From the Department of Internal Medicine, University of Texas Southwestern Medical School, Dallas, Texas 75390-8857

Progesterone-induced maturation of Xenopus oocytes is a well known example of nongenomic signaling by steroids; however, little is known about the early signaling events involved in this process. Previous work has suggested that G proteins and G protein-coupled receptors may be involved in progesterone-mediated oocyte maturation as well as in other nongenomic steroid-induced signaling events. To investigate the role of G proteins in nongenomic signaling by progesterone, the effects of modulating Galpha and Gbeta gamma levels in Xenopus oocytes on progesterone-induced signaling and maturation were examined. Our results demonstrate that Gbeta gamma subunits, rather than Galpha , are the principal mediators of progesterone action in this system. We show that overexpression of Gbeta gamma inhibits both progesterone-induced maturation and activation of the MAPK pathway, whereas sequestration of endogenous Gbeta gamma subunits enhances progesterone-mediated signaling and maturation. These data are consistent with a model whereby endogenous free Xenopus Gbeta gamma subunits constitutively inhibit oocyte maturation. Progesterone may induce maturation by antagonizing this inhibition and therefore allowing cell cycle progression to occur. These studies offer new insight into the early signaling events mediated by progesterone and may be useful in characterizing and identifying the membrane progesterone receptor in oocytes.


* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Div. of Endocrinology, Dept. of Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, TX 75390-8857. Tel.: 214-648-4793; Fax: 214-648-8917; E-mail: stephen.hammes@email.swmed.edu.


Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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