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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
G Protein  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.
Hammes
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 G and G levels in Xenopus oocytes on
progesterone-induced signaling and maturation were examined. Our
results demonstrate that G subunits, rather than G , are the
principal mediators of progesterone action in this system. We show that
overexpression of G inhibits both progesterone-induced maturation
and activation of the MAPK pathway, whereas sequestration of endogenous
G subunits enhances progesterone-mediated signaling and
maturation. These data are consistent with a model whereby endogenous
free Xenopus G 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.
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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Copyright © 2000 by the American Society for Biochemistry and Molecular Biology.
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