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Originally published In Press as doi:10.1074/jbc.M203623200 on May 24, 2002

J. Biol. Chem., Vol. 277, Issue 32, 28683-28689, August 9, 2002
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The Phosphorylation Site Located in the A Region of Retinoic X Receptor alpha  Is Required for the Antiproliferative Effect of Retinoic Acid (RA) and the Activation of RA Target Genes in F9 Cells*

Julie BastienDagger , Sylvie Adam-StitahDagger , Jean-Luc Plassat, Pierre Chambon, and Cécile Rochette-Egly§

From the Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP/Collège de France, BP 163, 67404 Illkirch Cedex, France

Mouse F9 embryocarcinoma cells constitute a well established cell autonomous model system for investigating retinoic acid (RA) signaling in vitro. RA induces the differentiation of F9 cells grown as monolayers into endodermal-like cells and decreases their rate of proliferation. Knock-out of the retinoic X receptor alpha  (RXRalpha ) gene abolishes endodermal differentiation and the induction of several endogenous RA-responsive genes. RXRalpha null cells are also drastically impaired in their antiproliferative response to RA. The role of the RXRalpha phosphorylation site located in the N-terminal A region (Ser22) has been investigated here by establishing cell lines re-expressing RXRalpha either wild type or mutated at the phosphorylation site (RXRalpha S22A) in a RXRalpha -null background. We show that Ser22 is dispensable for RA-induced endodermal differentiation but is crucial for the expression of several RA-responsive genes. Ser22 is also indispensable for the antiproliferative effect of RA and necessary for the RA-induced down-regulation of p21CIP and p27KIP CKIs proteins that are known to be involved in the control of cell cycle progression.

* This work was supported by funds from CNRS, INSERM, the Collège de France, the Association pour la Recherche sur le Cancer, and Bristol-Myers Squibb.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 Supported by the Ministère de l'Education Nationale et de la Recherche Scientifique et Technique.

§ To whom correspondence should be addressed: IGBMC, BP 163, 67 404 Illkirch Cedex, CU de Strasbourg, France. Tel.: 33-3-88-65-34-59; Fax: 33-3-88-65-32-01; E-mail: cegly@igbmc.u-strasbg.fr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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