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Originally published In Press as doi:10.1074/jbc.M008270200 on February 15, 2001

J. Biol. Chem., Vol. 276, Issue 21, 17800-17807, May 25, 2001
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Bcl-xL Expression Correlates with Primary Macrophage Differentiation, Activation of Functional Competence, and Survival and Results from Synergistic Transcriptional Activation by Ets2 and PU.1*

Lidia SevillaDagger , Arnaud Zaldumbide§, Francoise Carlotti§, Manal Abdel Dayem, Philippe Pognonec, and Kim E. Boulukos

From the Institute of Signalisation, Developmental Biology and Cancer, INSERM 470, Centre de Biochimie, Université de Nice, Faculté des Sciences, 06108 Nice, France

Depriving primary bone marrow-derived macrophages of colony-stimulating factor-1 (CSF-1) induces programmed cell death by apoptosis. We show that cell death is accompanied by decreases in the expression of anti-apoptotic Bcl-xL protein and the Ets2 and PU.1 proteins of the Ets transcription factor family. Macrophages require both priming and triggering signals independent of CSF-1 to kill neoplastic cells or microorganisms, and this activation of macrophage competence is accompanied by increased expression of bcl-xL, ets2, and PU.1. Furthermore, we show that only Ets2 and PU.1, but not Ets1, function in a synergistic manner to transactivate the bcl-x promoter. The synergy observed between PU.1 and Ets2 is dependent on the transactivation domains of both proteins. Although other transcription factors like Fos, c-Jun, Myc, STAT3, and STAT5a are implicated in the activation of macrophage competence or in CSF-1 signaling, no synergy was observed between Ets2 and these transcription factors on the bcl-x promoter. We demonstrate that the exogenous expression of both Ets2 and PU.1 in macrophages increases the number of viable cells upon CSF-1 depletion and that Ets2 and PU.1 can functionally replace Bcl-xL in inhibiting Bax-induced apoptosis. Together, these results demonstrate that PU.1 and Ets2 dramatically increase bcl-x activation, which is necessary for the cytocidal function and survival of macrophages.

* 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 European Communities Grant ERBFMBICT972684 and by the Foundation pour la Recherche Medicale.

§ Supported by Ministère de L'Education Nationale de La Recherche et de la Technologie.

Supported by Association pour la Recherche contre le Cancer Grant 9691. To whom correspondence should be addressed. Tel. and Fax: 33-4-92-07-64-13; E-mail: boulukos@unice.fr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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