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J Biol Chem, Vol. 275, Issue 17, 12941-12947, April 28, 2000
From The c-FOS protooncogene is rapidly
induced by a wide variety of extracellular stimuli including mitogenic
signals. Regulation of c-FOS expression is tightly
dependent on the serum response element localized within its promoter.
Two transcription factors, the serum response factor (SRF) and the
ternary complex factor, bind to the serum response element and play a
key role in the regulation of the c-FOS promoter activity.
In the present study, we show that two death effectors (CH11 and TRAIL)
severely impaired the transcriptional activity of the c-FOS
promoter in Jurkat T cells. This inhibition can be accounted for by the
specific cleavage by caspase 3 of the SRF both in vitro and
in vivo, since acetyl-DEVD-aldehyde prevented SRF cleavage
and abolished the inhibitory effect of CH11 and TRAIL on the
c-FOS promoter activity. Moreover, phorbol myristate
acetate, a potent anti-apoptotic effector, was found to protect SRF
completely from cleavage by caspase 3 and also to prevent the
inhibition of the c-FOS promoter activity by death effectors. Survival factors play an essential function in the regulation of cell growth mainly by regulating the expression of
immediate early gene such as c-FOS. In this line, cleavage of SRF at the onset of apoptosis could abrogate the ability of the cell
to induce inappropriate survival pathways. All together, our results
are consistent with a role of SRF at the interface between cell
survival and death pathways.
Cleavage of the Serum Response Factor during Death
Receptor-induced Apoptosis Results in an Inhibition of the
c-FOS Promoter Transcriptional Activity*
§,,,,
INSERM U526, Activation des Cellules
Hématopoïétiques, Physiopathologie de la Survie et
de la Mort Cellulaires et Infections Virales, Faculté de
Médecine, 28 Avenue de Valombrose, 06107 Nice Cedex 2 and
¶ Centre de Biochimie, CNRS, Institut de Recherche sur la
Signalisation, la Biologie du Développement et le Cancer,
CNRS UMR 6543, Centre A. Lacassagne, 33 Avenue de Valombrose,
06189 Nice, France
*
This work was supported by INSERM, the University of Nice,
Sophia-Antipolis, Association pour la Recherche sur le Cancer Grant 9502, and Ligue Nationale Contre le Cancer.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. Tel.: (33) 4 93 37 76 76; Fax: (33) 4 93 81 78 52; E-mail: auberger@unice.fr.
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