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Nucleic Acids Research 2004 32(15):4480-4490; doi:10.1093/nar/gkh773
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Published online 23 August 2004

Nucleic Acids Research, Vol. 32 No. 15 © Oxford University Press 2004; all rights reserved

Transcriptional repression by p53 promotes a Bcl-2-insensitive and mitochondria-independent pathway of apoptosis

Nelly Godefroy, Sylvina Bouleau, Gaëtan Gruel1, Flore Renaud, Vincent Rincheval, Bernard Mignotte, Diana Tronik-Le Roux1 and Jean-Luc Vayssière*

Université de Versailles/Saint Quentin-en-Yvelines, FRE 2445, Laboratoire de Génétique et Biologie Cellulaire and Ecole Pratique des Hautes Etudes, Laboratoire de Génétique Moléculaire et Physiologique, 45 avenue des Etats-Unis, 78035 Versailles cedex, France and 1 Commissariat à l'Energie Atomique (CEA), Laboratoire de Génomique et Radiobiologie de l'Hématopoïèse, Service de Génomique Fonctionnelle, 2 rue Gaston Crémieux 91057 Evry, France

* To whom correspondence should be addressed. Tel: +33 1 39 25 36 60; Fax: +33 1 39 25 36 55; Email: vayssiere{at}genetique.uvsq.fr

Received June 18, 2004; Revised and Accepted July 28, 2004

p53 can induce apoptosis in various ways including transactivation, transrepression and transcription-independent mechanisms. What determines the choice between them is poorly understood. In a rat embryo fibroblast model, caspase inhibition changed the outcome of p53 activation from standard Bcl-2-regulated apoptosis to caspase-independent and Bcl-2-insensitive cell death, a phenomenon not described previously. Here, we show that caspase inhibition affects cell death commitment decisions by modulating the apoptotic functions of p53. Indeed, in the Bcl-2-sensitive pathway, transactivation-dependent signalling is activated leading to a rapid MDM2-mediated degradation of p53. In contrast, in the Bcl-2-insensitive pathway, p53 is stable and this is associated with transrepression-dependent signalling. A study with microarrays identified these genes regulated by p53 in the absence of active caspases.


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