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p53- and Drug-Induced Apoptotic Responses Mediated by BH3-Only Proteins Puma and Noxa
Andreas Villunger,1,2*Ewa M. Michalak,1Leigh Coultas,1Franziska Müllauer,2Günther Böck,2Michael J. Ausserlechner,2Jerry M. Adams,1Andreas Strasser1*
Apoptosis provoked by DNA damage requires the p53 tumor suppressor,but which of the many p53-regulated genes are required has remainedunknown. Two genes induced by this transcription factor, noxaand puma (bbc3), stand out, because they encode BH3-only proteins,proapoptotic members of the Bcl-2 family required to initiateapoptosis. In mice with either noxa or puma disrupted, we observeddecreased DNA damage–induced apoptosis in fibroblasts,although only loss of Puma protected lymphocytes from cell death.Puma deficiency also protected cells against diverse p53-independentcytotoxic insults, including cytokine deprivation and exposureto glucocorticoids, the kinase inhibitor staurosporine, or phorbolester. Hence, Puma and Noxa are critical mediators of the apoptoticresponses induced by p53 and other agents.
1 The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. 2 Institute for Pathophysiology, University of Innsbruck, Austria.
* To whom correspondence should be addressed. E-mail: strasser{at}wehi.edu.au (A.S.) and andreas.villunger{at}uibk.ac.at (A.V.)
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