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Originally published in Science Express on 18 September 2003
Science 7 November 2003:
Vol. 302. no. 5647, pp. 1036 - 1038
DOI: 10.1126/science.1090072

Reports

p53- and Drug-Induced Apoptotic Responses Mediated by BH3-Only Proteins Puma and Noxa

Andreas Villunger,1,2* Ewa M. Michalak,1 Leigh Coultas,1 Franziska Müllauer,2 Günther Böck,2 Michael J. Ausserlechner,2 Jerry M. Adams,1 Andreas Strasser1*

Apoptosis provoked by DNA damage requires the p53 tumor suppressor, but which of the many p53-regulated genes are required has remained unknown. Two genes induced by this transcription factor, noxa and puma (bbc3), stand out, because they encode BH3-only proteins, proapoptotic members of the Bcl-2 family required to initiate apoptosis. In mice with either noxa or puma disrupted, we observed decreased DNA damage–induced apoptosis in fibroblasts, although only loss of Puma protected lymphocytes from cell death. Puma deficiency also protected cells against diverse p53-independent cytotoxic insults, including cytokine deprivation and exposure to glucocorticoids, the kinase inhibitor staurosporine, or phorbol ester. Hence, Puma and Noxa are critical mediators of the apoptotic responses 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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