FOXO3a-dependent regulation of Puma in response to cytokine/growth factor withdrawal

doi:10.1084/jem.20060353

Published online 26 June 2006 doi:10.1084/jem.20060353
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 7, 1657-1663

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BRIEF DEFINITIVE REPORT

FOXO3a-dependent regulation of Puma in response to cytokine/growth factor withdrawal

Han You¹^,2, Marc Pellegrini¹^,2, Katsuya Tsuchihara¹^,2, Kazuo Yamamoto¹^,2, Georg Hacker³, Miriam Erlacher⁴, Andreas Villunger⁴, and Tak W. Mak¹^,2

¹ The Campbell family Institute for Breast Cancer Research, University Health Network, Toronto, Ontario M5G 2C1, Canada ² Department of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario M5G 2M9, Canada ³ Institute for Medical Microbiology, Technische Universitat Munchen, D-81675 Munich, Germany ⁴ Division of Experimental Pathophysiology and Immunology, BIOCENTER, Innsbruck Medical University, Innsbruck, A-6020 Austria

CORRESPONDENCE Tak W. Mak: tmak{at}uhnres.utoronto.ca

Puma is an essential mediator of p53-dependent and -independentapoptosis in vivo. In response to genotoxic stress, Puma isinduced in a p53-dependent manner. However, the transcriptionfactor driving Puma up-regulation in response to p53-independentapoptotic stimuli has yet to be identified. Here, we show thatFOXO3a up-regulates Puma expression in response to cytokineor growth factor deprivation. Importantly, dysregulated Aktsignaling in lymphoid cells attenuated Puma induction upon cytokinewithdrawal. Our results suggest that Puma, together with anotherBH3 only member, Bim, function as FOXO3a downstream targetsto mediate a stress response when PI3K/Akt signaling is down-regulated.

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