The Journal of Experimental Medicine
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Published online December 11, 2006
doi:10.1084/jem.20061563
The Journal of Experimental Medicine, Vol. 203, No. 13, 2793-2799
The Rockefeller University Press, 0022-1007 $30.00
© 2006 Shreeram et al.
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BRIEF DEFINITIVE REPORT

 Regulation of ATM/p53-dependent suppression of myc-induced lymphomas by Wip1 phosphatase

Sathyavageeswaran Shreeram1, Weng Kee Hee1, Oleg N. Demidov1, Calvina Kek1, Hiroshi Yamaguchi2, Albert J. Fornace, Jr.3, Carl W. Anderson4, Ettore Appella2, and Dmitry V. Bulavin1

1 Institute of Molecular and Cell Biology, Singapore, 138673
2 Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD 20892
3 Department of Genetics and Complex Diseases, Harvard School Of Public Health, Boston, MA 02115
4 Biology Department, Brookhaven National Laboratory, Upton, NY 11973

CORRESPONDENCE D.V. Bulavin: dvbulavin{at}imcb.a-star.edu.sg

The ataxia telangiectasia mutated (ATM) kinase is a key tumor suppressor that regulates numerous cell cycle checkpoints as well as apoptosis. Here, we report that ATM is a critical player in the regulation of apoptosis and lymphomagenesis in the presence of c-myc. In turn, deletion of the inhibitory ATM phosphatase, Wip1, results in ATM up-regulation and suppression of Eµ-myc–induced B cell lymphomas. Using mouse genetic crosses, we show that the onset of myc-induced lymphomas is dramatically delayed in Wip1-null mice in an ATM- and p53-, but not p38 MAPK– or Arf-, dependent manner. We propose that Wip1 phosphatase is critical for regulating the ATM-mediated tumor surveillance network.


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