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J. Biol. Chem., Vol. 281, Issue 49, 38080-38088, December 8, 2006

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Physical and Functional Interaction of the p14^ARF Tumor Suppressor with Ribosomes^*

Helen Rizos¹, Heather A. McKenzie, Ana Luisa Ayub, Sarah Woodruff, Therese M. Becker, Lyndee L. Scurr², Joachim Stahl, and Richard F. Kefford

From the Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, New South Wales 2145, Australia and the Max-Delbrück-Centrum für Molekulare Medizin, Robert-Rössle-Strasse 10, D-13125 Berlin-Buch, Germany

Alterations in the p14^ARF tumor suppressor are frequent in many human cancers and are associated with susceptibility to melanoma, pancreatic cancer, and nervous system tumors. In addition to its p53-regulatory functions, p14^ARF has been shown to influence ribosome biogenesis and to regulate the endoribonuclease B23, but there remains considerable controversy about its nucleolar role. We sought to clarify the activities of p14^ARF by studying its interaction with ribosomes. We show that p14^ARF and B23 interact within the nucleolar 60 S preribosomal particle and that this interaction does not require rRNA. In contrast to previous reports, we found that expression of p14^ARF does not significantly alter ribosome biogenesis but inhibits polysome formation and protein translation in vivo. These results suggest a ribosome-dependent p14^ARF pathway that regulates cell growth and thus complements p53-dependent p14^ARF functions.

Received for publication, October 5, 2006

^* This work was supported by the National Health and Medical Research Council, the University of Sydney, and the New South Wales Health Department. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

² Cameron Melanoma Research Fellow, Melanoma and Skin Cancer Research Institute, University of Sydney.

¹ National Health and Medical Research Council RD Wright Fellow, University of Sydney. To whom correspondence should be addressed: Westmead Inst. for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead NSW 2145, Australia. Tel.: 61-2-9845-9509; Fax: 61-2-9845-9102; E-mail: helen_rizos{at}wmi.usyd.edu.au.

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