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Originally published In Press as doi:10.1074/jbc.M210479200 on October 15, 2002

J. Biol. Chem., Vol. 277, Issue 52, 50934-50940, December 27, 2002
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DNA Damage-induced Translocation of the Werner Helicase Is Regulated by Acetylation*

Gil BlanderDagger §, Noa ZalleDagger §, Yaron DanielyDagger , Jan TaplickDagger , Matthew D. Gray||, and Moshe OrenDagger **

From the Dagger  Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel and the || Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195-7470

Werner syndrome is a rare autosomal recessive disorder involving the premature appearance of features reminiscent of human aging. Werner syndrome occurs by mutation of the WRN gene, encoding a DNA helicase. WRN contributes to the induction of the p53 tumor suppressor protein by various DNA damaging agents. Here we show that UV exposure leads to extensive translocation of WRN from the nucleolus to nucleoplasmic foci in a dose-dependent manner. Ionizing radiation also induces WRN translocation, albeit milder, partially through activation of the ATM kinase. The nucleoplasmic foci to which WRN is recruited display partial colocalization with PML nuclear bodies. The translocation of WRN into nucleoplasmic foci is significantly enhanced by the protein deacetylase inhibitor, Trichostatin A. Moreover, Trichostatin A delays the re-entry of WRN into the nucleolus at late times after irradiation. WRN is acetylated in vivo, and this is markedly stimulated by the acetyltransferase p300. Importantly, p300 augments the translocation of WRN into nucleoplasmic foci. These findings support the notion that WRN plays a role in the cellular response to DNA damage and suggest that the activity of WRN is modulated by DNA damage-induced post-translational modifications of WRN and possibly WRN-interacting proteins.

* This work was supported in part by Grant RO1 CA 40099 from the NCI, National Institutes of Health, the USA-Israel Binational Science Foundation, the Kadoorie Charitable Foundations, the Cooperation Program in Cancer Research of the German Cancer Research Center (DKFZ) and Israel's Ministry of Science (MOS), the Robert Bosch Foundation (Germany), and the Yad Abraham Center for Cancer Diagnosis and Therapy.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Both authors contributed equally to this work.

Supported by postdoctoral Grant 01-182-01-TBE from the American Cancer Society.

** To whom correspondence should be addressed. Tel.: 972-8-9342358; Fax: 972-8-9465223; E-mail: Moshe.Oren@weizmann.ac.il.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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