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Nucleic Acids Research 2005 33(3):1021-1030; doi:10.1093/nar/gki246
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Published online 17 February 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

Mms22p protects Saccharomyces cerevisiae from DNA damage induced by topoisomerase II

E. L. Baldwin1, A. C. Berger3, A. H. Corbett3 and N. Osheroff1,2,*

1 Department of Biochemistry, Vanderbilt University School of Medicine Nashville, TN 37232-0146, USA 2 Department of Medicine (Hematology/Oncology), Vanderbilt University School of Medicine Nashville, TN 37232-0146, USA 3 Department of Biochemistry, Emory University School of Medicine Atlanta, GA 30322, USA

*To whom correspondence should be addressed at Department of Biochemistry, 654 Robinson Research Building, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, USA. Tel: +615 322 4338; Fax: +615 343 1166; Email: neil.osheroff{at}vanderbilt.edu

Received November 19, 2004. Accepted January 24, 2005.

The cleavage reaction of topoisomerase II, which creates double-stranded DNA breaks, plays a central role in both the cure and initiation of cancer. Therefore, it is important to understand the cellular processes that repair topoisomerase II-generated DNA damage. Using a genome-wide approach with Saccharomyces cerevisiae, we found that {Delta}mre11, {Delta}xrs2, {Delta}rad50, {Delta}rad51, {Delta}rad52, {Delta}rad54, {Delta}rad55, {Delta}rad57 and {Delta}mms22 strains were hypersensitive to etoposide, a drug that specifically increases levels of topoisomerase II-mediated DNA breaks. These results confirm that the single-strand invasion pathway of homologous recombination is the major pathway that repairs topoisomerase II-induced DNA damage in yeast and also indicate an important role for Mms22p. Although {Delta}mms22 strains are sensitive to several DNA-damaging agents, little is known about the function of Mms22p. {Delta}mms22 cultures accumulate in G2/M, and display an abnormal cell cycle response to topoisomerase II-mediated DNA damage. MMS22 appears to function outside of the single-strand invasion pathway, but levels of etoposide-induced homologous recombination in {Delta}mms22 cells are lower than wild-type. MMS22 is epistatic with RTT101 and RTT107, genes that encode its protein binding partners. Finally, consistent with a role in DNA processes, Mms22p localizes to discrete nuclear foci, even in the absence of etoposide or its binding partners.


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