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J. Biol. Chem., Vol. 281, Issue 19, 13717-13723, May 12, 2006

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Involvement of Topoisomerase III in Telomere-Telomere Recombination^*

Hung-Ji Tsai¹, Wei-Hsiang Huang¹, Tsai-Kun Li¹, Yun-Luen Tsai, Kou-Juey Wu, Shun-Fu Tseng, and Shu-Chun Teng^¶2

From the Department of Microbiology, College of Medicine, National Taiwan University, No. 1, Sec. 1, Jen-Ai Road, Taipei 10018, Taiwan, the Institute of Biochemistry, National Yang-Ming University, Taipei 11221, Taiwan, and the ^¶Institute of Internal Medicine, National Taiwan University Hospital, Taipei 10018, Taiwan

Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of telomerase. In both mammalian tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative (ALT) recombination mechanism. In yeast, Sgs1p and its associated type IA topoisomerase, Top3p, may work coordinately in removing Holliday junction intermediates from a crossover-producing recombination pathway. Previous studies have also indicated that Sgs1 helicase acts in a telomere recombination pathway. Here we show that topoisomerase III is involved in telomere-telomere recombination. The recovery of telomere recombination-dependent survivors in a telomerase-minus yeast strain was dependent on Top3p catalytic activity. Moreover, the RIF1 and RIF2 genes are required for the establishment of TOP3/SGS1-dependent telomere-telomere recombination. In human Saos-2 ALT cells, human topoisomerase III (hTOP3) also contributes to telomere recombination. Strikingly, the telomerase activity is clearly enhanced in surviving si-hTOP3 Saos-2 ALT cells. Altogether, the present results suggest a potential role for hTOP3 in dissociating telomeric structures in telomerase-deficient cells, providing therapeutic implications in human tumors.

Received for publication, January 23, 2006 , and in revised form, March 15, 2006.

^* This work was supported by National Science Council Grant NSC 93-2320-B-002-38 and National Health Research Institute of Taiwan Grant NHRI-EX94-9328SI (to S. C. T.). 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.

¹ These authors contributed equally to this work.

² To whom correspondence should be addressed. Tel.: 886-2-2312-3456 (ext. 8282); Fax: 886-2-23915293; E-mail: scteng{at}ha.mc.ntu.edu.tw.

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