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Bloom Helicase and DNA Topoisomerase III Are Involved in the Dissolution of Sister Chromatids

Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan,¹ Ludwig-Maximilians-Universitat, Lehrstuhl fur Tieranatomie II, Veterinarstrasse 13, D-80539 Munchen, Germany,² Biosystems Science, School of Advanced Sciences, The Graduate University for Advanced Studies, Shonan Village, Hayama, Kanagawa 240-0193, Japan,³ Department of Medical Genetics and Radiation Biology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan,⁴ Shujitsu University, School of Pharmacy, Nishigawara, Okayama 703-8516, Japan,⁵ Tohoku University 21st Century COE Program "Comprehensive Research and Education Center for Planning of Drug Development and Clinical Evaluation," Sendai, Miyagi 980-8578, Japan⁶

Received 24 April 2006/ Returned for modification 26 May 2006/ Accepted 2 June 2006

Bloom's syndrome (BS) is an autosomal disorder characterized by predisposition to a wide variety of cancers. The gene product whose mutation leads to BS is the RecQ family helicase BLM, which forms a complex with DNA topoisomerase III (Top3). However, the physiological relevance of the interaction between BLM and Top3 within the cell remains unclear. We show here that Top3 depletion causes accumulation of cells in G₂ phase, enlargement of nuclei, and chromosome gaps and breaks that occur at the same position in sister chromatids. The transition from metaphase to anaphase is also inhibited. All of these phenomena except cell lethality are suppressed by BLM gene disruption. Taken together with the biochemical properties of BLM and Top3, these data indicate that BLM and Top3 execute the dissolution of sister chromatids.

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