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Published online October 8, 2007
doi:10.1083/jcb.200702183
The Journal of Cell Biology, Vol. 179, No. 1, 53-63
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Otsuki et al.
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Article

 Functional interactions between BLM and XRCC3 in the cell

Makoto Otsuki1, Masayuki Seki1, Eri Inoue1, Akari Yoshimura1, Genta Kato1, Saki Yamanouchi1, Yoh-ichi Kawabe1, Shusuke Tada1, Akira Shinohara2, Jun-ichiro Komura5, Tetsuya Ono5, Shunichi Takeda3, Yutaka Ishii4, and Takemi Enomoto1,6

1 Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
2 Institute for Protein Research, Graduate School of Science, Osaka University, Suita, Osaka 565-0871, Japan
3 Department of Radiation Genetics, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan
4 Shujitsu University, School of Pharmacy, Nishigawara, Okayama 703-8516, Japan
5 Department of Cell Biology, Graduate School of Medicine, Tohoku University, Aoba-ku, Sendai, 980-8575 Japan
6 21st Century Centers of Excellence Program, Comprehensive Research and Education Center for Planning of Drug development and Clinical Evaluation, Tohoku University, Sendai, Miyagi 980-8578, Japan

Correspondence to M. Seki: seki{at}mail.pharm.tohoku.ac.jp

Bloom's syndrome (BS), which is caused by mutations in the BLM gene, is characterized by a predisposition to a wide variety of cancers. BS cells exhibit elevated frequencies of sister chromatid exchanges (SCEs), interchanges between homologous chromosomes (mitotic chiasmata), and sensitivity to several DNA-damaging agents. To address the mechanism that confers these phenotypes in BS cells, we characterize a series of double and triple mutants with mutations in BLM and in other genes involved in repair pathways. We found that XRCC3 activity generates substrates that cause the elevated SCE in blm cells and that BLM with DNA topoisomerase III{alpha} suppresses the formation of SCE. In addition, XRCC3 activity also generates the ultraviolet (UV)- and methyl methanesulfonate (MMS)–induced mitotic chiasmata. Moreover, disruption of XRCC3 suppresses MMS and UV sensitivity and the MMS- and UV-induced chromosomal aberrations of blm cells, indicating that BLM acts downstream of XRCC3.

Abbreviations used in this paper: BS, Bloom's syndrome; HJ, Holliday junction; hXRCC3, human XRCC3; MMS, methyl methanesulfonate; SCE, sister chromatid exchange; TOP3{alpha}, topoisomerase III{alpha}.


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