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Nucleic Acids Research Advance Access originally published online on March 30, 2009
Nucleic Acids Research 2009 37(10):3367-3376; doi:10.1093/nar/gkp200
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Nucleic Acids Research, 2009, Vol. 37, No. 10 3367-3376
© 2009
The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome Integrity, Repair and Replication

DIDS, a chemical compound that inhibits RAD51-mediated homologous pairing and strand exchange

Takako Ishida1, Yoshimasa Takizawa1, Takashi Kainuma1, Jin Inoue2, Tsutomu Mikawa2,3, Takehiko Shibata2, Hidekazu Suzuki4, Satoshi Tashiro4 and Hitoshi Kurumizaka1,*

1Laboratory of Structural Biology, Graduate School of Advanced Science and Engineering, Waseda University, 2-2 Wakamatsu-cho, Shinjuku-ku, Tokyo 162-8480, 2RIKEN Advanced Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, 3RIKEN SPring-8 center, 1-1-1 Kouto, Sayo, Sayo, Hyogo 679-5148 and 4Department of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan

*To whom correspondence should be addressed. Tel: +81 3 5369 7315; Fax: +81 3 5367 2820; Email: kurumizaka{at}waseda.jp

Received December 4, 2008. Revised March 11, 2009. Accepted March 11, 2009.

RAD51, an essential eukaryotic DNA recombinase, promotes homologous pairing and strand exchange during homologous recombination and the recombinational repair of double strand breaks. Mutations that up- or down-regulate RAD51 gene expression have been identified in several tumors, suggesting that inappropriate expression of the RAD51 activity may cause tumorigenesis. To identify chemical compounds that affect the RAD51 activity, in the present study, we performed the RAD51-mediated strand exchange assay in the presence of 185 chemical compounds. We found that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) efficiently inhibited the RAD51-mediated strand exchange. DIDS also inhibited the RAD51-mediated homologous pairing in the absence of RPA. A surface plasmon resonance analysis revealed that DIDS directly binds to RAD51. A gel mobility shift assay showed that DIDS significantly inhibited the DNA-binding activity of RAD51. Therefore, DIDS may bind near the DNA binding site(s) of RAD51 and compete with DNA for RAD51 binding.


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