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Molecular and Cellular Biology, April 2007, p. 2812-2820, Vol. 27, No. 8
0270-7306/07/$08.00+0     doi:10.1128/MCB.02043-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Cooperative Roles of Vertebrate Fbh1 and Blm DNA Helicases in Avoidance of Crossovers during Recombination Initiated by Replication Fork Collapse{triangledown} ,{dagger}

Masaoki Kohzaki,1,2 Atsushi Hatanaka,1 Eiichiro Sonoda,1 Mitsuyoshi Yamazoe,1 Koji Kikuchi,1 Nguyen Vu Trung,1,3 Dávid Szüts,4 Julian E. Sale,4 Hideo Shinagawa,5 Masami Watanabe,2 and Shunichi Takeda1*

Department of Radiation Genetics, Kyoto University Graduate School of Medicine, Yoshidakonoe, Sakyo-ku, Kyoto 606-8501, Japan,1 Research Reactor Institute, Kyoto University, Kumatori, Sennan-gun, Osaka 590-0494, Japan,2 Department of Medical Microbiology, Hanoi Medical University, 01 Ton That Tung, Dong Da, Hanoi, Vietnam,3 Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Hills Road, Cambridge CB2 2QH, United Kingdom,4 Department of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan5

Received 1 November 2006/ Returned for modification 18 December 2006/ Accepted 2 January 2007

Fbh1 (F-box DNA helicase 1) orthologues are conserved from Schizosaccharomyces pombe to chickens and humans. Here, we report the disruption of the FBH1 gene in DT40 cells. Although the yeast fbh1 mutant shows an increase in sensitivity to DNA damaging agents, FBH1–/– DT40 clones show no prominent sensitivity, suggesting that the loss of FBH1 might be compensated by other genes. However, FBH1–/– cells exhibit increases in both sister chromatid exchange and the formation of radial structures between homologous chromosomes without showing a defect in homologous recombination. This phenotype is reminiscent of BLM–/– cells and suggests that Fbh1 may be involved in preventing extensive strand exchange during homologous recombination. In addition, disruption of RAD54, a major homologous recombination factor in FBH1–/– cells, results in a marked increase in chromosome-type breaks (breaks on both sister chromatids at the same place) following replication fork arrest. Further, FBH1BLM cells showed additive increases in both sister chromatid exchange and the formation of radial chromosomes. These data suggest that Fbh1 acts in parallel with Bloom helicase to control recombination-mediated double-strand-break repair at replication blocks and to reduce the frequency of crossover.

* Corresponding author. Mailing address: Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan. Phone: 81 75 753 4410. Fax: 81 75 753 4419. E-mail: stakeda{at}rg.med.kyoto-u.ac.jp

{triangledown} Published ahead of print on 5 February 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, April 2007, p. 2812-2820, Vol. 27, No. 8
0270-7306/07/$08.00+0     doi:10.1128/MCB.02043-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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