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Molecular and Cellular Biology, January 2005, p. 34-43, Vol. 25, No. 1
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.1.34-43.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Fanconi Anemia Protein FANCD2 Promotes Immunoglobulin Gene Conversion and DNA Repair through a Mechanism Related to Homologous Recombination{dagger}

Kazuhiko Yamamoto,1,{ddagger} Seiki Hirano,1 Masamichi Ishiai,1 Kenichi Morishima,2 Hiroyuki Kitao,1 Keiko Namikoshi,1 Masayo Kimura,1 Nobuko Matsushita,1 Hiroshi Arakawa,3 Jean-Marie Buerstedde,3 Kenshi Komatsu,2 Larry H. Thompson,4 and Minoru Takata1*

Department of Immunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Okayama,1 Department of Genome Repair Dynamics, Radiation Biology Centre, Kyoto University, Yoshida-konoe, Sakyo-ku, Kyoto, Japan,2 GSF, Institute for Molecular Radiobiology, Neuherberg, Munich, Germany,3 Biology and Biotechnology Research Program, Lawrence Livermore National Laboratory, Livermore, California4

Received 14 May 2004/ Returned for modification 4 June 2004/ Accepted 8 October 2004

Recent studies show overlap between Fanconi anemia (FA) proteins and those involved in DNA repair mediated by homologous recombination (HR). However, the mechanism by which FA proteins affect HR is unclear. FA proteins (FancA/C/E/F/G/L) form a multiprotein complex, which is responsible for DNA damage-induced FancD2 monoubiquitination, a key event for cellular resistance to DNA damage. Here, we show that FANCD2-disrupted DT40 chicken B-cell line is defective in HR-mediated DNA double-strand break (DSB) repair, as well as gene conversion at the immunoglobulin light-chain locus, an event also mediated by HR. Gene conversions occurring in mutant cells were associated with decreased nontemplated mutations. In contrast to these defects, we also found increased spontaneous sister chromatid exchange (SCE) and intact Rad51 foci formation after DNA damage. Thus, we propose that FancD2 promotes a subpathway of HR that normally mediates gene conversion by a mechanism that avoids crossing over and hence SCEs.

* Corresponding author. Mailing address: Department of Immunology and Molecular Genetics, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan. Phone: 81-86-462-1111. Fax: 81-86-464-1187. E-mail: mtakata{at}med.kawasaki-m.ac.jp.

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

{ddagger} Present address: Division of Hematology/Oncology, Mount Sinai School of Medicine, New York, NY 10029.

Molecular and Cellular Biology, January 2005, p. 34-43, Vol. 25, No. 1
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.1.34-43.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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