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Molecular and Cellular Biology, December 2004, p. 10733-10741, Vol. 24, No. 24
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.24.10733-10741.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

DNA Cross-Link Repair Protein SNM1A Interacts with PIAS1 in Nuclear Focus Formation

Masamichi Ishiai,1 Masayo Kimura,1 Keiko Namikoshi,1 Mitsuyoshi Yamazoe,2 Kazuhiko Yamamoto,1,{dagger} Hiroshi Arakawa,3 Kazunaga Agematsu,4 Nobuko Matsushita,1 Shunichi Takeda,2 Jean-Marie Buerstedde,3 and Minoru Takata1*

Department of Immunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Okayama,1 Department of Radiation Genetics, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto,2 Department of Infectious Immunology, Graduate School of Medicine, Shinshu University, Matsumoto, Nagano, Japan,4 GSF, Institute for Molecular Radiobiology, Neuherberg Munich, Germany3

Received 6 August 2004/ Returned for modification 27 August 2004/ Accepted 21 September 2004

The yeast SNM1/PSO2 gene specifically functions in DNA interstrand cross-link (ICL) repair, and its role has been suggested to be separate from other DNA repair pathways. In vertebrates, there are three homologs of SNM1 (SNM1A, SNM1B, and SNM1C/Artemis; SNM1 family proteins) whose functions are largely unknown. We disrupted each of the SNM1 family genes in the chicken B-cell line DT40. Both SNM1A- and SNM1B-deficient cells were sensitive to cisplatin but not to X-rays, whereas SNM1C/Artemis-deficient cells exhibited sensitivity to X-rays but not to cisplatin. SNM1A was nonepistatic with XRCC3 (homologous recombination), RAD18 (translesion synthesis), FANCC (Fanconi anemia), and SNM1B in ICL repair. SNM1A protein formed punctate nuclear foci depending on the conserved SNM1 (metallo-ß-lactamase) domain. PIAS1 was found to physically interact with SNM1A, and they colocalized at nuclear foci. Point mutations in the SNM1 domain, which disrupted the interaction with PIAS1, led to mislocalization of SNM1A in the nucleus and loss of complementation of snm1a cells. These results suggest that interaction between SNM1A and PIAS1 is required for ICL repair.

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

Molecular and Cellular Biology, December 2004, p. 10733-10741, Vol. 24, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.24.10733-10741.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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