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Genes to Cells (2005) 10, 321-332. doi:10.1111/j.1365-2443.2005.00836.x
© 2005 Blackwell Publishing or its licensors
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Role of NAD-dependent deacetylases SIRT1 and SIRT2 in radiation and cisplatin-induced cell death in vertebrate cells

Nobuko Matsushita1, Yasunari Takami2, Masayo Kimura1, Seiji Tachiiri3, Masamichi Ishiai1, Takeo Nakayama2 and Minoru Takata1,*

1 Department of Immunology and Molecular Genetics, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan
2 Department of Biochemistry, Miyazaki Medical College, Kihara, Kiyotake, Miyazaki 889-1692, Japan
3 Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshida Konoe, Sakyo-ku, Kyoto 606-8501, Japan

Yeast Sir2 is a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a central role in transcriptional silencing, chromosomal stability, DNA damage response and aging. In mammals, Sir2-like genes constitute a seven-member family whose function is largely unknown. To investigate the role of the Sir2 family in vertebrates, we have disrupted Sir2 homologues SIRT1 and SIRT2 in the p53-deficient chicken cell line DT40. Both SIRT1–/– and SIRT2–/– cells had mild growth defects. Colony survival assays showed moderate and mild sensitivity to cisplatin in SIRT1–/– and SIRT2–/– cells, respectively, while SIRT1–/–, but not SIRT2–/– cells, were sensitive to ionizing radiation (IR). Cells rendered doubly deficient in SIRT1 and SIRT2 exhibited the same levels of IR and cisplatin sensitivity as SIRT1–/– cells. SIRT1–/– cells appeared to be defective neither in DNA double strand break repair nor in G2/M checkpoints, but were more susceptible to cell death induction following IR than wild-type cells. Furthermore, both SIRT1- and SIRT2-deficient cells were more sensitive to pro-apoptotic stimuli including cisplatin and staurosporine. Our results indicate that SIRT1 and SIRT2 regulate stress-induced cell death pathways in a p53-independent manner.

Communicated by: Fumio Hanaoka

*Correspondence: E-mail: mtakata{at}med.kawasaki-m.ac.jp




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