@article{oai:repo.qst.go.jp:00043364,
 author = {Furuno-Fukushi, Ikuko and Ichi, Masumura Ken and Furuse, Takeshi and Noda, Yuko and Takahagi, Masahiko and Saito, Toshiyuki and Fujimori, Yuko and Suzuki, Hiroshi and Wynshaw-boris, Anthony and Nohmi, Takehiko and Tatsumi, Kouichi and 福士 育子 and 増村 健一 and 古瀬 健 and 野田 攸子 and 高萩 真彦 and 齋藤 俊行 and 藤森 ゆう子 and 能美 健彦 and 巽 紘一},
 issue = {5},
 journal = {Radiation Research},
 month = {Nov},
 note = {Deletion mutations were efficiently recovered in mouse liver after total-body irradiation with X rays by using a transgenic mouse "gpt-delta" system that harbored a lambda EG10 shuttle vector with the red and gam genes for Spi(-) (sensitive to P2 lysogen interference) selection. We incorporated this system into homozygous Atm-knockout mice as a model of the radiosensitive hereditary disease ataxia telangiectasia (AT). Lambda phages recovered from the livers of X-irradiated mice with the Atm(+/+) genotype showed a dose-dependent increase in the Spi(-) mutant frequency up to sixfold at 50 Gy over the unirradiated control of 2.8 x 10(-6). The livers from Atm(-/-) mice yielded a virtually identical dose-response curve for X rays with a background fraction of 2.4 x 10(-6). Structural analyses revealed no significant difference in the proportion of -1 frameshifts and larger deletions between Atm(+/+) and Atm(-/-) mice, although larger deletions prevailed in X-ray-induced Spi(-) mutants irrespective of Atm status. While a possible defect in DNA repair after irradiation has been strongly indicated in the literature for nondividing cultured cells in vitro from AT patients, the Atm disruption does not significantly affect radiation mutagenesis in the stationary mouse liver in vivo.},
 pages = {549--558},
 title = {Effect of Atm Disruption on Spontaneously Arising and Radiation-Induced Deletion Mutations in Mouse Liver},
 volume = {160},
 year = {2003}
}