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Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues
https://repo.qst.go.jp/records/45365
https://repo.qst.go.jp/records/45365c5698d39-f075-438f-9c4b-eb576dd11b27
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2008-12-25 | |||||
| タイトル | ||||||
| タイトル | Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Uehara, Yosihiko
× Uehara, Yosihiko× Ikehata, Hironobu× Hirayama, Ryoichi× Furusawa, Yoshiya× Ando, Koichi× Ono, Tetsuya× et.al× 上原 芳彦× 平山 亮一× 古澤 佳也× 安藤 興一 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | With the goal of understanding the role of non-homologous end-joining repair in the maintenance of genetic information at the tissue level, we studied mutations induced by radiation and subsequent repair of DNA double-strand breaks in Ku70 gene-deficient lacZ transgenic mice. The local mutation frequencies and types of mutations were analyzed on a lacZ gene that had been chromosomally integrated, which allowed us to monitor DNA sequence alterations within this 3.1-kbp region. The mutagenic process leading to the development of the most frequently observed small deletions in wild-type mice after exposure to 20 Gy of X rays was suppressed in Ku70 mice in the three tissues examined: spleen, liver and brain. Examination of DNA break rejoining and the phosphorylation of histone H2AX in Ku70-deficient and -proficient mice revealed that Ku70 deficiency decreased the frequency of DNA rejoining, suggesting that DNA rejoining is one of the causes of radiation-induced deletion mutations. Limited but statistically significant DNA rejoining was found in the liver and brain of Ku70-deficient mice 3.5 days after irradiation, showing the presence of a DNA double-strand break repair system other than non-homologous end joining. These data indicate a predominant role of non-homologous end joining in the production of radiation-induced mutations in vivo. | |||||
| 書誌情報 |
Radiation Research 巻 170, 号 2, p. 216-223, 発行日 2008-08 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0033-7587 | |||||
