2008年8月
Absence of Ku70 gene obliterates X-ray-induced lacZ mutagenesis of small deletions in mouse tissues
RADIATION RESEARCH
- 巻
- 170
- 号
- 2
- 開始ページ
- 216
- 終了ページ
- 223
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1667/RR1283.1
- 出版者・発行元
- RADIATION RESEARCH SOC
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. (C) 2008 by Radiation Research Society.
- リンク情報
-
- DOI
- https://doi.org/10.1667/RR1283.1
- J-GLOBAL
- https://jglobal.jst.go.jp/detail?JGLOBAL_ID=200902265205871875
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/18666816
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000258007100010&DestApp=WOS_CPL
- ID情報
-
- DOI : 10.1667/RR1283.1
- ISSN : 0033-7587
- J-Global ID : 200902265205871875
- PubMed ID : 18666816
- Web of Science ID : WOS:000258007100010