The experimental verification of saturated repair model by using repair reporter genes.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26550025
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Kyoto University
• Principal Investigator: Komatsu Kenshi 京都大学, 放射線生物研究センター, 研究員 (80124577)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 相同組換え修復 / 非相同末端再結合 / 細胞生存曲線の肩 / saturated repair model

Outline of Final Research Achievements

Present results confirmed the saturation of DNA repair by using the reporter genes, in which the homologous recombination repair functions within a limited region at a low dose. In contrast, non-homologous end-joining has constant activity irrespective of the radiation dose. As a result, the cells exposed to a low dose can survive due to both functional repair pathways: homologous recombination and non-homologous end-joining, while non-homologous end-joining is sole repair pathway at a higher dose. Thus, biological model based on repair activity of cells became plausible to explain the quasi-threshold of radiation survival curve.

Free Research Field

放射線生物学