Epigenetic regulation of cellular robustness in DNA damage response

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K12203
• 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: Ikura Tsuyoshi 京都大学, 放射線生物研究センター, 准教授 (70335686)
• Co-Investigator(Renkei-kenkyūsha): MATSUDA Tomonari 京都大学, 工学研究科附属 流域圏総合環境質研究センター, 准教授 (50273488)
• Research Collaborator: IKURA Masae
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 放射線障害 / エピジェネティクス / TIP60 / アセチル化 / 細胞ロバストネス

Outline of Final Research Achievements

We investigated the mechanism of acquired radio-resistance in cells after gamma irradiation, focusing on histone modifications and protein networks via histone modifications around DNA damage sites. In order to clarify this, we performed chromatin immunoprecipitation (Chromatin IP) after infection I-Sce1 adenovirus, which produce DNA double-strand break, in the acquired radio-resistance HeLa/DR-GFP cells, using anti-histone H2AX acetylation, phosphorylation or histone H4 acetylation antibodies. As a result, no remarkable change of histone modifications was observed between the acquired radio-resistance and non-resistant HeLa/DR-GFP cells. We also analyzed DNA repair efficiency using HeLa/DR-GFP system between these cells. As a result, DNA repair efficiency in acquired radio-resistance HeLa/DR-GFP cells is comparable to that in non-resistant HeLa/DR-GFP cells.

Free Research Field

放射線生物学