Acetylation network via TIP60 complex focusing on damaged chromatin dynamics

2016 Fiscal Year Final Research Report

• Project/Area Number: 26281020
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• 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) ; TASHIRO Satoshi 広島大学, 原爆放射線医科学研究所, 教授 (20243610)
• Research Collaborator: IKURA Masae
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: アセチル化 / ヒストンH2AX / TIP60 / リン酸化 / DNA損傷応答

Outline of Final Research Achievements

We investigated how damaged chromatin dynamics via histone H2AX acetylation by TIP60 histone acetyltransferase complex affects the activation of DNA damage signaling via H2AX-phosphorylation. We found that both acetylation and phosphorylation of H2AX after induction of DNA damage are not required for the initial recruitment of NBS1 to DNA damage sites but for the maintenance of NBS1 at DNA damage sites in different ways. Our findings demonstrate that the phosphorylation of H2AX function as an anchor to maintain NBS1 at DNA damage sites whereas, the acetylation of H2AX by TIP60 complex has an important role to prevent the spreading of NBS1 signaling to undamaged regions.

Free Research Field

放射線生物学