| Project/Area Number |
16H02954
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Fukuoka University (2017-2019)
Osaka University (2016) |
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Principal Investigator |
Kuraoka Isao 福岡大学, 理学部, 教授 (60335396)
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| Co-Investigator(Kenkyū-buntansha) |
塩井 成留実 (青木成留実) 福岡大学, 理学部, 助教 (50510187)
竹立 新人 福岡大学, 理学部, 助教 (20846505)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
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| Keywords | DNA修復 / 転写 / DNA鎖切断 / 環境 / 放射線 / DNA損傷 / 修復 / 転写産物 / 影響評価 / ゲノム修復 |
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| Outline of Final Research Achievements |
Ionizing radiation directly affects DNA structure by inducing DNA breaks, particularly, DSBs. Secondary effects are the generation of reactive oxygen species that oxidize proteins and lipids, and also induce several damages to DNA. Oxidative DNA damage induces genomic instability and may lead to mutagenesis and carcinogenesis. These DNA lesions interfere not only with replication but also with transcription. Thus, it is thought that the blockage of transcriptional machinery at the damaged DNA site of the transcribed strand triggers transcription-coupled DNA repair and recruits other DNA repair factors to repair the transcription-blocking lesions on the transcribed strand.
Here, we designed new vector construct that can be detect DNA repair pathways with transcription in vivo and found that transcription-coupled double strand break repair can be too quick to analyze the mechanism.
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| Academic Significance and Societal Importance of the Research Achievements |
ヒト細胞において，DNA損傷に対する反応はより多種多様である。例えば，ヒト体細胞においてはほとんどが休止期の細胞，つまり複製より転写の方がより機能し，DNA損傷の影響は転写反応に現れてくると考えられる。本研究はDNA鎖切断がヒトの転写機構において，どのように影響を与え，それを回避していくのかを明らかにする実験を行った。この結果は転写における放射線細胞障害の解明に貢献していると思われる。
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