| Project/Area Number |
18K18193
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 63020:Radiation influence-related
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 細胞周期 / DNA修復 / DNA複製 / ゲノム安定性維持 |
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| Outline of Final Research Achievements |
A gene, named PARI, was previouly reported as a anti-recombinase of homologous recombination. In this study we reveal how PARI changes its localization during cell cycle progression. We established U2OS cell line stably expressed GFP tagged PARI. PARI-GFP was accumulated at induced DNA damage site by micro-irradiation. In addition, to visualize cell cycle in live-cell, cell cycle indicatior Fucci was introduced to PARI-GFP cell. By using In-cell analyzer and Fucci-PARI-GFP cell, we also developed a screening system for cell cycle dependent regulatory factor of PARI. These techniques could hold the key to understanding the complex mechanism of the maintainance of genomic stability and further investigations would be warranted.
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| Academic Significance and Societal Importance of the Research Achievements |
遺伝情報をコードするゲノムDNAは生命の維持に重要であるが、生体内では様々な要因により常にDNA損傷を受けており、細胞内にはこの損傷を修復しゲノムを安定に維持するための分子機構がある。本研究では、近年報告が相次ぐ細胞周期依存的ゲノム安定性維持機構の制御について組換抑制因子PARIに着目して解析するものであり、細胞周期によってDNA損傷に対して異なる修復経路を選択するメカニズムをライブセルイメージングを用いて可視化しようとする新しい研究である。
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