Sequence specific detection and manipulation of epigenetic status
| Project/Area Number |
16H03281
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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 |
Biomolecular chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
Imanishi Miki 京都大学, 化学研究所, 講師 (80362391)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2018: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2017: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2016: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
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| Keywords | 核酸結合タンパク質 / 核酸修飾 / メチル化シトシン / TALE / TALEタンパク質 / エピゲノム |
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| Outline of Final Research Achievements |
Methylated cytosine (5mC) is important for the regulation of transcription, and is involved in development, differentiation, carcinogenesis, etc. Furthermore, the importance of RNA methylation is also becoming clear. In this study, with the aim of developing a technique for DNA/RNA sequence-specific detection and control of the methylation status in living cells, I focused on the following points; (1) Development of DNA binding protein capable of selectively recognizing cytosine methylation in a specific genomic sequence, (2) detection of methylation in living cells using designed methylation discrimination protein, and (3) Detection and control of RNA methylation status.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究で得られたメチル化シトシン選択性を有するDNA結合ユニットを利用することで、メチル化状態に依存したゲノム改変や転写調節が実現する。すなわち、正常細胞には影響を及ぼさず、メチル化機構に異常をきたしたガン細胞のみに作用するといった、副作用の少ない遺伝子標的治療への応用も期待される。また、本システムを利用して、従来の網羅的なメチル化解析に続くステップである「個々のメチル化の意義」に答えることで、エピゲノムの重要性が示唆されている発ガン、発生、分化、体内時計のメカニズム解明や創薬標的の決定、未だ萌芽的なRNAメチル化研究の推進に貢献すると期待される。
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Report
(4 results)
Research Products
(24 results)
