| Project/Area Number |
18K06204
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 44010:Cell biology-related
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| Research Institution | University of Tsukuba |
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Principal Investigator |
Numata Osamu 筑波大学, 生命環境系, 名誉教授 (50189354)
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| Co-Investigator(Kenkyū-buntansha) |
中野 賢太郎 筑波大学, 生命環境系, 教授 (50302815)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | テトラヒメナ / アクチン / 細胞骨格ホメオスタシス / アクチン重合阻害剤 / 転写調節 / LITAF / YEATS / 転写調節配列 / YEATSファミリータンパク質 / TCXI1 / オートファジー / ATG8 / ユビキチン化 / フィンブリン |
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| Outline of Final Research Achievements |
The mechanisms regulating the intracellular concentration of actin are unknown. We have discovered the phenomenon of Tetrahymena acquiring resistance to the inhibitor of actin polymerization, latrunculin A (LA). This is accompanied by the induction of dozens of gene transcriptions. To elucidate the mechanism of this transcriptional regulation, we examined three transcriptional regulators (LITAF, YEATS, and TCXI1) whose expression levels increased after LA treatment, but found no association. Next, we examined the transcriptional regulatory region upstream of the ACT2 gene, which is significantly upregulated, and found the sequences TRR1-3. Deletion of all of these sequences halved the amount of ACT2 protein after LA treatment. They are now searching for transcriptional regulators that bind to TRR1-3 in order to elucidate the substance of the transcriptional regulatory mechanism.
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| Academic Significance and Societal Importance of the Research Achievements |
筋収縮や細胞運動、細胞質分裂で重要な働きをするアクチンの細胞内濃度の制御機構は不明である。我々は、アクチン重合阻害剤ラトランキュリンA(LA)に対するテトラヒメナの耐性獲得現象を発見した。これには、数十種類の遺伝子転写誘導とアクチン分子の活発な合成分解が伴う。この分子機構の根底には、アクチンの最適な量と品質を感知・制御する「細胞骨格ホメオスタシス」の存在が伺えた。本研究の核心は、「細胞がアクチンの量をどのように感知し、制御するか？」という問いに、LAで撹乱した状態から、テトラヒメナが適切な細胞骨格機能を回復する過程を調べ、解答を得ることである。
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