| Project/Area Number |
18K08574
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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 55010:General surgery and pediatric surgery-related
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
福田 信治 愛媛大学, プロテオサイエンスセンター, 講師 (70398238)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | exocyst / 細胞極性 / 細胞生存 / 乳腺上皮細胞 / 乳がん / Par3 / ゲノム編集 / CRISPR/Cas9 |
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| Outline of Final Research Achievements |
In this study, we analyzed the intracellular dynamics of the exocyst complex, which regulates cell survival through binding to the cell polarity factor partitioning defective 3 (Par3). we also examined the role of factors that bind to the exocyst subunit. Using mouse mammary epithelial cells NMuMG, we established knock-in cells with GFP, mScarleti or Halo tag attached to the C-terminus of the exocyst complex subunits, and clarified the details of the intracellular dynamics of each subunit by live cell imaging analysis. These results provide insights for understanding the mechanism of cell survival regulation by exocyst.
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| Academic Significance and Societal Importance of the Research Achievements |
細胞極性の消失は多くのがん組織で認められており、がんの悪性度を見極める上で１つの指標となっている。exocyst複合体は、細胞極性因子Partitioning defective 3 (Par3)との結合を介して細胞極性形成や細胞生存を制御するが、その分子機構は不明な点が多い。本研究は、ゲノム編集とライブセルイメージングを組み合わせる事でexocyst複合体の細胞内動態を明らかにした。本研究成果は、exocystによる細胞極性制御、細胞生存制御のメカニズムを理解するための分子基盤となる。
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