| Project/Area Number |
18K05438
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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 38030:Applied biochemistry-related
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| Research Institution | Shimane University |
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Principal Investigator |
Matsuo Yasuhiro 島根大学, 学術研究院農生命科学系, 准教授 (70596832)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ストレス応答 / シグナル伝達 / 細胞増殖 / 分裂酵母 / 有糸分裂期制御 / グルコース制限への応答 / 微小管形成への関与 / 塩ストレスへの応答 / マルチコピーサプレッサー / cAMP/PKA経路 / 染色体分配制御 / 塩ストレス応答 / 細胞周期 / 有糸分裂期 / PKA経路 |
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| Outline of Final Research Achievements |
The mechanism, which is cells response to high concentration stress, was investigated in Schizosaccharomyces pombe in this study. The cAMP/PKA pathway regulated the mitosis progression. Loss of functional Pka1 caused the chromosome mis-segregation phenotype and showed the TBZ-sensitive phenotype. These phenotypes were rescued by Mal3-overespression, which was isolated as multi-copy suppressor. The Mal3-overexpressed cells formed monopolar spindle formation and rescued in the pka1 mutant or in the limitation of glucose, indicating that Pka1 regulates the formation of proper microtubules. The pka1 mutant also showed the salt-sensitive phenotype and rescued by rst2 deletion, which is a transcription factor that regulates transition from mitosis to meiosis. These findings indicate that the cAMP/PKA pathway regulates the mitotic progression.
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| Academic Significance and Societal Importance of the Research Achievements |
高濃度のストレスに応答するPKA経路の機能欠損が染色体分配の異常を引き起こすことを明らかにした。また、有糸分裂期の異常を引き起こす温度感受性変異体が示す単極性微小管形成や生育阻害をPKAの機能欠損やグルコース制限によって、抑圧されることがわかった。以上のことから、高濃度ストレス応答経路であるPKA経路が、細胞周期の有糸分裂期の制御に関与していることを明らかにした。また、PKA経路の標的因子を多数単離したため、高濃度ストレス応答経路の詳細な制御メカニズム解明に近づくことができた。
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