| Project/Area Number |
26291058
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Plant molecular biology/Plant physiology
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| Research Institution | Nagoya University |
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Principal Investigator |
ITO Masaki 名古屋大学, 生命農学研究科, 准教授 (10242851)
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| Co-Investigator(Kenkyū-buntansha) |
町田 泰則 名古屋大学, 理学(系)研究科(研究院), 教授 (80175596)
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| Co-Investigator(Renkei-kenkyūsha) |
SUZUKI Takamasa 中部大学, 応用生物学部, 講師 (50535797)
KUWATA Keiko 名古屋大学, トランスフォーマティブ生命分子研究所, 特任助教 (70624352)
NAKAMICHI Norihito 名古屋大学, トランスフォーマティブ生命分子研究所, 特任助教 (90513440)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2016: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
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| Keywords | 細胞周期 / 細胞増殖 / 転写制御 / タンパク質分解 / RNA代謝 / 環境ストレス / 細胞分裂 / 植物 / 核内倍加 / G2/M期制御 / 非対称分裂 |
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| Outline of Final Research Achievements |
For controlling plant organ growth in changing environment, it is important to properly regulate proliferation of component cells in growing organs. It has been believed that regulation at G2/M in the cell cycle is particularly important for plants that show endoreplication in their organ growth. In our genetic studies using Arabidopsis mutant with deregulated activity of mitotic regulator APC/C that acts as E3 ubiquitin ligase, we showed the possibility that a novel mechanism of cell cycle checkpoint may exist and may inhibit G2/M progression when nuclear mRNA metabolism is occasionally impaired. We also showed that MYB3R transcription factors, known as central regulators of G2/M-specific genes, play an important role in growth inhibition under salt stress, partially through its roles in gibberellin signal transduction where MYB3Rs physically interact with DELLA proteins and mediate the growth inhibition caused by the action of DELLA.
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