Elucidation of mechanism of cold-inducible gene expression in plant
| Project/Area Number |
17K15413
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied molecular and cellular biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Kidokoro Satoshi 東京大学, 大学院農学生命科学研究科(農学部), 助教 (70588368)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 植物 / 低温ストレス応答 / 転写制御 / 低温ストレス / カルシウムシグナル / 低温 / 発現制御 |
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| Outline of Final Research Achievements |
In plants, DRE-binding protein 1/C-repeat binding factors (DREB1/CBFs) function as master switches in cold stress-responsive gene expression. The expression of the DREB1 genes is strongly induced in the early stage of the cold stress responses. CAMTA3 and CAMTA5 transcription factors activate the DREB1 expression by a rapid temperature decrease. We tried to elucidate activation mechanisms of CAMTA proteins for inducing the DREB1 expression in response to the cold stress. We pre-treated Arabidpopsis seedling to calcium channel inhibitors and then treated them to the cold stress. But the DREB1 expression was not altered between the mock and pre-treated seedlings. Because CAMTA proteins contain conserved domains for interacting calmodulins (CaMs) that can bind to Ca2+. We screened proteins that can interact with CAMTAs with co-immunoprecipitation and LC-MS/MS analysis. We obtained sevreal proteins including CaMs and CaM-like as candidates of the interacting proteins.
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| Academic Significance and Societal Importance of the Research Achievements |
CAMTA転写因子は通常生育時から発現することから、DREB1の遺伝子発現を誘導するためには低温ストレス特異的な活性化が必要であると考えられた。CAMTA転写因子はCa2+結合タンパク質であるカルモジュリンとの相互作用ドメインを持つことから、その活性化にはカルシウムシグナルが関わると予想された。しかし、その実態は不明であった。本研究成果により同定された相互作用因子の解析を進めてCAMTA転写因子を介したDREB1の発現制御機構が解明されることで、低温に応答したカルシウムシグナルからCAMTA転写因子の活性化へとつながるシグナル伝達系全体の理解が進むことが期待される。
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Report
(5 results)
Research Products
(14 results)
