| Project/Area Number |
22K15143
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 44030:Plant molecular biology and physiology-related
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
ZHANG YE 奈良先端科学技術大学院大学, 先端科学技術研究科, 助教 (10899470)
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| Project Period (FY) |
2022-04-01 – 2025-03-31
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| Project Status |
Granted (Fiscal Year 2023)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2023: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2022: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | plant stem cell / DNA damage / cell division / regeneration / stem cell / brassinosteroid / DNA damage response |
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| Outline of Research at the Start |
Stem cells in the root are less tolerant to DNA damage and would undergo programmed cell death. Afterward cells neighboring to the dead stem cells undergo replenishing divisions to restore the stem cell niche. This study explores brassinosteroid's roles in regulating stem cell regeneration.
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| Outline of Annual Research Achievements |
Firstly, I have optimized the plant growth conditions and the microscope settings for live imaging to reveal the spatiotemporal dynamics of hormone signaling levels and key gene expressions.
Secondly, to test whether internalization of BRL3-BR plays a physiologically relevant role in the transient activation of replenishing cell division that enables proper cellular organization in the regenerated tissues, I have generated an internalization-deficient version of BRL3. I have managed to monitor and evaluate the endocytosis activity of the mutated version of BRL3.
Thirdly, to explore whether the BRL3-centered regulatory network can be applied to tissue regeneration processes in general, I have developed a novel method to induce specific cell death in the root meristem. I have verified the cell killing specificity and efficiency of this system. I have also optimized the induction condition of this system.
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| Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
In this year, I have generated the endocytosis deficient version of BRL3 and have performed preliminary experiment on the endocytosis behavior of wid-type and mutated BRL3 protein.
As a modification of my original plan, I have also developed a novel method to induce cell death in specific cell types in the root meristem. Such system shall facilitate the evaluation of the BRL3-centered regulatory network in more general tissue regeneration scenarios. However, the completion of planned experiments using the cell death induction system takes time because plant lines transformation and crossing are time-consuming
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| Strategy for Future Research Activity |
Due to the delay and changes of my original research plan, I have applied one year extension of the period of this research project. In the year 2024, I will first complete the phenotypical analysis of the transgenic lines carrying endocytosis deficient BRL3. Then I will focus on testing the roles of BRL3 and its upstream- and downstream-factors in the tissue regeneration processes triggered by cell death in various specific cell types. These work will help to elucidate how replenishing cell divisions are transiently activated to ensure the proper cellular organization in the regenerated tissues.
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