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Study on brassinosteroid-mediated regulation of stem cell regeneration in roots

研究課題

研究課題/領域番号 22K15143
研究種目

若手研究

配分区分基金
審査区分 小区分44030:植物分子および生理科学関連
研究機関奈良先端科学技術大学院大学

研究代表者

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)

研究期間 (年度) 2022-04-01 – 2025-03-31
研究課題ステータス 交付 (2023年度)
配分額 *注記
4,680千円 (直接経費: 3,600千円、間接経費: 1,080千円)
2023年度: 2,340千円 (直接経費: 1,800千円、間接経費: 540千円)
2022年度: 2,340千円 (直接経費: 1,800千円、間接経費: 540千円)
キーワードplant stem cell / DNA damage / cell division / regeneration / stem cell / brassinosteroid / DNA damage response
研究開始時の研究の概要

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.

研究実績の概要

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.

現在までの達成度 (区分)
現在までの達成度 (区分)

2: おおむね順調に進展している

理由

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

今後の研究の推進方策

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.

報告書

(2件)
  • 2023 実施状況報告書
  • 2022 実施状況報告書
  • 研究成果

    (3件)

すべて 2023

すべて 雑誌論文 (1件) (うち査読あり 1件) 学会発表 (2件) (うち国際学会 1件)

  • [雑誌論文] DNA double-strand breaks enhance brassinosteroid signaling to activate quiescent center cell division in Arabidopsis2023

    • 著者名/発表者名
      Takahashi Naoki、Suita Kazuki、Koike Toshiya、Ogita Nobuo、Zhang Ye、Umeda Masaaki
    • 雑誌名

      Journal of Experimental Botany

      巻: 75 号: 5 ページ: 1364-1375

    • DOI

      10.1093/jxb/erad424

    • 関連する報告書
      2023 実施状況報告書
    • 査読あり
  • [学会発表] Brassinosteroid receptor-mediated regulation of tissue regeneration in Arabidopsis2023

    • 著者名/発表者名
      Zhang Ye
    • 学会等名
      International Conference of Arabidopsis Research
    • 関連する報告書
      2023 実施状況報告書
    • 国際学会
  • [学会発表] Brassinosteroid receptor-mediated regulation of tissue regeneration in Arabidopsis2023

    • 著者名/発表者名
      Zhang Ye
    • 学会等名
      The 65th Annual Meeting of the Japanese Society of Plant Physiologists
    • 関連する報告書
      2023 実施状況報告書

URL: 

公開日: 2022-04-19   更新日: 2024-12-25  

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