グルコース駆動型TOR-FIE-PRC2シグナリング制御 プラント開発
Ruiqiang Ye1,2, Meiyue Wang3,4,5, Hao Du6,7
1Department of Molecular Biology and Centre for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA. ye@molbio.mgh.harvard.edu.
Nature
|September 14, 2022
まとめ
植物におけるグルコース活性化されたラパミシン (TOR) キナーゼの標的は,ヒストンのメチル化を調節することによって細胞の運命を制御する. この栄養信号伝達経路は 植物のオルガノゲネシスと 花期への移行に影響します
科学分野:
- 植物生物学
- エピジェネティクス
- 分子信号
背景:
- 栄養素とエネルギーは 植物の発達に不可欠です
- ラパミシン (TOR) キナーゼのターゲットは成長を制御するために栄養信号を統合します.
- TORが発達的移行と分化に果たす役割は十分に理解されていません.
研究 の 目的:
- アラビドプシス・タリアナの表遺伝的変異と発達プログラムに,グルコース活性化されたTORキナーズがどのように影響するかを調査する.
- 細胞の運命を制御する TOR 標的を特定し特徴づけること.
主な方法:
- K27 (H3K27me3) でヒストンH3トリメチル化の全ゲノム解析
- TORのターゲットとして,FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) を特定する.
- FIEのリン酸化部位変異分析
- トランスクリプトーム再プログラム分析
- グルコース-TOR-FIE-ポリコンブ抑制複合体2 (PRC2) 信号経路の調査
主要な成果:
- グルコース活性化されたTORキナーゼは,アラビドプシスの全ゲノムH3K27me3レベルを制御する.
- FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) はTORの直接的な標的であり,TORによるそのリン酸化が核転移を推進する.
- FIEのリン酸化が妨げられ,H3K27me3が失効し,トランスクリプトームが変化し,臓器生成が損なわれます.
- グルコース-TOR-FIE-PRC2経路は,ヴァルナライゼーション誘発の花の移行を調節する.
結論:
- グルコース-TOR-FIE-PRC2信号軸は栄養チェックポイントとして機能します.
- この経路は幹細胞の運命を 制御する遺伝子を 黙らせます
- 栄養信号は表遺伝子組を直接再プログラムし 植物における発達移行に影響を与えます
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