植物免疫を調節するBIK1のリガンド誘発モヌビキチン化
Xiyu Ma1,2, Lucas A N Claus3,4, Michelle E Leslie5,6
1Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX, USA.
Nature
|May 15, 2020
まとめ
植物免疫受容体は 病原体のパターンを検知し 防御を活性化します この研究では,ボトリチス誘発キナーゼ1 (BIK1) がモヌビキチン化され,フラゲリンセンシング2 (FLS2) - ブラッシノステロイド無感性1関連キナーゼ1 (BAK1) 複合体から免疫を誘発する.
科学分野:
- 植物免疫
- 分子信号
- 細胞のプロセス
背景:
- 植物免疫受容体 (PRR) は,微生物に関連した分子パターン (MAMP) を認識し,防御反応を開始します.
- 受容体型の細胞質キナーゼ (RLCKs) はPRRに関連した重要な調節因子ですが,その活性化メカニズムはほとんど不明です.
- ボトライト誘発キナーゼ1 (BIK1) は,植物免疫シグナル伝達に関与する重要なRLCKである.
研究 の 目的:
- 植物免疫におけるRLCK活性化に伴う分子メカニズムを解明する.
- PRR-RLCK複合体の動態を調節するタンパク質のリン酸化とユビキチン化の役割を調査する.
- BIK1がFLAGELLIN SENSING 2 (FLS2) - BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1) コンプレックスからどのように活性化され,放出されるかを理解する.
主な方法:
- 先進的な顕微鏡技術を用いてMAMP検出後のBIK1の動態を調査した.
- BIK1の改変に関与するE3ユビキチンリガスを特定するために遺伝的アプローチを使用した.
- リガンド結合への反応として,BIK1のリン酸化とモノビキチン化状態を分析した.
主要な成果:
- MAMPの知覚はBIK1のリン酸化を誘発し,その後モヌビキチネーションを起こす.
- アラビドプシスE3のユビキチンリガゼRING-H2 FINGER A3A (RHA3A) とRHA3BはBIK1のモノビキチン化を媒介する.
- FLS2- BAK1複合体からのBIK1放出と,その後の免疫信号の活性化には,モノビキチン化が不可欠である.
- BIK1のダイナミクスは,モヌビキチン化とエンドソームの局所化を含め,PRR FLS2とは異なる.
結論:
- リガンド誘発のモノビキチネーションは,PRR複合体からRLCKの活性化と放出を制御する重要な規制メカニズムである.
- リン酸化とユビキチネーションの相互作用は,PRR-RLCK複合体の活性化と植物免疫反応を制御する.
- この研究は,RLCKのダイナミックな調節を通して,植物免疫信号の活性化のための新しい経路を明らかにしています.
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