細菌の毒性の効果因子の宿主抑制は,感染に対する免疫を誘発する
Vardis Ntoukakis1, Tatiana S Mucyn, Selena Gimenez-Ibanez
1Sainsbury Laboratory, Colney, Norwich NR4 7UH, UK.
まとめ
植物は,毒性の因子を無効化することによって,細菌の病原体に抵抗します. トマトのPtoキナーゼは,E3リガースドメインのリン酸化により,AvrPtoBの分解を防止し,これは新しい植物免疫メカニズムである.
科学分野:
- 植物病理学 植物病理学
- 分子植物-微生物の相互作用
- 植物免疫 植物免疫とは
背景:
- 植物病原菌は,宿主の免疫を抑制するためにエフェクタータンパク質を供給します.
- プセドモナスのシリンガエエフェクタ AvrPtoB は,トマトのFenのような宿主タンパク質キナーゼを,そのE3リガゼドメインを通じて分解する.
- トマトのPtoキナーゼは,Fenに関連しており,AvrPtoBをPrf抵抗タンパク質で認識しています.
研究 の 目的:
- トマトのPtoキナーゼがAvrPtoB媒介による分解に抵抗するメカニズムを調査する.
- 植物がどのように効果因子不活性化により,病気に対する耐性を発揮するかを明らかにする.
主な方法:
- タンパク質の分解とユビキチネーションを研究するための生化学的分析.
- PtoとAvrPtoBの相互作用を分析するためのインビトロキナーゼアッセイ.
- 主要な機能ドメインを特定するためのサイト指向型変異.
主要な成果:
- AvrPtoBは,その触媒裂け目の中でFenをユビキチネートし,Prf.の分解と損失を引き起こしました.
- Ptoは,AvrPtoB媒介による分解に耐性がある.
- Ptoは,リン酸化によってAvrPtoB E3リガースドメインを無効化する.
結論:
- 植物は,細菌のエフェクタータンパク質を無効化することによって病原体に抵抗することができます.
- AvrPtoBのE3リガースドメインのPtoのリン酸化は,植物免疫の新たなメカニズムである.
- この研究は,宿主キナーゼが病原体の毒性因子を無効化する戦略を明らかにしています.
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