バクテリア感染時のRNF213によるリポポリサッカリドのユビキチル化
Elsje G Otten1, Emma Werner2, Ana Crespillo-Casado2
1MRC Laboratory of Molecular Biology, Cambridge, UK. gotten@mrc-lmb.cam.ac.uk.
Nature
|May 20, 2021
まとめ
ユビキティレーションは,タンパク質だけでなく,細菌のリポポリサッカリド (LPS) を標的にします. このプロセスはRNF213によって媒介され,抗菌的自己死と細胞自律的免疫を誘発する.
科学分野:
- 細胞微生物学
- 免疫学
- 生物化学
背景:
- ユビキティレーションは通常,タンパク質を修正し,細胞内細菌をオートファジーにマークします.
- 侵入した細菌に存在する特定の基質は未確認のままでした.
研究 の 目的:
- サイトゾール型サルモネラ菌のどこにでも存在する基質を特定する.
- RNF213の細菌の普遍化と抗菌自己死における役割を明らかにする.
主な方法:
- E3ユビキチンリガゼRNF213を用いて細菌のリポポリサカリド (LPS) のユビキティレーションを調査した.
- LPSの普遍化とLUBACの採用におけるRNF213ドメインの機能を分析した.
- バクテリアのクリアランスとオートファギーの誘導に対するRNF213欠乏の影響を評価した.
主要な成果:
- RNF213は,細胞性サルモネラ菌のLPSの脂質A分子を全域に存在させることが実証された.
- RNF213は細菌のユビキチンコートを生成し,LUBACを募集するのに不可欠です.
- LPSの普遍化は 抗菌性自己死と 細胞自律免疫を 引き起こすことが分かりました
結論:
- Ubiquitylationは,LPSのような非タンパク質分子を含むために,タンパク質基板を超えて広がります.
- RNF213によるLPSのユビキティレーションは,抗菌自死体の開始における重要なステップです.
- この発見は,宿主の防御メカニズムにおける翻訳後の改変の理解を広げています.
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