バクテリアのエフェクターは,異国食を誘発するV-ATPase-ATG16L1軸を明らかにする

Yue Xu¹, Ping Zhou², Sen Cheng³

¹College of Biological Sciences, China Agricultural University, 100094 Beijing, China; National Institute of Biological Sciences, Beijing, 102206 Beijing, China.

Cell

|July 23, 2019

まとめ

サルモネラ菌は

科学分野:

細胞生物学
微生物学
免疫学

背景:

細胞内細菌に対する宿主防御機構として重要なものです
エクセノファギーの正確な開始経路は,まだ完全に理解されていません.
バクテリアの病原体は,オートファギーを含む宿主の免疫反応を回避する戦略を進化させた.

研究の目的:

異国食を阻害する細菌因子を特定するためです
エクセノファギーの開始に関与する宿主機構を明らかにする.
細菌のエフェクターが宿主の防御メカニズムに干渉する方法を理解するためです

主な方法:

バクテリアのトランスポゾン検診を行い, 異国食を阻害するサルモネラエフェクターを特定した.
クレノファジーに不可欠な宿主因子を特定するためにCRISPRスクリーニングを使用しました.
タンパク質の相互作用と機能領域を調査するために生化学的測定と遺伝子変異を使用した.

主要な成果:

サルモネラ・クセノファギーの強力な抑制剤として,タイプIII分泌システム (T3SS) エフェクターであるSopFを特定した.
宿主V-ATPaseとATG16L1複合体は,真空の損傷時に異食性の開始を媒介することを発見した.
SopFは,V-ATPaseのATP6V0CのGln124をADP-リボシレートすることで,ATG16L1の徴集を阻害する.

結論:

V-ATPase-ATG16L1軸は,細胞内病原体の自己滅菌認識に不可欠である.
サルモネラSopFエフェクターは,この宿主軸を標的とし,細菌の増殖を促すことで,異食を抑制する.
この研究は細菌の免疫回避の新たなメカニズムと主体防衛の重要な経路を明らかにしています

キーワード:

ADPリボシライゼーション V-ATPASE についてオートファジー細菌と宿主の相互作用生まれつきの免疫タイプIIIの分泌システムエクソファギー

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