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Yersinia YopT inhibits RLH‐mediated NF‐κB and IRF3 signal transduction
Author(s) -
Li Dongyu,
Wang Haoyong,
Zhang Pingping,
Zhang Yanhong,
He Xiang,
Zhong Hui,
Guan Kai,
Min Min,
Gao Qi,
Wei Congwen
Publication year - 2020
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12842
Subject(s) - irf3 , biology , effector , signal transduction , innate immune system , microbiology and biotechnology , yersinia , cytoskeleton , rig i , pathogen , signal transducing adaptor protein , ubiquitin , immune system , bacteria , biochemistry , gene , immunology , cell , genetics
The Gram‐negative bacterial pathogen Yersinia delivers six effector proteins into the host cells to block the host innate immune response. One of the effectors, YopT, is a potent cysteine protease that causes the disruption of the actin cytoskeleton to inhibit phagocytosis of the pathogen; however, its molecular mechanism and relevance to pathogenesis need further investigation. In this report, we show that RIG‐I is a novel target of the YopT protein. Remarkably, YopT interacts with RIG‐I and inhibits rat liver homogenate‐mediated nuclear factor‐κB and interferon regulatory factor‐3 activation. Further studies revealed a YopT‐dependent increase in the K48‐polymerized ubiquitination of RIG‐I. These findings suggest that YopT negatively regulates RIG‐I‐mediated cellular antibacterial response by targeting RIG‐I.