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Pseudomonas syringae evades phagocytosis by animal cells via type III effector‐mediated regulation of actin filament plasticity
Author(s) -
Yoon SungJin,
Park YoungJun,
Kim JunSeob,
Lee Soohyun,
Lee SangHyun,
Choi Song,
Min JeongKi,
Choi Inpyo,
Ryu ChoongMin
Publication year - 2018
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.14426
Subject(s) - pseudomonas syringae , biology , effector , phagocytosis , microbiology and biotechnology , virulence , immunity , actin , pathogen , immune system , immunology , genetics , gene
Summary Certain animal and plant pathogenic bacteria have developed virulence factors including effector proteins that enable them to overcome host immunity. A plant pathogen, Pseudomonas syringae pv. tomato ( Pto ) secretes a large repertoire of effectors via a type III secretory apparatus, thereby suppressing plant immunity. Here, we show that Pto causes sepsis in mice. Surprisingly, the effector HopQ1 disrupted animal phagocytosis by inhibiting actin rearrangement via direct interaction with the LIM domain of the animal target protein LIM kinase, a key regulator of actin polymerization. The results provide novel insight into animal host–plant pathogen interactions. In addition, the current study firstly demonstrates that certain plant pathogenic bacteria such as Pto evade phagocytosis by animal cells due to cross‐kingdom suppression of host immunity.