Pseudomonas syringae evades phagocytosis by animal cells via type III effector-mediated regulation of actin filament plasticity.
Sung-Jin YoonYoung-Jun ParkJun-Seob KimSoohyun LeeSang-Hyun LeeSong ChoiJeong-Ki MinInpyo ChoiChoong Min RyuPublished in: Environmental microbiology (2018)
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.
Keyphrases
- type iii
- induced apoptosis
- cell cycle arrest
- biofilm formation
- signaling pathway
- regulatory t cells
- cell wall
- plant growth
- pseudomonas aeruginosa
- dendritic cells
- cell death
- metabolic syndrome
- immune response
- adipose tissue
- small molecule
- transcription factor
- insulin resistance
- high fat diet induced
- amino acid
- functional connectivity