Abstract
Ralstonia solanacearum is the causative agent of bacterial wilt in many plants. To identify R. solanacearum effectors that suppress pattern-triggered immunity (PTI) in plants, we transiently expressed R. solanacearum RS1000 effectors in Nicotiana benthamiana leaves and evaluated their ability to suppress the production of reactive oxygen species (ROS) triggered by flg22. Out of the 61 effectors tested, 11 strongly and five moderately suppressed the flg22-triggered ROS burst. Among them, RipE1 shared homology with the Pseudomonas syringae cysteine protease effector HopX1. By yeast two-hybrid screening, we identified jasmonate-ZIM-domain (JAZ) proteins, which are transcriptional repressors of the jasmonic acid (JA) signaling pathway in plants, as RipE1 interactors. RipE1 promoted the degradation of JAZ repressors and induced the expressions of JA-responsive genes in a cysteine–protease-activity-dependent manner. Simultaneously, RipE1, similarly to the previously identified JA-producing effector RipAL, decreased the expression level of the salicylic acid synthesis gene that is required for the defense responses against R. solanacearum. The undecuple mutant that lacks 11 effectors with a strong PTI suppression activity showed reduced growth of R. solanacearum in Nicotiana plants. These results indicate that R. solanacearum subverts plant PTI responses using multiple effectors and manipulates JA signaling at two different steps to promote infection.
Highlights
Plants are exposed to various abiotic and biotic stresses during their life cycle
To identify RS1000 effectors that affect plant pattern-triggered immunity (PTI) responses, we transiently expressed each effector protein in N. benthamiana leaves by agroinfiltration and evaluated its ability to suppress reactive oxygen species (ROS) burst triggered by flg22 treatment
Two type III effectors, AvrPtoB and HopM1, from pv. tomato (Pto) DC3000 with the ability to suppress PTI [13,14]
Summary
Plants are exposed to various abiotic and biotic stresses during their life cycle. To combat pathogens, plants have developed a specialized surveillance system, the so-called pattern-triggered immunity (PTI), to reject or attenuate infection by potential pathogens [1]. Salicylic acid (SA) mediates defense responses against biotrophic and hemibiotrophic pathogens, whereas jasmonic acid (JA) controls defense responses against necrotrophic pathogens [3,4]. In many cases, their signaling network shows an antagonistic relationship with each other to induce appropriate immune responses against various pathogens with different infection strategies. Upon Pto infection, the activation of JA signaling by COR antagonistically suppresses the SA-mediated signaling pathway, leading to the inhibition of stomatal closure and callose deposition to promote bacterial infection [9,10,11]
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