Metaeffector interactions modulate the type III effector-triggered immunity load of Pseudomonas syringae

Abstract

The bacterial plant pathogen Pseudomonas syringae requires type III secreted effectors (T3SEs) for pathogenesis. However, a major facet of plant immunity entails the recognition of a subset of P. syringae’s T3SEs by intracellular host receptors in a process called Effector-Triggered Immunity (ETI). Prior work has shown that ETI-eliciting T3SEs are pervasive in the P. syringae species complex raising the question of how P. syringae mitigates its ETI load to become a successful pathogen. While pathogens can evade ETI by T3SE mutation, recombination, or loss, there is increasing evidence that effector-effector (a.k.a., metaeffector) interactions can suppress ETI. To study the ETI-suppression potential of P. syringae T3SE repertoires, we compared the ETI-elicitation profiles of two genetically divergent strains: P. syringae pv. tomato DC3000 (PtoDC3000) and P. syringae pv. maculicola ES4326 (PmaES4326), which are both virulent on Arabidopsis thaliana but harbour largely distinct effector repertoires. Of the 529 T3SE alleles screened on A. thaliana Col-0 from the P. syringae T3SE compendium (PsyTEC), 69 alleles from 21 T3SE families elicited ETI in at least one of the two strain backgrounds, while 50 elicited ETI in both backgrounds, resulting in 19 differential ETI responses including two novel ETI-eliciting families: AvrPto1 and HopT1. Although most of these differences were quantitative, three ETI responses were completely absent in one of the pathogenic backgrounds. We performed ETI suppression screens to test if metaeffector interactions contributed to these ETI differences, and found that HopQ1a suppressed AvrPto1m-mediated ETI, while HopG1c and HopF1g suppressed HopT1b-mediated ETI. Overall, these results show that P. syringae strains leverage metaeffector interactions and ETI suppression to overcome the ETI load associated with their native T3SE repertoires.

Surface frustration re-patterning underlies the structural landscape and evolvability of fungal orphan candidate effectors

“…Another layer of complexity emerges from interference between the activity of several effectors, either through epistatic interactions (John et al, 2022) or by cross-suppression of immune recognition (Martel et al, 2022;Lazar et al, 2022). Finally, effectors may promote virulence not by directly targeting host processes but rather by altering the host microbiota (Snelders et al, 2020(Snelders et al, , 2021.…”

Insights intoPhakopsora pachyrhizieffector-effector interactions

“…Effectors may function redundantly with, cooperate with, assist, function as decoys for, or control other effectors to modulate host immunity. The identification of bacterial effectors of animal and plant pathogens that promote or antagonize the activity of other effectors has revealed the importance of effector interplay and given rise to the concept of metaeffectors (effectors of effectors) (Shames and Finlay 2012; Urbanus et al 2016; Martel et al 2022).…”

The immune receptor SNC1 monitors helper NLRs targeted by a bacterial effector

“…An important role of pathogen effectors is to antagonize PTI components, with some Type III Secretion System (T3SS) effectors of P. syringae also suppressing ETI [19][20][21] . For example, HopI1 greatly dampens HR triggered by several other effectors by unknown mechanisms 21 .…”