The ETS-ETI cycle: evolutionary processes and metapopulation dynamics driving the diversification of pathogen effectors and host immune factors

Martel, Alexandre; Ruiz-Bedoya, Tatiana; Breit-McNally, Clare; Laflamme, Bradley; Desveaux, Darrell; Guttman, David S.

doi:10.1016/j.pbi.2021.102011

Cited by 34 publications

(17 citation statements)

References 76 publications

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“…Cell-surface pattern recognition receptors, including receptor-like kinases (RLKs) and receptor-like proteins (RLPs), perceive conserved microbial molecular structures such as pathogen-associated molecular patterns (PAMPs) and elicit defence responses known as PAMP-triggered immunity (PTI), leading to resistance to a broad range of non-adapted pathogens (Boutrot and Zipfel 2017 ). However, pathogens that secrete into host cells virulence factors called effectors can cause diseases by suppressing the components involved in PTI (Martel et al 2021 ). Plants in turn evolved intracellular receptors, the majority of which belong to the family of nucleotide-binding leucine-rich repeat receptors (NLRs).…”

Section: Introductionmentioning

confidence: 99%

Structural basis of NLR activation and innate immune signalling in plants

et al. 2022

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Animals and plants have NLRs (nucleotide-binding leucine-rich repeat receptors) that recognize the presence of pathogens and initiate innate immune responses. In plants, there are three types of NLRs distinguished by their N-terminal domain: the CC (coiled-coil) domain NLRs, the TIR (Toll/interleukin-1 receptor) domain NLRs and the RPW8 (resistance to powdery mildew 8)-like coiled-coil domain NLRs. CC-NLRs (CNLs) and TIR-NLRs (TNLs) generally act as sensors of effectors secreted by pathogens, while RPW8-NLRs (RNLs) signal downstream of many sensor NLRs and are called helper NLRs. Recent studies have revealed three dimensional structures of a CNL (ZAR1) including its inactive, intermediate and active oligomeric state, as well as TNLs (RPP1 and ROQ1) in their active oligomeric states. Furthermore, accumulating evidence suggests that members of the family of lipase-like EDS1 (enhanced disease susceptibility 1) proteins, which are uniquely found in seed plants, play a key role in providing a link between sensor NLRs and helper NLRs during innate immune responses. Here, we summarize the implications of the plant NLR structures that provide insights into distinct mechanisms of action by the different sensor NLRs and discuss plant NLR-mediated innate immune signalling pathways involving the EDS1 family proteins and RNLs.

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Section: Introductionmentioning

confidence: 99%

Structural basis of NLR activation and innate immune signalling in plants

et al. 2022

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“…Microbial pathogens utilize several evolutionary strategies to modulate their ETI-load, with the most commonly invoked strategies being effector diversification via mutation or recombination, and gene loss (i.e., pseudogenization) [ 8 , 11 ]. For example, P .…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2022

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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.

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“…To enhance pathogenicity for successful establishment of growth, plant pathogens secrete effectors to compromise PTI. To combat this, plants have evolved sophisticated mechanisms for the recognition of pathogen effectors or their actions on host targets and induce a more effective and robust resistance response known as effectortriggered immunity (ETI; Martel et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Coactivators: Driving Force of Plant Immunity

et al. 2022

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Salicylic acid (SA) is a plant defense signal that mediates local and systemic immune responses against pathogen invasion. However, the underlying mechanism of SA-mediated defense is very complex due to the involvement of various positive and negative regulators to fine-tune its signaling in diverse pathosystems. Upon pathogen infections, elevated level of SA promotes massive transcriptional reprogramming in which Non-expresser of PR genes 1 (NPR1) acts as a central hub and transcriptional coactivator in defense responses. Recent findings show that Enhanced Disease Susceptibility 1 (EDS1) also functions as a transcriptional coactivator and stimulates the expression of PR1 in the presence of NPR1 and SA. Furthermore, EDS1 stabilizes NPR1 protein level, while NPR1 sustains EDS1 expression during pathogenic infection. The interaction of NPR1 and EDS1 coactivators initiates transcriptional reprogramming by recruiting cyclin-dependent kinase 8 in the Mediator complex to control immune responses. In this review, we highlight the recent breakthroughs that considerably advance our understanding on how transcriptional coactivators interact with their functional partners to trigger distinct pathways to facilitate immune responses, and how SA accumulation induces dynamic changes in NPR1 structure for transcriptional reprogramming. In addition, the functions of different Mediator subunits in SA-mediated plant immunity are also discussed in light of recent discoveries. Taken together, the available evidence suggests that transcriptional coactivators are essential and potent regulators of plant defense pathways and play crucial roles in coordinating plant immune responses during plant–pathogen interactions.

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The ETS-ETI cycle: evolutionary processes and metapopulation dynamics driving the diversification of pathogen effectors and host immune factors

Cited by 34 publications

References 76 publications

Structural basis of NLR activation and innate immune signalling in plants

Structural basis of NLR activation and innate immune signalling in plants

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

Transcriptional Coactivators: Driving Force of Plant Immunity

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