Abstract
Two modes of plant immunity against biotrophic pathogens, Effector Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), are triggered by recognition of pathogen effectors and Microbe-Associated Molecular Patterns (MAMPs), respectively. Although the jasmonic acid (JA)/ethylene (ET) and salicylic acid (SA) signaling sectors are generally antagonistic and important for immunity against necrotrophic and biotrophic pathogens, respectively, their precise roles and interactions in ETI and PTI have not been clear. We constructed an Arabidopsis dde2/ein2/pad4/sid2-quadruple mutant. DDE2, EIN2, and SID2 are essential components of the JA, ET, and SA sectors, respectively. The pad4 mutation affects the SA sector and a poorly characterized sector. Although the ETI triggered by the bacterial effector AvrRpt2 (AvrRpt2-ETI) and the PTI triggered by the bacterial MAMP flg22 (flg22-PTI) were largely intact in plants with mutations in any one of these genes, they were mostly abolished in the quadruple mutant. For the purposes of this study, AvrRpt2-ETI and flg22-PTI were measured as relative growth of Pseudomonas syringae bacteria within leaves. Immunity to the necrotrophic fungal pathogen Alternaria brassicicola was also severely compromised in the quadruple mutant. Quantitative measurements of the immunity levels in all combinatorial mutants and wild type allowed us to estimate the effects of the wild-type genes and their interactions on the immunity by fitting a mixed general linear model. This signaling allocation analysis showed that, contrary to current ideas, each of the JA, ET, and SA signaling sectors can positively contribute to immunity against both biotrophic and necrotrophic pathogens. The analysis also revealed that while flg22-PTI and AvrRpt2-ETI use a highly overlapping signaling network, the way they use the common network is very different: synergistic relationships among the signaling sectors are evident in PTI, which may amplify the signal; compensatory relationships among the sectors dominate in ETI, explaining the robustness of ETI against genetic and pathogenic perturbations.
Highlights
Pattern Triggered Immunity (PTI) and Effector Triggered Immunity (ETI) are forms of plant immunity defined by different modes of pathogen recognition [1,2,3]
A traditional approach, knocking out one mechanism at a time, has revealed little about major parts of the signaling network involved in two forms of immunity, Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI)
By simultaneously knocking out four major signaling mechanisms in the network, we demonstrated that a common network comprised of the four signaling mechanisms accounts for most of ETI and PTI triggered by particular molecules
Summary
Pattern Triggered Immunity (PTI) and Effector Triggered Immunity (ETI) are forms of plant immunity defined by different modes of pathogen recognition [1,2,3]. In ETI, a resistance (R) gene product, usually inside the plant cell, recognizes a corresponding virulencepromoting effector protein(s) delivered by a pathogen [6,7,8,9]. Recognition of pathogen attack in PTI and ETI leads to activation of partly overlapping sets of signaling sectors and defense responses [10,11]. Most efforts to obtain mutants defective in ETI yielded only mutations in genes encoding R proteins and proteins required for R protein function. These observations suggest that the ETI signaling network is robust against pathogenic and genetic perturbations. The mechanism leading to robust immunity in ETI is yet to be determined
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