Network Properties of Robust Immunity in Plants

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.

Arabidopsis PECTIN METHYLESTERASEs Contribute to Immunity against Pseudomonas syringae

“…For A. brassicicola growth assays, at least 15 leaf discs from five to six plants were pooled per biological sample. Disease severity, a proxy of fungal growth, was determined as previously described (Tsuda et al, 2009;Botanga et al, 2012). For PME assays, at least four leaf discs from one plant were combined for each biological sample.…”

The novel elicitor AsES triggers a defense response against Botrytis cinerea in Arabidopsis thaliana

“…MAMPs such as polypeptides, glycoproteins, lipids, glycolipids, and oligosaccharides, as well as DAMPs released by microbial hydrolytic enzymes from plant components, such as cell-wall fragments, have been characterized and are known to trigger defense responses that require the activation of SA-, JA-, and ET-induced signaling pathways [18][19][20]. The novel elicitor AsES (Patent EPC N • 12.720.221.6-1410) is a member of subtilisinrelated alkaline proteases and its proteolytic activity is necessary to induce systemic defense responses in strawberry plants against Colletotrichum acutatum, a hemibiotrophic pathogen that is the causal agent of anthracnose disease in strawberry [21].…”

Not to be suppressed? Rethinking the host response at a root-parasite interface

“…Similar to that for local responses, the salicylate and jasmonate pathways can have a neutral or synergistic role in promoting the systemic resistance responses [12,16].…”

“…The two main hormones that take part in defense signaling are salicylic acid and jasmonic acid, both of which show increased biosynthesis upon pathogen attack and have complex regulatory relationships with other hormone signaling pathways [12,13]. In addition to the network of transcriptional changes that accompany host defense signaling, a range of cellular responses are also activated at the local site of contact that restrict pathogen growth such as the production of reactive oxygen species and antimicrobial metabolites, activation of specific protein kinases and deposition of callose.…”