Abstract
Network robustness is a crucial property of the plant immune signaling network because pathogens are under a strong selection pressure to perturb plant network components to dampen plant immune responses. Nevertheless, modulation of network robustness is an area of network biology that has rarely been explored. While two modes of plant immunity, Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), extensively share signaling machinery, the network output is much more robust against perturbations during ETI than PTI, suggesting modulation of network robustness. Here, we report a molecular mechanism underlying the modulation of the network robustness in Arabidopsis thaliana. The salicylic acid (SA) signaling sector regulates a major portion of the plant immune response and is important in immunity against biotrophic and hemibiotrophic pathogens. In Arabidopsis, SA signaling was required for the proper regulation of the vast majority of SA-responsive genes during PTI. However, during ETI, regulation of most SA-responsive genes, including the canonical SA marker gene PR1, could be controlled by SA-independent mechanisms as well as by SA. The activation of the two immune-related MAPKs, MPK3 and MPK6, persisted for several hours during ETI but less than one hour during PTI. Sustained MAPK activation was sufficient to confer SA-independent regulation of most SA-responsive genes. Furthermore, the MPK3 and SA signaling sectors were compensatory to each other for inhibition of bacterial growth as well as for PR1 expression during ETI. These results indicate that the duration of the MAPK activation is a critical determinant for modulation of robustness of the immune signaling network. Our findings with the plant immune signaling network imply that the robustness level of a biological network can be modulated by the activities of network components.
Highlights
How network properties, such as robustness against network perturbations, emerge from biological networks has been a central question in systems biology [1,2]
We previously reported that the robustness level of the plant immune signaling network is higher during Effector-Triggered Immunity (ETI) than Pattern-Triggered Immunity (PTI)
Transcriptional induction of PR1 was completely dependent on SID2, which is a key salicylic acid (SA) biosynthetic enzyme, and completely dependent on SA signaling during PTI [26]
Summary
How network properties, such as robustness against network perturbations, emerge from biological networks has been a central question in systems biology [1,2]. In which defense responses are induced through signaling events initiated by recognition of pathogen attack, composes a major part of plant immunity [3]. PAMP/ Pattern-Triggered Immunity (PTI) and Effector-Triggered Immunity (ETI) are modes of plant innate immunity defined by the way pathogens are detected [4,5]. PTI is triggered by recognition of microbe/pathogen-associated molecular patterns (MAMPs/ PAMPs) by the cognate pattern-recognition receptors (PRRs), which are typically receptor-like kinases or receptor-like proteins [6]. The Arabidopsis intracellular NB-LRR R proteins RPS2 and RPM1 indirectly recognize perturbations of the PTI signaling component RIN4 by the effectors AvrRpt and AvrRpm1/AvrB, respectively, of a Gram-negative bacterial pathogen, Pseudomonas syringae [3]. In addition to proteinaceous effectors, some P. syringae strains deliver coronatine, which is a Author Summary
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