Since signaling machineries for two modes of plant-induced immunity, pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), extensively overlap, PTI and ETI signaling likely interact. In an Arabidopsis quadruple mutant, in which four major sectors of the signaling network, jasmonate, ethylene, PAD4, and salicylate, are disabled, the hypersensitive response (HR) typical of ETI is abolished when the Pseudomonas syringae effector AvrRpt2 is bacterially delivered but is intact when AvrRpt2 is directly expressed in planta. These observations led us to discovery of a network-buffered signaling mechanism that mediates HR signaling and is strongly inhibited by PTI signaling. We named this mechanism the ETI-Mediating and PTI-Inhibited Sector (EMPIS). The signaling kinetics of EMPIS explain apparently different plant genetic requirements for ETI triggered by different effectors without postulating different signaling machineries. The properties of EMPIS suggest that information about efficacy of the early immune response is fed back to the immune signaling network, modulating its activity and limiting the fitness cost of unnecessary immune responses.
Bibliographical noteFunding Information:
We are grateful to Narayana Upadhyaya and Peter Dodds of CSIRO for providing the AvrRpm1sp-Cya (pNR527) plasmid. We thank Amanda Thao for technical assistance in RNA-Seq library construction, the University of Minnesota Genomics Center (www.genomics.umn.edu) for sequencing of the RNA-Seq libraries, and the Minnesota Supercomputing Institute (www.msi.umn.edu) for a high performance computing environment. This work was supported by grants from National Science Foundation, IOS-1121425 and MCB-1518058 to F.K., IOS-1025642 to A.C. and IOS-1353854 to J.G., and a grant from Ajinomoto Co. to F.K.
- deep perturbation
- fitness cost of immunity
- network resilience
- plant immune signaling network