Recognition of microbial challenges leads to enhanced immunity at both the local and systemic levels. In Arabidopsis, EFR and PEPR1/PEPR2 act as the receptor for the bacterial elongation factor EF-Tu (elf18 epitope) and for the endogenous PROPEP-derived Pep epitopes, respectively. The PEPR pathway has been described to mediate defence signalling following microbial recognition. Here we show that PROPEP2/PROPEP3 induction upon pathogen challenges is robust against jasmonate, salicylate, or ethylene dysfunction. Comparative transcriptome profiling between Pep2- and elf18-treated plants points to co-activation of otherwise antagonistic jasmonate- and salicylate-mediated immune branches as a key output of PEPR signalling. Accordingly, as well as basal defences against hemibiotrophic pathogens, systemic immunity is reduced in pepr1 pepr2 plants. Remarkably, PROPEP2/PROPEP3 induction is essentially restricted to the pathogen challenge sites during pathogen-induced systemic immunity. Localized Pep application activates genetically separable jasmonate and salicylate branches in systemic leaves without significant PROPEP2/PROPEP3 induction. Our results suggest that local PEPR activation provides a critical step in connecting local to systemic immunity by reinforcing separate defence signalling pathways.
Local microbial recognition involving PEPR pattern recognition receptors leads to a systemic immune response via the Salicylate and Jasmonate hormone signaling pathways.
- Genome-wide profiling for Pep2-responsive genes in Arabidopsis thaliana shows co-activation of salicylate (SA)- and jasmonate (JA) pathways as an important output of PEPR-mediated signalling.
- Molecular genetic studies indicate a critical role for PEPRs in pathogen- and microbial pattern-induced systemic immunity.
- Activation of a PEPR-PROPEP feedback loop is restricted to the pathogen-challenged sites during pathogen-induced systemic immunity.
- Exogenous application of Pep peptides confers systemic immunity through distinct defence signalling branches.