Danger-associate peptide regulates root immunity in Arabidopsis

Plant elicitor peptides (Peps) are recognized by two receptor-like kinases, PEPR1 and PEPR2, and trigger plant immunity responses and root growth inhibition. In this study, we reveal that the Pep-PEPR system triggers root immunity responses in Arabidopsis. Pep1 incubation initiated callose and lignin deposition in roots of wild type but not in that of pepr1 pepr2 mutant seedlings. The plasma membrane-associated kinase BIK1, which serves downstream of the Pep-PEPR signaling pathway, was essential for Pep1-induced root immunity responses. Interestingly, disruption of PEPR1/2-associated coreceptor BAK1 enhanced the deposition of both callose and lignin induced by Pep1 in roots. Ethylene and salicylic acid signaling are involved in Pep1-induced root immunity responses. Furthermore, we showed that the successful phytopathogen, P. syringae (DC3000) could effectively suppress Pep1-trigged root callose and lignin accumulation. These results demonstrated the endogenous Pep-triggered root immunity responses and pathogenic suppression of the Pep-PEPR signaling pathway. •Pep-PEPR system elicits immune response in root.•BIK1 and BAK1 involved in the Pep-induced defense response in roots.•Ethylene and Salicylic acid modulate root immunity induced by Pep1.•Suppression of Pep-induced root defense response by phytopathogen.