The pathogen-induced peptide CEP14 is perceived by the receptor-like kinase CEPR2 to promote systemic disease resistance in Arabidopsis.

Abstract

Secreted plant peptides that trigger cellular signaling are crucial for plant growth, development, and adaptive responses to environmental stresses. In Arabidopsis (Arabidopsis thaliana), the C-TERMINALLY ENCODED PEPTIDE (CEP) family is a class of secreted signaling peptides that is phylogenetically divided into two groups: group I (CEP1-CEP12) and group II (CEP13-CEP15). Several group I CEP peptides regulate root architecture and nitrogen starvation responses, whereas the biological activity and roles of group II CEPs remain unknown. Here, we report that a group II CEP peptide, CEP14, functions as a pathogen-induced elicitor of Arabidopsis immunity. In response to infection by the bacterial pathogen Pseudomonas syringae, CEP14 expression was highly induced via the salicylic acid pathway in Arabidopsis leaves and roots. In the absence of pathogen attack, treatment of Arabidopsis plants with synthetic CEP14 peptides was sufficient to trigger immune responses. Genetic and biochemical analyses demonstrated that the receptor-like kinase CEP RECEPTOR 2 (CEPR2) perceives CEP14 to trigger plant immunity. The SOMATIC EMBRYOGENESIS RECEPTOR KINASES (SERKs) BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) and SERK4 also participated in CEP14 perception by forming CEP14-induced complexes with CEPR2. Overexpression of CEP14 largely enhanced Arabidopsis resistance to P. syringae, while CEP14 or CEPR2 mutation significantly attenuated Arabidopsis systemic resistance to P. syringae. Taken together, our data reveal that the pathogen-induced CEP14 peptide, which is perceived by the CEPR2-BAK1/SERK4 receptor complexes, acts as an endogenous elicitor to promote systemic disease resistance in Arabidopsis.