Lyso-phosphatidylethanolamine triggers immunity against necrotrophs by promoting JA-signaling and ROS-homeostasis

Abstract

Abstract Modulation of the plant defense response by bioactive molecules is of increasing interest. However, despite plant cell lipids being one of the major cellular components, their role in plant immunity remains elusive. We found that the exogenous application of the cell-membrane localized phospholipid lyso-phosphatidylethanolamine (LPE) reprograms the plant transcript profile in favor of defense-associated genes thereby priming the plant immune system. Exogenous LPE application at different Arabidopsis accessions increases resistance against the necrotrophic pathogens, Botrytis cinerea and Cochliobolus heterostrophus. We found that the immunity-promoting effect (IPE) of LPE is repealed in the jasmonic acid (JA) receptor mutant coi1, but multiplied in the JA-hypersensitive mutant feronia (fer-4). The JA-signaling repressor JAZ1 is degraded following LPE administration, suggesting that JA-signaling is promoted by LPE. Following LPE-treatment, reactive oxygen species (ROS) accumulation is affected in coi1 and fer-4. The application of ROS-scavengers compromises the LPE-mediated immune response suggesting that ROS are crucial for the LPE-mediated IPE. Moreover, FER signaling inhibitors of the RALF family are strongly expressed after LPE application, and RALF23 is internalized in stress granules, suggesting the LPE-mediated repression of FER-signaling by promoting RALF function. The in-situ increase of LPE-abundance in the LPE-biosynthesis mutant lpeat1 and lpeat2 elevates plant resistance to B. cinerea, in contrast to the endogenous LPE-deficient mutant pla2-alpha. We show that LPE increases plant resistance against necrotrophs by promoting JA-signaling and ROS-homeostasis, thereby paving the way for the LPE-targeted genomic engineering of crops to raise their ability to resist biotic threats.