Bacterial rhamnolipids and their 3-hydroxyalkanoate precursors activateArabidopsisinnate immunity through two independent mechanisms

Abstract

Plant innate immunity is activated upon perception of invasion pattern molecules by plant cell-surface immune receptors. Several bacteria of the generaPseudomonasandBurkholderiaproduce rhamnolipids (RLs) froml-rhamnose and (R)-3-hydroxyalkanoate precursors (HAAs). RL and HAA secretion is required to modulate bacterial surface motility, biofilm development, and thus successful colonization of hosts. Here, we show that the lipidic secretome from the opportunistic pathogenPseudomonas aeruginosa, mainly comprising RLs and HAAs, stimulatesArabidopsisimmunity. We demonstrate that HAAs are sensed by the bulb-type lectin receptor kinase LIPOOLIGOSACCHARIDE-SPECIFIC REDUCED ELICITATION/S-DOMAIN-1-29 (LORE/SD1-29), which also mediates medium-chain 3-hydroxy fatty acid (mc-3-OH-FA) perception, in the plantArabidopsis thaliana. HAA sensing induces canonical immune signaling and local resistance to plant pathogenicPseudomonasinfection. By contrast, RLs trigger an atypical immune response and resistance toPseudomonasinfection independent of LORE. Thus, the glycosyl moieties of RLs, although abolishing sensing by LORE, do not impair their ability to trigger plant defense. Moreover, our results show that the immune response triggered by RLs is affected by the sphingolipid composition of the plasma membrane. In conclusion, RLs and their precursors released by bacteria can both be perceived by plants but through distinct mechanisms.