Recognition of pathogen-derived sphingolipids in Arabidopsis

In plants, many invading microbial pathogens are recognized by cell-surface pattern recognition receptors, which induce defense responses. Here, we show that the ceramide Phytophthora infestans–ceramide D (Pi-Cer D) from the plant pathogenic oomycete P. infestans triggers defense responses in Arabidopsis. Pi-Cer D is cleaved by an Arabidopsis apoplastic ceramidase, NEUTRAL CERAMIDASE 2 (NCER2), and the resulting 9-methyl–branched sphingoid base is recognized by a plasma membrane lectin receptor–like kinase, RESISTANT TO DFPM-INHIBITION OF ABSCISIC ACID SIGNALING 2 (RDA2). 9-Methyl–branched sphingoid base is specific to microbes and induces plant immune responses by physically interacting with RDA2. Loss of RDA2 or NCER2 function compromised Arabidopsis resistance against an oomycete pathogen. Thus, we elucidated the recognition mechanisms of pathogen-derived lipid molecules in plants. Description Extracellular processing raises alarm Plants that lack defensive responses to given microbial pathogens can fail miserably, as the potato plant did when faced with the oomycete pathogen Phytophthora infestans, the cause of the potato blight that contributed to famines in the mid-19th century. Kato et al. show how the small mustard plant Arabidopsis defends against this same oomycete. A sphingolipid from the oomycete’s cell membrane is cleaved by a ceramidase that the plant puts out into the apoplast. One of the cleavage products is a branched sphingoid base that is then recognized by a lectin receptor–like kinase on the plant cell surface, kicking off the plant’s immune responses. Without the apoplastic ceramidase or the cell surface lectin, the plant’s ability to defend against this oomycete pathogen is compromised. —PJH Extracellular cleavage and cell surface reception turn a plant pathogen’s membrane lipid into an alarm signal to promote plant defense.