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This study identifies lysophosphatidylethanolamine (LPE18:1) as a previously unknown lipid-based immune signal in plant innate immunity. When plants detect the bacterial pathogen Pseudomonas syringae, a secreted phospholipase A2 enzyme (PLA2) is rapidly released into the apoplast, where it cleaves bacterial membrane phospholipids to produce LPE18:1. This pathogen-derived lipid signal subsequently activates salicylic acid biosynthesis via ICS1 and NPR1-mediated defense gene expression, linking NLR receptor activation to spatially localized immune responses.
Why it matters
Understanding how plants convert pathogen membrane components into immune-activating signals could inform the development of more disease-resistant crops, reducing reliance on pesticides in agriculture. The authors also suggest evolutionary conservation of this mechanism across plants and mammals, which could have broader implications for innate immunity research.
β οΈ Preprint β Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhΓ€ngigen Experten begutachtet. Die Ergebnisse sind vorlΓ€ufig und sollten mit Vorsicht interpretiert werden.
In plants, effector-triggered immunity (ETI) is initiated when NLR receptors recognize pathogen effectors, yet the molecular signals linking this recognition to downstream defense activation remain poorly defined, in contrast to the well-characterized immunogenic signals of pattern-triggered immunity. Here, we show that a lysophospholipid is a previously unidentified ETI-mediating immune signal generated through host enzymatic conversion of pathogen membrane lipids. Upon recognition of avirulent Pseudomonas syringae, secretory phospholipase A2 (PLA2) is rapidly induced and secreted into the apoplast, where it hydrolyzes bacterial phosphatidylethanolamine to produce lysophosphatidylethanolamines (LPEs), predominantly LPE18:1. Genetic ablation of PLA2 compromises local immunity, hypersensitive response confinement, and defense gene activation, all of which are fully rescued by exogenous LPE18:1. Mechanistically, LPE18:1 promotes ICS1-dependent salicylic acid biosynthesis and NPR1-mediated transcriptional reprogramming. Together, these findings support pathogen-derived LPE18:1 as a previously unrecognized lipid-based immune signal that links NLR activation to spatially confined defense responses. The evolutionary conservation of secretory PLA2 enzymes and lysophospholipid signaling from plants to mammals suggests that host-directed enzymatic remodeling of pathogen membranes into immune-activating lipid signals may constitute a fundamental and ancient strategy of innate immunity.
Source: Secreted phospholipase A2Ξ± generates a pathogen-derived lysophospholipid to signal local immunity