Plasma membrane-nucleo-cytoplasmic coordination of a receptor-like cytoplasmic kinase promotes EDS1-dependent plant immunity

Plants use cell-surface immune receptors to recognize pathogen-specific patterns to evoke basal immunity. ENHANCED DISEASE SUSCEPTIBILITY (EDS1) is known to be crucial for plant basal immunity, whereas its activation mechanism by pattern recognition remains enigmatic. Here, we show that the fungal pattern chitin induced the plasma membrane-anchored receptor-like cytoplasmic kinase PBS1-LIKE 19 (PBL19) to undergo nuclear translocation in Arabidopsis. The palmitoylation-deficient PBL19(C3A) variant constantly resided in the nucleus, triggering transcriptional self-amplification mainly through WRKY8 and EDS1-dependent constitutive immunity. Unexpectedly, the metacaspase-cleaved PBL19 lacking the N-terminal nuclear localization sequence specifically interacted with and phosphorylated EDS1 in the cytoplasm. Phosphodeficient EDS1 attenuated PBL19(C3A)-induced constitutive immunity, while phosphomimetic EDS1 complemented the loss of PBL19 for fungal resistance. Collectively, these findings reveal a compelling model wherein the plasma membrane, nuclear and cytoplasmic pools of PBL19 temporally coordinate distinct roles of immune signal receiver, amplifier and effector to boost plant antifungal immunity via EDS1. How the plant immune signalling hub EDS1 is activated by pathogen elicitors remains enigmatic. Li et al. show that fungal elicitor perception can induce EDS1 phosphorylation by a plasma membrane tethering kinase after elegant subcellular coordination.

Automated summary

Plants use cell-surface immune receptors to recognize pathogen-specific patterns and evoke basal immunity. Researchers have discovered that the fungal pattern chitin can induce nuclear translocation of PBL19 in Arabidopsis and its interaction with EDS1 in the cytoplasm. These findings reveal the important role of PBL19 in plant antifungal immunity.