Plant Receptor Kinase BTL2 Integrates Local and Systemic Defense by Activating Phytocytokine Signaling and Modulating Defense Hormone Signaling

The response to pathogens and the coordination of local and long-distance signaling are critical for plants to combat diseases. Plant receptor kinase (RK) BAK1 and its closest homolog SERK4 function as co-receptors of multiple pattern recognition receptors (PRRs) in initiating pattern-triggered immunity (PTI). However, some pathogen effectors can target BAK1/SERK4 for degradation or perturbation, which leads to the compromised or abolished PTI. We recently identified an RK, BAK TO LIFE 2 (BTL2), as a backup surveillance system that detects disruptions of BAK1/SERK4 to sustain phytocytokine signaling and ensure plant immunity. Under normal growth condition, BAK1/SERK4 phosphorylate BTL2 to maintain its inactive state. Upon depletion of BAK1/SERK4, BTL2 is activated through autophosphorylation, allowing it to interact with multiple phytocytokine receptors and activate Ca2+-permeable channels CNGC19/20, triggering robust local immune responses mediated by intracellular immune receptors. Furthermore, we demonstrate that BTL2 plays a pivotal role in systemic acquired resistance (SAR) against pathogen invasions. In the btl2 mutant, salicylic acid (SA), a key defense hormone for SAR, fails to accumulate in distal leaves following the immunogenic elicitor flg22 treatment of local leaves. Conversely, jasmonic acid (JA) biosynthesis and responses, which usually antagonizes SA responses, are elevated in the distal tissues of the btl2 mutant compared to wild-type plants upon flg22 treatment. As a result, the btl2 mutant exhibits reduced sensitivity to SA-triggered SAR. We hypothesize that BTL2 interacts with PRRs of mobile phytocytokines and/or damage-associated molecular pattern (DAMP) in mediating plant systemic resistance. These findings reveal that BTL2 integrates local and systemic defense signaling to protect plants against pathogens.