Loss of Arabidopsis ferroxidases LPR1 and LPR2 enhances plant immunity by promoting leaf iron deposition.

Iron (Fe) is a critical nutrient for both plants and their pathogens, and its distribution and homeostasis critically influence the outcome of plant-pathogen interactions. Low Phosphate Root 1 (LPR1) and LPR2 are ferroxidases that regulate Fe translocation in the xylem, but their role in plant immunity remains unknown. Here, we report that loss of LPR1 and LPR2 in Arabidopsis thaliana confers enhanced resistance to both virulent (Pseudomonas syringae pv. Tomato DC3000, Pst) and avirulent (Pst-avrRpt2) bacterial strains. This enhanced resistance is associated with excessive Fe deposition in the leaves of the lpr1 lpr2 double mutant. This resistance is further enhanced by exogenous Fe supplementation and attenuated under Fe-limited conditions. Mechanistically, this iron deposition leads to a more robust reactive oxygen species (ROS) burst, accelerated hypersensitive response (HR) cell death, and enhanced callose deposition upon pathogen challenge. Furthermore, the lpr1 lpr2 mutant exhibits constitutively elevated expression of defense genes, including both effector-triggered immunity (ETI) and PAMP-triggered immunity (PTI) markers, and displays a primed state upon infection with either Pst-avrRpt2 or Pst. Collectively, our findings uncover LPR1 and LPR2 as novel negative regulators of plant immunity that limit defense activation by preventing excessive Fe deposition in leaves and maintaining a normal cellular iron homeostasis. This work establishes a critical link between iron distribution/homeostasis and defense activation and provides a potential strategy for enhancing disease resistance through Fe modulation.