Complex regulation of Citron OGD2-dependent resistance to citrus canker caused by Xanthomonas citri subsp. citri

Iron is an essential nutrient for all organisms. Feruloyl-COA 6-hydroxylase 1 (F6′H1) plays a pivotal role in iron uptake in plant roots by catalyzing the biosynthesis of iron-mobilizing scopoletin, a secondary metabolite also possessing antimicrobial activity. However, it remains unclear whether F6′H1-mediated iron uptake affects plant resistance to foliar pathogens and how such a process might be regulated. Here, we show that enhanced expression of 2-oxoglutarate-dependent dioxygenases 2 (CmOGD2), a homolog of F6′H1 in Citron C-05 (Citrus medica L.), confers resistance to citrus canker caused by Xanthomonas citri subsp. citri (Xcc). CmOGD2-mediated pathogen resistance is achieved by promoting iron uptake and the accumulation of reactive oxygen species (ROS), which likely results in ferroptosis. Furthermore, CmOGD2 interacts with the enolase CmENO2 to destabilize CmZAT10.1, a transcriptional activator of CmOGD2, thereby forming a negative feedback loop that limits CmOGD2 expression. Notably, the Xcc effector pthA4 interferes with the CmOGD2–CmENO2 interaction, likely via a decoy mechanism, leading to CmZAT10.1 accumulation. These findings reveal complex regulatory mechanisms underlying the critical role of CmOGD2 in mediating Xcc resistance through iron- and ROS-dependent ferroptosis.