Seminars

Plants must continuously balance growth and immunity by maintaining low basal levels of defense hormones while remaining poised to trigger rapid responses to pathogen attack. Although jasmonic acid (JA) and salicylic acid (SA) are central regulators of plant immunity, the mechanisms that coordinate their homeostasis with developmental programs remain poorly understood. Here, we identify the developmental transcription factor JACKDAW (JKD), previously characterized for its role in root patterning, as a key regulator of hormone-dependent basal immunity. We show that JKD directly regulates a defense-associated transcriptional network by repressing JA signaling while promoting SA biosynthesis. JKD binds promoters of key hormone-responsive genes and physically interacts with MYC2, TCP14, and JAZ3 to fine-tune JA-mediated defense responses. Consistent with this mechanism, loss of JKD function enhances resistance to the necrotrophic pathogen Botrytis cinerea in both Arabidopsis and tomato. Remarkably, enhanced disease resistance occurs without detectable defects in vegetative growth or reproductive development, demonstrating that modulation of JKD activity uncouples immunity from the classical growth-defense tradeoff. Together, our findings establish JKD as a molecular bridge between developmental and immune signaling pathways, uncover a mechanism that maintains immune hormone homeostasis under non-stress conditions, and provide a conceptual framework for engineering disease-resistant crops without compromising growth.