Hormone-Mediated Signaling of Reactive Oxygen Species Under Abiotic Stress

Abiotic stresses trigger the generation of reactive oxygen species (ROS) in various subcellular compartments of plant cells, where they perform a dual function: acting as cytotoxic agents during acute stress and as highly specific signaling modulators under mild or chronic stress. However, the fundamental question of how the cell distinguishes between toxic and signaling ROS pools—and how phytohormones coordinate this distinction—remains unresolved. This review re-examines the molecular logic of the hormone-redox interface, focusing on the post-translational modifications of NADPH oxidases (RBOHs) and antioxidant enzymes as a key mechanism for the rapid tuning of signals. Moving beyond traditional linear cascade models, we propose the concept of a “dynamic hormonal code,” in which abscisic acid acts as the primary initiator of apoplastic ROS bursts via SnRK2-dependent phosphorylation, while salicylates and jasmonates modulate the duration and amplitude of these bursts, thereby determining the outcome—ranging from programmed cell death to systemic resistance. Known mechanisms of the hormonal code have been established (e.g., ABA → SnRK2 → RBOH; SA/JA antagonism mediated by NPR1; and the redox relay involving PRXIIB/GPX3 → ABI2). This review goes beyond simple hormone combinatorics by proposing a conceptual framework: the hormonal code encodes ROS signals through parameters of time, amplitude, and cellular compartment. Particular attention is paid to recent discoveries regarding the roles of auxin and brassinosteroids in reconfiguring chloroplast redox homeostasis during flooding and heat shock. Generalizing these data, we propose an integrated model of spatiotemporal regulation that explains how feedback loops involving ROS, Ca2+ waves, and hormone receptors facilitate systemic acclimation. Thus, targeting key crosstalk nodes—specifically SnRK2 and TOR kinase complexes—offers new strategies for engineering stress-resilient crops in the face of climate change.