Targeted alterations in iron homeostasis underlie plant defense responses.

Iron (Fe) is a ubiquitous redox-active element essential for most life. The formation of localized cell wall appositions, the oxidative burst and the production of pathogenesis-related proteins are hallmarks of plant defense responses. Here, we report that iron is a central mediator linking these three phenomena. We show that in response to pathogen attack, reactive Fe 3+ , but not Fe 2+ , is deposited at cell wall appositions where it accumulates and mediates the oxidative burst. We provide evidence that the bulk secretion of Fe 3+ provoked by pathogen attack leads to intracellular iron depletion, and that H 2 O 2 itself induces ATP-dependent intracellular iron efflux. Finally, we demonstrate that this intracellular iron depletion promotes the transcription of pathogenesis-related genes in concert with H 2 O 2 . This work identifies iron as an underlying factor associated with the oxidative burst and regulating cereal defenses, and establishes links between disease-related iron homeostasis in plants and animals.