Abstract
Plants use sophisticated strategies to balance their responses to oxidative stress. Programmed cell death is one outcome that is regulated by reactive oxygens in various cellular contexts, including the hypersensitive response (HR) associated with successful pathogen recognition. We focus on the Arabidopsis bZIP transcription factor AtbZIP10 that binds G- and C-box consensus sequences. AtbZIP10 shuttles between nucleus and cytoplasm, likely via interaction with the export receptor AtXPO1. Surprisingly, AtbZIP10 can be retained outside nucleus by LSD1, a protein that protects Arabidopsis cells from death in the face of various oxidative stress signals. Our genetic analyses demonstrate that AtbZIP10 is a positive mediator of the uncontrolled cell death observed in lsd1 mutants. Additionally, AtbZIP10 and LSD1 act antagonistically in both pathogen-induced HR and basal defense responses. LSD1 likely functions as a cellular hub, where its interaction with AtbZIP10 and additional, as yet unidentified, proteins contributes significantly to plant oxidative stress responses.