Redox regulation of the transcription factor HAT1 limits basal defenses and promotes responses to infection in <i>Arabidopsis thaliana</i>

Plants precisely regulate defense responses to balance energy allocation between growth and immunity. Here, we showed in <i>Arabidopsis thaliana</i> that the homeodomain-leucine zipper protein 1 (HAT1) functions as a redox-controlled mediator that restricts defense responses by competing with the master immune regulator NPR1 for interaction with the transcription factor TGA3. Under normal conditions, oxidative modification of HAT1 at Cys¹⁹⁶, Cys²⁰², Cys²⁴², and Cys²⁴⁵ enhanced its binding affinity for TGA3, effectively competing with NPR1 for binding to TGA3 and sequestering TGA3 from target genes to maintain immune suppression. During immune activation in response to a bacterial pathogen, the phytohormone salicylic acid facilitated the reduction of HAT1 by the thioredoxins TRXh3 and TRXh5, thereby destabilizing the HAT1-TGA3 interaction. Salicylic acid also promoted the formation of NPR1-TGA3 complexes that activated defense gene expression. This redox switch mechanism enabled plants to dynamically regulate TGA3 transcriptional activity through reversible redox modification of HAT1. Our findings elucidate how HAT1 serves as a molecular brake to prevent immune overactivation while permitting dynamic response modulation.