[Abstract unavailable

No abstract

SUMMARY Systemic acquired resistance (SAR) is a broad-spectrum plant immune response involving profound transcriptional changes that are regulated by the co-activator NPR1. Nuclear translocation of NPR1 is a critical regulatory step, but how it is regulated in the nucleus is unknown. Here, we show that turnover of nuclear NPR1 protein plays an important role in modulating its target gene transcription. In the absence of pathogen challenge, NPR1 is continuously cleared from the nucleus by the proteasome, which restricts its co-activator activity to prevent untimely activation of SAR. Surprisingly, inducers of SAR promote turnover of NPR1 by phosphorylation of residues Ser11/Ser15, thereby facilitating its recruitment to a Cullin3-based ubiquitin ligase. Genetic experiments showed that turnover of phosphorylated NPR1 is required for full induction of target genes and establishment of SAR. These in vivo data demonstrate unique dual roles for co-activator turnover in both preventing and stimulating gene transcription to regulate plant immunity.