Abscisic acid promotes proteasome‐mediated degradation of the transcription coactivator NPR1 in Arabidopsis thaliana

Summary Proteasome‐mediated turnover of the transcription coactivator NPR 1 is pivotal for efficient activation of the broad‐spectrum plant immune responses known as localized acquired resistance ( LAR ) and systemic acquired resistance (SAR) in adjacent and systemic tissues, respectively, and requires the CUL 3‐based E3 ligase and its adaptor proteins, NPR 3 and NPR 4, which are receptors for the signaling molecule salicylic acid ( SA ). It has been shown that SA prevents NPR 1 turnover under non‐inducing and LAR / SAR ‐inducing conditions, but how cellular NPR 1 homeostasis is maintained remains unclear. Here, we show that the phytohormone abscisic acid ( ABA ) and SA antagonistically influence cellular NPR 1 protein levels. ABA promotes NPR 1 degradation via the CUL 3 NPR 3/ NPR 4 complex‐mediated proteasome pathway, whereas SA may protect NPR 1 from ABA ‐promoted degradation through phosphorylation. Furthermore, we demonstrate that the timing and strength of SA and ABA signaling are critical in modulating NPR 1 accumulation and target gene expression. Perturbing ABA or SA signaling in adjacent tissues alters the temporal dynamic pattern of NPR 1 accumulation and target gene transcription. Finally, we show that sequential SA and ABA treatment leads to dynamic changes in NPR 1 protein levels and target gene expression. Our results revealed a tight correlation between sequential SA and ABA signaling and dynamic changes in NPR 1 protein levels and NPR 1‐dependent transcription in plant immune responses.