Figure 2. NPRs are regulators of two opposing hormone-mediated immune responses.
NPR1 normally exists as a high molecular weight oligomer in the cytoplasm. In response to salicylic acid (SA) - induced changes in cellular redox, NPR1 monomers are released into the nucleus. At resting state, NPR1, which is phosphorylated (red circles) at Ser55/Ser59, interacts with WRKY, a transcriptional repressor of PR genes. Sumoylated (light blue oval) NPR1, which is phosphorylated at Ser11/Ser15 but dephosphorylated at Ser55/Ser59, interacts with the transcriptional activator TGA3 to promote PR gene expression and establishment of systemic acquired resistance (SAR). NPR3 and NPR4 mediate SA-dependent degradation of NPR1 by the proteasome. NPR3 and NPR4 also promote the SA-enhanced degradation of JAZ transcriptional repressors to induce JA gene expression, resulting in activation of JA synthesis and signaling during early effector-triggered immune (ETI) responses.