Hyo-Jun Leea, Young-Joon Parka, Pil Joon Seob, Ju-Heon Kima, Hee-Jung Simc, Sang-Gyu Kimc and Chung-Mo Parka,d,1
aDepartment of Chemistry, Seoul National University, Seoul 151-742, Korea
bDepartment of Chemistry, Chonbuk National University, Jeonju 561-756, Korea
cCenter for Genome Engineering, Institute for Basic Science, Daejeon 305-811, Korea
dPlant Genomics and Breeding Institute, Seoul National University, Seoul 151-742, Korea
1Correspondence to Chung-Mo Park
In plants, necrotic lesions occur at the site of pathogen infection through the hypersensitive response, which is followed by induction of systemic acquired resistance (SAR) in distal tissues. Salicylic acid (SA) induces SAR by activating NONEXPRESSER OF PATHOGENESIS-RELATED GENES1 (NPR1) through an oligomer-to-monomer reaction. However, SA biosynthesis is elevated only slightly in distal tissues during SAR, implying that SA-mediated induction of SAR requires additional factors. Here, we demonstrated that SA-independent systemic signals induce a gene encoding SNF1-RELATED PROTEIN KINASE 2.8 (SnRK2.8), which phosphorylates NPR1 during SAR. The SnRK2.8-mediated phosphorylation of NPR1 is necessary for its nuclear import. Notably, although SnRK2.8 transcription and SnRK2.8 activation are independent of SA signaling, the SnRK2.8-mediated induction of SAR requires SA. Together with the SA-mediated monomerization of NPR1, these observations indicate that SA signals and SnRK2.8-mediated phosphorylation coordinately function to activate NPR1 via a dual-step process in developing systemic immunity in Arabidopsis thaliana.