Systemic Immunity Requires SnRK2.8-Mediated Nuclear Import of NPR1 in Arabidopsis. Issue 12 (15th December 2015)

• Record Type: Journal Article
• Authors: Lee, Hyo-Jun; Park, Young-Joon; Seo, Pil Joon; Kim, Ju-Heon; Sim, Hee-Jung; Kim, Sang-Gyu; Park, Chung-Mo
• Is Part Of: The Plant Cell. Volume 27:Issue 12(2015)
• Page Start: 3425
• Page End: 3438
• Publication Date: 2015-12-15
• DOI: 10.1105/tpc.15.00371
• Languages: English
• ISSNs: 1040-4651

Abstract

Abstract : Phosphorylation of NPR by the protein kinase SnRK2.8 allows nuclear import of NPR1, an essential step in systemic acquired resistance. Abstract: 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 .