Salicylic acid engages central metabolic regulators SnRK1 and TOR to govern immunity by differential phosphorylation of NPR1.

Abstract

Immunity requires a delicate balance between combating infection and preserving metabolic functions. However, the mechanisms by which immune responses are coordinated with cellular metabolism remain largely unknown. Here, we show that NONEXPRESSER OF PR GENES 1 (NPR1), the central plant immune regulator of salicylic acid (SA)-mediated defense responses, is controlled by a cascade of post-translational modifications (PTMs) involving two master nutrient-sensing kinases. In the absence of pathogen challenge, TARGET OF RAPAMYCIN (TOR) inhibits NPR1 through phosphorylation at Ser-55/59. During defense responses, elevated SA reduces sugar phosphate levels and enhances SNF1-RELATED PROTEIN KINASE 1 (SnRK1) activity, which in turn inhibits TOR signaling and phosphorylates NPR1 at Ser-557, a modification required for subsequent PTMs and NPR1 activation. Together, our findings identify SA as a coordinator of growth and immunity in response to pathogen challenge by modulating the central metabolic regulators SnRK1 and TOR, which antagonistically control NPR1 immune activity through differential phosphorylation.