Salicylic acid (SA) is a plant immune signal produced after pathogen challenge to induce systemic acquired resistance. It is the only major plant hormone for which the receptor has not been firmly identified. Systemic acquired resistance in Arabidopsis requires the transcription cofactor nonexpresser of PR genes 1 (NPR1), the degradation of which acts as a molecular switch. Here we show that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as adaptors of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in an SA-regulated manner. Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance. Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity. Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge. Plant resistance to pathogen challenge is thought to be mediated through salicylic acid (SA) signalling; here NPR3 and NPR4, paralogues of the transcription cofactor NPR1, are identified as receptors of SA. Salicylic acid is the only major plant hormone for which a receptor has not been firmly identified. It is produced in plants in response to pathogen challenge, and induces systemic acquired resistance against secondary infection. This process requires the transcription cofactor NPR1, which indicated that NPR1 might be a salicylic acid receptor, but NPR1 alone does not bind to the hormone. Here, Xinnian Dong and colleagues identify the NPR1 paralogues NPR3 and NPR4 as salicylic acid receptors with different binding affinities. The authors propose a model for the regulation of NPR1 by NPR3 and NPR4 in response to different levels of salicylic acid.

NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants