Figure 1.

Regulatory convergence and mutual potentiation of salicylic acid (SA) and N-hydroxypipecolic acid (NHP) biosynthesis and signaling. Upstream immunity-associated signals [e.g., reactive oxygen species (ROS), Ca²⁺] lead to activation/repression of TGACG SEQUENCE-SPECIFIC BINDING PROTEIN 1 (TGA1)/4 transcriptional activators and CALMODULIN-BINDING TRANSCRIPTION ACTIVATOR (CAMTA) transcriptional repressors. Along with the antagonistic SA receptors NONEXPRESSER OF PR GENES 1 (NPR1; co-activator) and NPR3/4 (co-repressors), TGA1/4 and CAMTA1/2/3 control expression of CALMODULIN-BINDING PROTEIN 60-LIKE G (CBP60g) and SAR DEFICIENT 1 (SARD1) that encode functionally redundant master transcription factors of plant immunity. SARD1 and CBP60g directly bind the promoters of SA biosynthetic (ICS1, EDS5, and PBS3) and NHP biosynthetic genes (ALD1, SARD4, and FMO1). Central immune regulators ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) and PHYTOALEXIN DEFICIENT 4 (PAD4; which mediate both pattern-triggered immunity and effector-triggered immunity) are also required for SA and NHP accumulation. Downstream of their biosynthesis, SA directly activates while NHP indirectly activates the SA receptor NPR1. NPR1 then promotes TGA-directed transcription of key defense genes for local/basal and systemic immune responses. Created with BioRender.com.