Excess nitric oxide alters cellular pH to restrict salicylic acid movement and systemic immunity.

Plants carrying a mutation in S-nitrosoglutathione reductase 1 (GSNOR1) accumulate high nitric oxide (NO) and exhibit impaired immunity characterized by reduced pathogen-responsive salicylic acid (SA) accumulation and failure to activate normal SA signaling. We show that this reduced SA responsiveness in gsnor1 plants arises from impaired vascular-associated movement of SA, thereby compromising systemic acquired resistance (SAR). Elevated NO perturbs cellular pH homeostasis, acidifying the apoplast and alkalinizing the cytosol, which likely interferes with phloem-associated SA movement and renders gsnor1 plants unresponsive to foliar SA. In contrast, SA supplied via root drench restores SA signaling and SAR in gsnor1, likely because sustained xylem delivery bypasses the mutant's defect in SA entry into the symplast. NO-mediated modulation of pH and its downstream effects on solute and ion transport in mammals suggest a conserved role for NO in regulating transport processes across biological systems. Our study provides previously unknown insights into how spatial NO gradients fine-tune immune signaling in plants and potentially across the organismal scale.