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

Abstract

Plants carrying a mutation in <i>S</i>-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 <i>gsnor1</i> 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 <i>gsnor1</i> plants unresponsive to foliar SA. In contrast, SA supplied via root drench restores SA signaling and SAR in <i>gsnor1</i>, 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.