Short-Term Exposure to Nitrogen Dioxide Provides Basal Pathogen Resistance

Nitrogen dioxide (NO 2 ) forms in plants under stress conditions, but little is known about its physiological functions. Here, we explored the physiological functions of NO 2 in plant cells using short-term fumigation of Arabidopsis ( Arabidopsis thaliana ) for 1 h with 10 µL L −1 NO 2. Although leaf symptoms were absent, the expression of genes related to pathogen resistance was induced. Fumigated plants developed basal disease resistance, or pattern-triggered immunity, against the necrotrophic fungus Botrytis cinerea and the hemibiotrophic bacterium Pseudomonas syringae . Functional salicylic acid and jasmonic acid (JA) signaling pathways were both required for the full expression of NO 2 -induced resistance against B. cinerea . An early peak of salicylic acid accumulation immediately after NO 2 exposure was followed by a transient accumulation of oxophytodienoic acid. The simultaneous NO 2 -induced expression of genes involved in jasmonate biosynthesis and jasmonate catabolism resulted in the complete suppression of JA and JA-isoleucine (JA-Ile) accumulation, which was accompanied by a rise in the levels of their catabolic intermediates 12-OH-JA, 12-OH-JA-Ile, and 12-COOH-JA-Ile. NO 2 -treated plants emitted the volatile monoterpene α-pinene and the sesquiterpene longifolene (syn. junipene), which could function in signaling or direct defense against pathogens. NO 2 -triggered B. cinerea resistance was dependent on enhanced early callose deposition and CYTOCHROME P450 79B2 ( CYP79B2 ), CYP79B3 , and PHYTOALEXIN DEFICIENT3 gene functions but independent of camalexin, CYP81F2 , and 4-OH-indol-3-ylmethylglucosinolate derivatives. In sum, exogenous NO 2 triggers basal pathogen resistance, pointing to a possible role for endogenous NO 2 in defense signaling. Additionally, this study revealed the involvement of jasmonate catabolism and volatiles in pathogen immunity.