FIGURE 2.

A simplified model showing pathways, chemicals, and proteins involved in SAR. Infection with avirulent (avr) pathogen induces accumulation of SA and nitric oxide (NO) in a digalactosyldiacylglycerol (DGDG)-dependent manner. NO operates in a feedback loop with reactive oxygen species (ROS), which catalyze oxidation of C18 unsaturated fatty acids (FA) present on monogalactosyldiacylglycerol (MGDG) and DGDG lipids. Oxidation of C18 FAs at C9 carbon (indicated by the arrows) generates azelaic acid (AzA), which triggers biosynthesis of glycerol-3-phosphate (G3P) via upregulation of genes encoding G3P biosynthetic enzymes (glycerol kinase, GK and G3P dehydrogenase, G3Pdh). G3P-mediated signaling is dependent on DIR1 and AZI1, which interact with each other and require G3P for the stability of their respective transcripts. Conversely, DIR1 and AZI1 are also required for G3P biosynthesis, suggesting that G3P and DIR1/AZI1 regulate SAR via a feedback loop. In the SA branch, EDS1 regulates both SA and AzA levels. NPR1 is a key downstream component in the SA branch which is nitrosylated by NO.