Figure 1. Proposed salicylic acid biosynthetic and metabolic pathway in plants. Pathway for SA biosynthesis through isochorismate synthase (ICS), which, in bacteria also requires pyruvate lyase (PL). Modification of SA leads to the formation of two major metabolites, salicylic acid 2-O--d-glucoside and methyl salicylate.

Figure 2. Establishment of systemic acquired resistance in plants. Necrotizing pathogens trigger the accumulation of salicylic acid (SA), pathogenesis-related (PR) protein expression and the release of a yet unknown phloem-mobile signal at the site of infection. This leads to an increase in SA levels and to the production of volatile methyl salicylate in distal parts of the plant and subsequently to the expression of PR proteins, which is tightly linked to the onset of resistance.

Figure 3. Structures of chemical inducers of systemic acquired resistance (SAR). Comparison of the structures of salicylic acid (SA) and its analogue 2,6 dichloroisonicotinic acid (INA) and benzothiadiazole (BTH).

Figure 4. Proposed model illustrating the role of SA, NPR1 and its interaction partners TGA factors and NIMIN proteins in defence gene regulation. (a) In healthy plants, NPR1 forms oligomeric complexes in the cytoplasm. The subunits are supposed to be held together by intermolecular disulfide bridges (–S–S–). (b) Necrotizing pathogens induce the accumulation of SA possibly leading to a redox change in the affected cells. Subsequently, oligomeric NPR1 is reduced (–SH) and the active, monomeric form translocates to the nucleus. There, it interacts with TGA factors which bind to a positive regulatory element termed LS7 to activate PR-1 gene expression. NIMIN1 forms a ternary complex with NPR1 and TGA factors and dampens PR-1 gene expression.