Figure 8.

Model for the salicylic acid (SA)‐mediated activation of the tobacco (Nt) PR‐1a gene late in systemic acquired resistance (SAR). Low levels of SA elicited by pathogen attack induce the expression of NIMIN2 genes. At this stage, premature PR‐1a induction via the TGA–NPR1 complex is inhibited by binding of NIMIN2‐type proteins to the C‐terminal end of NPR1. Inability to confine the pathogen leads to a further increase in SA levels in the noninfected leaves of the plant, eventually resulting in the release of NIMIN2, the activation of NPR1 and induction of the PR‐1a gene. The model implies that PR genes are activated at distinct threshold levels of SA (indicated by the step), and that direct measurement of the ambient cellular SA concentration occurs through SA‐sensitive complexes formed between the NPR1 C‐terminal end and NIMIN2 proteins. NIMIN, NIM1‐INTERACTING; NPR1, NONEXPRESSOR OF PATHOGENESIS‐RELATED PROTEINS1; PR, PATHOGENESIS‐RELATED.