FIGURE 2.

Redox-modulated processes in the SA-mediated control of gene expression. Model for the transcriptional control of genes representing three main groups of SA-regulated genes: SA-induced non-expressor of pathogenesis-related (PR) genes 1 (NPR1) -dependent late genes (PR1, Left); SA-induced NPR1-independent early genes [glutaredoxin C9 (GRXC9), Medium]; and JA/ET-induced SA-repressed genes [Octadecanoid-Responsive AP2/ERF domain protein 59 (ORA59), Right]. The temporal dynamics of the redox changes (Δ Redox) occurring during the defense response to stress are represented by the bar at the left, where blue indicates reductive states and red indicates oxidative states. The temporal dynamics in the formation of transcriptionally active and inactive complexes in the promoter of PR1, GRXC9, and ORA59, according to redox changes dynamics, are included in each panel. The places where ROS/SA, and JA/ET signals act in these pathways, is indicated by red arrows. The components identified (or suspected) as redox sensors in these pathways, whose mechanisms of action are discussed in the text, are indicated in color. TGA factors (red) are involved in the three pathways. Homodimers or heterodimers of TGA2 and TGA3 (T2T3) or TGA2 and TGA5 (T2T5) factors act as platforms for the formation of transcriptionally inactive and active complexes. Active complexes promote recruitment of RNA polymerase II (RNAPII) and gene transcription (red arrows at promoters). NPR1 (yellow) is the master co-activator for SA-inducible NPR1-dependent pathway and is redox-regulated by oxido-reduction of Cys residues. TRXh5 and GRXC9 (green) are oxidoreductases coded by SA-inducible genes, which catalyze reduction of NPR1 and of a still unknown component in GRXC9 and ORA59 promoters. Other transcriptional factors and co-factors not directly involved in redox regulation are shown in gray tones.