Simplified model of the molecular machinery involved in the transcriptional regulation of the SA signaling pathway (A), the JA signaling pathway (B), or the antagonism of SA on the JA signaling pathway (C). By inducing reduction and monomerization of NPR1, SA activates NPR1 (star-shaped), which then triggers gene expression in the nucleus. JA-responsive genes are kept in check by JAZ repressors in the absence of JA. In the presence of JA, MYC or ERF transcription factors activate JA-responsive genes, but only if SA is absent. Activation of both the SA and JA signaling pathways leads to antagonism of JA-responsive gene expression by SA. There are indications for roles in SA/JA crosstalk for cytosolic NPR1, and nuclear localized TGAs, GRX480, and WRKYs. See text for details on the molecular processes underlying the transcriptional control, like redox signaling, sequestration, degradation, phosphorylation, and chromatin modification. Solid lines indicate established (in)activities and dashed lines hypothesized (in)activities, where black arrows specify activation and red blocks suppression. Red crosses indicate that gene transcription is hampered.