The role of AP2/ERF transcription factors in SA/JA crosstalk.

Salicylic acid (SA) and jasmonic acid (JA) play major roles in the regulation of the plant immune signaling network. Their signaling pathways cross-communicate to fine-tune the activation of defenses. We aim to unravel how SA exerts its antagonistic effect on the expression of JA-dependent genes, such as PDF1.2, in Arabidopsis. Previously, we showed that SA targets the GCC-box promoter motif, which is present in promoters of JA/ET-regulated genes and is a binding site for AP2/ERF transcription factors (Van der Does et al., 2013; Plant Cell 25: 744–761). Protein levels of ORA59, an AP2/ERF that activates PDF1.2, were downregulated after SA treatment. Using the protein synthesis inhibitor cycloheximide (CHX), we further showed that de novo protein synthesis is required for SA/JA crosstalk. Because AP2/ERFs can also act as negative regulators of JA-responsive gene expression, we hypothesized that newly synthesized SA-induced AP2/ERFs may contribute to SA/JA crosstalk as well. We screened microarray and RNA sequencing data of SA-treated plants to select SA-induced AP2/ERFs and AP2/ERFs containing an EAR repression domain. We tested 17 loss-of-function ap2/erf mutants and although some were affected in JA-responsiveness, they were all found to still exhibit SA/JA crosstalk, indicating that the tested AP2/ERFs are not essential for SA/JA crosstalk or act redundantly. In addition, a loss-of-function mutation in TOPLESS (TPL), encoding a co-repressor of JA signaling that interacts with EAR-domain AP2/ERFs, did not affect SA/JA crosstalk either. Collectively, our data suggest that SA antagonizes JA signaling by targeting positive JA signaling regulators, possibly via newly synthesized factors.