Roles of Defense Hormones in the Regulation of Ozone-Induced Changes in Gene Expression and Cell Death

Apoplast, the diffusional space between plant cell plasma membranes, is an important medium for signaling within and between the cells. Apoplastic reactive oxygen species (ROS) are crucial signaling molecules in various biological processes. ROS signaling is interconnected with the response to several hormones, including jasmonic acid (JA), salicylic acid (SA) and ethylene. Using ozone (O3) to activate apoplastic ROS signaling, we performed global and targeted analysis of transcriptional changes and cell death assays to dissect the contribution of hormone signaling and various transcription factors (TFs) in the regulation of gene expression and cell death. The contributions of SA, JA, and ethylene were assessed through analysis of single, double, and triple mutants deficient in biosynthesis or signaling for all three hormones. Even in the triple mutant, the global gene expression responses to O3 were mostly similar to the wild-type. Cell death in the JA receptor mutant coi1-16 was suppressed by impairment of the NADPH oxidase RBOHF, suggesting a role for a ROS signal in limiting the spread of cell death. In response to apoplastic ROS, there is not a single signaling pathway that regulates gene expression or cell death. Instead, several pathways regulate the apoplastic ROS response via combinatorial or overlapping mechanisms.