O-3-Induced Priming Defense Associated With the Abscisic Acid Signaling Pathway Enhances Plant Resistance to Bemisia tabaci

Elevated ozone (O-3) modulates phytohormone signals, which subsequently alters the interaction between plants and herbivorous insects. It has been reported that elevated O-3 activates the plant abscisic acid (ABA) signaling pathway, but its cascading effect on the performance of herbivorous insects remains unclear. Here, we used the ABA-deficient tomato mutant notabilis (not) and its wild type, Ailsa Craig (AC), to determine the role of ABA signaling in mediating the effects of elevated O-3 on Bemisia tabaci in field open-top chambers (OTCs). Our results showed that the population abundance and the total phloem-feeding duration of B. tabaci were decreased by O-3 exposure in AC plants compared with not plants. Moreover, elevated O-3 and B. tabaci infestation activated the ABA signaling pathway and enhanced callose deposition in AC plants but had little effect on those in not plants. The exogenous application of a callose synthesis inhibitor (2-DDG) neutralized O-3-induced resistance to B. tabaci, and the application of ABA enhanced callose deposition and exacerbated the negative effects of elevated O-3 on B. tabaci. However, the application of 2-DDG counteracted the negative effects of O-3 exposure on B. tabaci in ABA-treated AC plants. Collectively, this study revealed that callose deposition, which relied on the ABA signaling pathway, was an effective O-3-induced priming defense of tomato plants against B. tabaci infestation.