Fungal endophyte-induced volatile oil accumulation in Atractylodes lancea plantlets is mediated by nitric oxide, salicylic acid and hydrogen peroxide

Inoculation with endophytic fungus Gilmaniella sp. induced multiple responses in host plantlets of Atractylodes lancea, including the burst of NO, SA, H2O2, and the accumulation of volatile oil. To investigate the pathways that the three signal molecules affect the volatile oil production, the plantlets were treated with NO specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO), SA synthesis inhibitor trans-cinnamic acid (trans-CA), membrane NADPH oxidase inhibitor diphenylene iodonium (DPI) and catalase (CAT). The results showed pretreatment of plantlets with cPTIO, DPI/CAT and trans-CA inhibited the burst of signal molecules and volatile oil accumulation induced by the fungus. Exogenous NO donor SNP could promote SA and H2O2 production as well as volatile oil accumulation. Combined application of trans-CA and DPI/CAT could inhibit the promotion effects of exogenous NO. Exogenous SA and H2O2 had no effects on NO production, but they could reverse the total inhibitory effects of cPTIO, CAT/DPI and trans-CA toward volatile oil accumulation. Exogenous H2O2 had promotion effect on SA production, yet CAT/DPI could not significantly prevent SA synthesis. These data indicated NO mediates violate oil accumulation induced by the fungus through SA and H2O2 dependent pathways. H2O2 can regulate SA production, but does not act as upstream signal molecule.