Jasmonic acid is involved in the signaling pathway for fungal endophyte-induced volatile oil accumulation of Atractylodes lancea plantlets

BACKGROUND: Jasmonic acid (JA) is a well-characterized signaling molecule in plant defense responses. However, its relationships with other signal molecules in secondary metabolite production induced by endophytic fungus are largely unknown. Atractylodes lancea (Asteraceae) is a traditional Chinese medicinal plant that produces antimicrobial volatiles oils. We incubated plantlets of A. lancea with the fungus Gilmaniella sp. AL12. to research how JA interacted with other signal molecules in volatile oil production. RESULTS: Fungal inoculation increased JA generation and volatile oil accumulation. To investigate whether JA is required for volatile oil production, plantlets were treated with JA inhibitors ibuprofen (IBU) and nordihydroguaiaretic acid. The inhibitors suppressed both JA and volatile oil production, but fungal inoculation could still induce volatile oils. Plantlets were further treated with the nitric oxide (NO)-specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO), the H(2)O(2) inhibitors diphenylene iodonium (DPI) and catalase (CAT), and the salicylic acid (SA) biosynthesis inhibitors paclobutrazol and 2-aminoindan-2-phosphonic acid. With fungal inoculation, IBU did not inhibit NO production, and JA generation was significantly suppressed by cPTIO, showing that JA may act as a downstream signal of the NO pathway. Exogenous H(2)O(2) could reverse the inhibitory effects of cPTIO on JA generation, indicating that NO mediates JA induction by the fungus through H(2)O(2)-dependent pathways. With fungal inoculation, the H(2)O(2) scavenger DPI/CAT could inhibit JA generation, but IBU could not inhibit H(2)O(2) production, implying that H(2)O(2) directly mediated JA generation. Finally, JA generation was enhanced when SA production was suppressed, and vice versa. CONCLUSIONS: Jasmonic acid acts as a downstream signaling molecule in NO- and H(2)O(2)-mediated volatile oil accumulation induced by endophytic fungus and has a complementary interaction with the SA signaling pathway.