Complementary action of jasmonic acid on salicylic acid in mediating fungal elicitor-induced flavonol glycoside accumulation of Ginkgo biloba cells

• Published in: Plant, cell and environment cell and environment, 2009-08, Vol.32 (8), p.960-967
• Main Authors: XU, MAOJUN, DONG, JUFANG, WANG, HUIZHONG, HUANG, LUQI
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cyclopentanes - metabolism; Fatty Acids, Unsaturated - metabolism; Flavonols - biosynthesis; Fundamental and applied biological sciences. Psychology; Fungal Proteins - metabolism; Gene Expression Regulation, Plant; Genes, Plant; Ginkgo biloba; Ginkgo biloba - genetics; Ginkgo biloba - metabolism; Glycosides - biosynthesis; Mixed Function Oxygenases - genetics; Mixed Function Oxygenases - metabolism; Oxylipins - metabolism; PB90; Phytophthora - metabolism; Phytophthora boehmeriae; Plants, Genetically Modified - genetics; Plants, Genetically Modified - metabolism; Salicylic Acid - metabolism; secondary metabolites; signal interaction; Signal Transduction
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1111/j.1365-3040.2009.01976.x

The antagonistic action between jasmonic acid (JA) and salicylic acid (SA) in plant defence responses has been well documented. However, their relationship in secondary metabolite production is largely unknown. Here, we report that PB90, a protein elicitor from Phytophthora boehmeriae, triggers JA generation, SA accumulation and flavonol glycoside production of Ginkgo biloba cells. JA inhibitors suppress not only PB90-triggered JA generation, but also the elicitor-induced flavonol glycoside production. However, the elicitor can still enhance flavonol glycoside production even though the JA generation is totally inhibited. Over-expression of SA hydrolase gene NahG not only abolishes SA accumulation, but also suppresses the elicitor-induced flavonol glycoside production when JA signalling is inhibited. Interestingly, expression of NahG does not inhibit the elicitor-induced flavonol glycoside accumulation in the absence of JA inhibitors. Moreover, JA levels are significantly enhanced when SA accumulation is impaired in the transgenic cells. Together, the data suggest that both JA and SA are involved in PB90-induced flavonol glycoside production. Furthermore, we demonstrate that JA signalling might be enhanced to substitute for SA to mediate the elicitor-induced flavonol glycoside accumulation when SA signalling is impaired, which reveals an unusual complementary relationship between JA and SA in mediating plant secondary metabolite production.