Background : Ginseng root rot is a devastating disease caused by the fungus, Ilyonectria mors-panacis that generally attacks younger roots (-2 years), leading to defects in root quality, ginsenoside accumulation and also life cycle of the plant. Hence, there is an indispensable need to develop strategies resulting in tolerance against ginseng root rot. The protective role of silicon during pathogen infestation is well documented in other plant systems and a previous study demonstrated that silica nanoparticles are absorbed and accumulated more than the bulk silica in maize. However, the role of silica in ginseng-root rot pathosystem is unknown. Methods and Results : In the present study, we evaluated the effect of silica nanoparticles (N-SiO2) in Panax ginseng during I. mors-panacis infection. Long term analysis (30 dpi) revealed a striking 50% reduction in disease severity index upon 1 mM and 2 mM treatment of N-SiO2. However, N-SiO2 did not have any direct antifungal activity against I. mors-panacis. Candidate genes and metabolites based approach revealed jasmonic acid (JA) mediated sterol accumulation and incresed ginsenside biosyntesis as the key transcriptional reprogramming events orchestrated by N-SiO2 during the fungal infection. Conclusion : In a nut shell, N-SiO2 administration induces transcriptional reprogramming in ginseng roots, leading to increased phytosterol and ginsenosides synthesis resulting in enhanced tolerance against I. mors-panacis.

Carotenoid compounds in embryos of wild-type(WT) and viviparous mutants of maize(Zea mays L.) were analyzed using high performance liquid ehromatography (HPLC) with a photodiode array detector. Zeaxanthin accumulates in WT embryos as the major carotenoid. Phytoene accumulates in vp2 and vp5. Phytofluene in w3 and ζ-carotene in the vp9 mutant embryos. This indicates that the vp2 and vp5 mutants impair phytoene desaturase from 15-cis-phytoene to 15-cis-phytofluene. The w3 mutant has neither an isomerase from 15-cis-phytofluene to all-trans-phytofuene nor phytofluene desaturase from phytofluene to ζ-carotene. The vp9 mutant does not have the ζ-carotene desaturase from ζ-carotene to lycopene. Our analysis shows that the terminal carotenoid. γ-carotene(β,ψ-carotene), accumulates in the vp7 mutant embryos. The ε-carotene(ε,ε-carotene), a product of δ-carotene(ε,ψ-carotene) in some plants, however, has not been found in maize embryos. The vp7 mutant impairs a cyclization step from γ-carotene to both β-carotene and α-carotene. We suggest that monocyclic γ-carotene is the sole precursor of both bicyclic β-carotene(β,β-carotene) and α-carotene(β,ε-carotene) in maize.