Chitosan triggers tolerance to Pythium myriotylum infection in ginger (Zingiber officinale) by modulating multiple defense signaling pathways

Abstract

In this study, we evaluated the potential of abscisic acid, brassinolide, isoxaben, hexanoic acid, β-aminobutyric acid, oligogalacturonic acid, flagellin 22, chitosan, methyl salicylate and pipecolic acid in suppressing the soft rot disease in ginger (Zingiber officinale) caused by the necrotrophic oomycete pathogen Pythium myriotylum. Of the ten elicitors tested, the treatment with 100 μM chitosan curtailed the disease severity in ginger to ∼36%. We examined the differential modulation in different parameters between the chitosan treated P. myriotylum inoculated (CTI) and the untreated inoculated (UTI) ginger plants. The ROS generator RBOHD was induced in CTI plants whereas the different ROS scavengers were modulated variously between the two regimens. While the biosynthetic and signaling genes of the jasmonic acid and ethylene were induced in CTI plants, salicylic acid signaling genes were suppressed. The chitosan treatment induced the HR marker gene HSR203J in ginger and suppressed the expression of cell death markers HIN1, AIF1 and AIF2. Similarly, while the lignin biosynthetic genes were mostly upregulated, the cell wall homeostasis genes EXLA2, INV3 and WAK2-LIKE were suppressed. Total phenylpropanoids declined in both the regimens, but the level of decline was less in the CTI plants. The histopathology showed retarded pathogen ingress in CTI plants. Well diffusion assays revealed non-toxicity of chitosan to the pathogen. The data highlight that the orchestration pattern of defense pathways in chitosan primed ginger and the pathogen induced basal defense pathways operated in a resistant plant host are loosely parallel. The results demonstrate the ability of chitosan to prime standing ginger plants against soft rot disease and implicate the potential of integrating chitosan for the sustainable management of ginger soft rot.