Defence-related biochemical changes by elicitor of malformation pathogen,Fusarium mangiferae, in mango

Abstract

Malformation of mango (Mangifera indica L.) induced by Fusarium moniliforme var. subglutinans is a plant disease of international importance. The paper reports the downstream defence responses at the initial stage in a susceptible host (cultivar Amrapali) after treatment with biotic (isolated from the pathogen cell wall) (BEL) and abiotic (salicylic acid, SA) elicitors, and inoculation of vegetative buds with the pathogen (IVB). The SA was further tested to induce resistance in field trials. The inoculation and application of elicitors increased b-1, 3 glucanase that causes lysis of fungal hyphae by many folds. Hydrogen peroxide (H 2 O 2 ) (active oxygen species) that induces hypersensitive cell death was reduced to the minimum level after treatment with BEL. The reduction of H 2 O 2 in the inoculated vegetative buds was also substantial; however, comparatively less with SA treatment. Consequently, there was no hypersensitive cell death in the malformed mango. Salicylic acid that enhances H 2 O 2 content by suppressing H 2 O 2 -degradation by catalase, increased marginally with the SA treatment and in the IVB, but reduced with the BEL. The reduction of SA in BEL-treated buds concomitantly reduced its H 2 O 2 content. The activity of catalase, suppressor of resistance mechanism, was reduced in all the treatments, but the reduction was not enough to arrest H 2 O 2 -degradation. Magiferin (1, 3, 6, 7-tetrahdroxyxanthone C 2 -b-D glucoside), a defence metabolite of mango, increased substantially in all the treatments; maximum with the BEL. A pathogenesis-related (PR) protein of 20 KDa that resists symptom development appeared in all the treatments except the control. But light colour of the spots for the PR-protein indicated low protein accumulation. The maximum accumulation was with the IVB followed by SA and BEL treatments. The amount of total protein reduced considerably in all the treatments. The SA treatment on healthy plants failed to induce defence against malformation. Contrarily, the treatment on malformed seedlings restored normal growth within two months. Hence, SA acted better over the infected plants in presence of the pathogen. Thus, a signal transduction system involving SA and H 2 O 2 remained nonfunctional and enough defence chemicals could not be synthesised. Defence genes that produce phenolic and b-1, 3 glucanase, however, became activated and saved the plants from death although could not prevent symptom manifestations.