Abstract
Plant growth promoting rhizobacteria have been proposed as effective biocontrol agents against several fungal and bacterial plant pathogens. However, there is limited knowledge regarding their effect against viruses. In this study, Bacillus amyloliquefaciens strain MBI600 (MBI600), active ingredient of the biological fungicide Serifel® (BASF SE), was tested for its antiviral action in tomato plants. Drench, foliar or soil amendment applications of MBI600 reduced up to 80% the incidence of Tomato spotted wilt virus under two different sets of environmental conditions. In addition, drench application of MBI600 delayed Potato virus Y systemic accumulation. Transcriptional analysis of a range of genes associated with salicylic acid (SA)- or jasmonic acid - related defense, priming or basal defense against viruses, revealed the induction of the SA signaling pathway in tomato after MBI600 treatment, and discrete gene expression patterns in plant response to TSWV and PVY infection.
Highlights
® of the biological fungicide Serifel (BASF SE), was tested for its antiviral action in tomato plants
To MBI600 triple drench application, the MBI600 single drench application in air-dried potting medium during sowing of tomato seeds resulted in a significant reduction of Tomato spotted wilt virus (TSWV) incidence compared to the water treatment (P < 0.0001 in all cases)
Representative tomato plants treated with each of water, BTH or MBI600 at 30 days post inoculation with TSWV are illustrated in Fig. 1c and Supplementary Fig. S1
Summary
® of the biological fungicide Serifel (BASF SE), was tested for its antiviral action in tomato plants. Systemic resistance can be categorized in two forms: (i) induced systemic resistance (ISR) activated by plant-growth promoting rhizobacteria (PGPR) and fungi (PGPF), and (ii) systemic acquired resistance (SAR) activated by a variety of pathogens or chemical compounds[6,7]. In both cases, systemic resistance is related to differential gene expression that is tightly linked to hormonal production[8]. The defense mechanism triggered by PGPR against viruses depends on the complicated interactions among PGPR, host plant and virus, involving mostly the salicylate (SA) signaling pathway and in some cases both SA and jasmonate (JA) pathways[13,18,19]
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