Transcriptome of silicon-induced resistance against Ralstonia solanacearum in the silicon non-accumulator tomato implicates priming effect

Silicon induced resistance (SiIR) in tomato against bacterial wilt caused by Ralstonia solanacearum. The mechanism of SiIR is ambiguous. Therefore we tracked the expression of twelve defense marker genes over time using qRT-PCR. Besides up-regulated expression of the jasmonic acid/ethylene marker genes JERF3, TSRF1and ACCO during SiIR, the expression of the oxidative stress markers FD-I and POD and the basal defense marker AGP-1g were also up-regulated. The expression of defense marker genes was generally induced upon challenging the silicon-treated plants with R. solanacearum and reached its highest levels at 72 h post inoculation. A global transcriptome profiling was performed to uncover further changes at this time point using the TOM2 microarray. Significant regulation of additional 16 genes was revealed after silicon treatment in plants challenged with R. solanacearum. Twelve genes, involved in defense, signal transduction, response to stresses, transcription, ubiquitinylation and metabolism, were up-regulated. A JAZ1-similar gene showed the highest level of up-regulation indicating prior induction and fine tuning of jasmonic acid signaling. Thus, we conclude that silicon primed plants, thereby alleviating biotic stress imposed by the pathogen. The primed state could be mediated via ethylene, jasmonic acid and/or reactive oxygen species signaling pathways. We also suggest that the protective role of silicon can not only be explained with its mechanical properties.

Research highlights
► This paper reveals for the first time gene expression underlying silicon-induced resistance (SiIR) in a silicon non-accumulator plant, tomato, in response to challenge with a bacterial pathogen, and that SiIR is expressed in form of priming.
► The paper presents a follow-up on transcript level of our biochemical and immunohistochemical work on silicon induced resistance, and confirms our histochemical observations of induction of basal resistance (e.g. PMPP 64: 233–243, 68: 41–50, 70: 120–129).
► From the transcription profile we could develop a hypothetical model of the SiIR, in which JA/ET and/ROS signaling pathways could be involved.
► We also suggest that the protective role of silicon can not only be explained with its mechanical properties.