Thiamin priming to control early blight in potato: investigation of its effectiveness and molecular mechanisms

Background: Previous reports in several plant species have shown that thiamin applied on foliage primes plant immunity and is effective in controlling fungal, bacterial, and viral diseases. However, the effectiveness of thiamin against potato (Solanum tuberosum) pathogens has seldom been investigated. Additionally, the transcriptomics and metabolomics of immune priming by thiamin have not previously been investigated. Here, we tested the effect of thiamin application against Alternaria solani, a necrotrophic fungus that causes early blight disease on potato foliage, and identified associated changes in gene expression and metabolite content. Results: Foliar applications of thiamin reduced lesion size by approximately 33% when applied at an optimal concentration of 10 mM. However, the effect of thiamin on preventing lesion growth was temporally limited, as we observed a reduction of lesion size when leaves were inoculated 4 h, but not 24 h, following thiamin treatment. Additionally, we found that the effect of thiamin on lesion size was restricted to the site of application and was not systemic. Gene expression analysis via RNA-seq showed that thiamin induced the expression of genes involved in the synthesis of salicylic acid (SA) and phenylpropanoids to higher levels than the pathogen alone, as well as fatty acid metabolism genes that may be related to jasmonic acid biosynthesis. Thiamin also delayed the downregulation of photosynthesis-associated genes in plants inoculated with A. solani, which is a typical plant response to pathogens, but could also induce a similar repression of primary metabolic pathways in non-infected leaves. Metabolite analyses revealed that thiamin treatment in the absence of pathogen decreased the amounts of several organic compounds involved in the citric acid cycle as well as sugars, sugar alcohols, and amino acids. Conclusions: Our study indicates that thiamin priming of plant defenses may occur through perturbation of primary metabolic pathways and a re-allocation of energy resources towards defense activities.