Integration of Transcriptomic and Metabolomic Profiling as a Source of Insight into Key Candidate Genes and Metabolic Pathways Associated with Maize Resistance to Fusarium spp.
Maciej Lenort, Agnieszka Tomkowiak, Jan Bocianowski, Kinga Stuper-Szablewska, Tomasz Kosiada, Karolina Jarzyniak, Roksana Bobrowska, Łukasz Wolko, Przemysław Gawrysiak, Wiktoria PadiasekFusarium spp. infections substantially reduce maize productivity, making the identification of molecular and metabolic mechanisms underlying host resistance important for breeding. This study aimed to characterize the maize response to Fusarium infection by integrating pathogen colonization, the expression of 17 candidate genes, and metabolite profiles. Five maize genotypes differing in resistance were inoculated with a mixture of Fusarium spores and analyzed at 0, 6, 12, 24, and 48 h post-inoculation. Six Fusarium species were identified, with F. poae and F. culmorum predominating in susceptible genotypes. Colonization exceeded 70% in susceptible samples, whereas resistant genotypes generally showed 0–2% colonization. Gene expression patterns were strongly genotype- and time-dependent, with 24 h post-inoculation representing a major point of transcriptional activation. Several genes were strongly induced in the susceptible genotype, whereas selected genes, including Putrescine hydroxycinnamoyltransferase (LOC103649226), showed constitutive or induced expression associated with resistant genotypes. Resistant lines, particularly SMH 57524 and SMH 57624, showed higher concentrations of selected phenolic acids and luteolin glycosides and higher peroxidase, polyphenol oxidase, and catalase activities. Regression analyses revealed significant associations between candidate gene expression and the accumulation of selected metabolites, including ferulic, diferulic, p-coumaric, and caffeic acids, as well as lutein, with both positive and negative relationships being detected. These findings indicate that maize resistance to Fusarium is associated with coordinated transcriptional, metabolic, and redox responses and identify gene–metabolite relationships relevant to the molecular characterization of resistance.