Revealing gene–metabolite interactions in wheat defenses against Pyrenophora tritici-repentis in resistant and susceptible genotypes

Wheat defenses against Pyrenophora tritici-repentis (Ptr), the cause of tan spot disease, are complex and require further characterization. We previously identified two wheat genotypes, Robigus (resistant) and Hereward (susceptible), and characterized their differentially expressed genes (DEGs) and accumulated metabolites (DAMs) following challenge with Ptr. In this study we uncover coordinated shifts in gene expression and metabolism triggered by Ptr. The DEGs and DAMs from each genotype were integrated using regularized canonical correlation analysis, yielding scale-free networks with 69 745 edges in Robigus and 760 433 in Hereward. In Robigus, hub genes were upregulated at 48 and 96 h post-inoculation and included hst2 (encoding hydroxycinnamoyl-CoA:shikimate hydroxycinnamoyl transferase 2), located within a QTL for Ptr resistance (QTs.fcu-5D locus), a receptor-like kinase, and a late embryogenesis abundant protein (which play roles in cell wall organization). Pathway enrichment showed significant involvement of catalytic activity, chitinase activity, and cell wall metabolic processes. In contrast, Hereward hub genes were mostly downregulated, except for a hexosyltransferase, with enriched pathways related to energy metabolism, such as ATP binding and phosphorylation. These results suggest that cell wall modifications and chitinase activity are part of an effective defense response against Ptr, whereas costly energetic processes may contribute to tan spot susceptibility.