Postdoctoral Research Associate University of Florida Belle Glade, Florida
Body of Abstract: Wheat plants defend themselves against the yield-reducing pathogen Pyrenophora tritici-repentis (Ptr) in an inverse gene-for-gene manner, and the intricacies of this system are not yet fully understood. We have previously identified two wheat genotypes with high resistance (cv. Robigus) and susceptibility (cv. Hereward) to Ptr, which the differentially expressed genes (DEGs) and accumulated metabolites (DAMs) have been defined from transcriptomic and metabolomic profiles of both cultivars during Ptr challenge in comparison to controls. This study aims to identify the key shifts in both gene expression and metabolism triggered by Ptr infection. We performed Regularized Canonical Correlation Analysis (RCCA) using the DEG and DAMs from each genotype. Using a correlation threshold of 0.6, we obtained scale-free networks comprised of 760433 edges in Hereward and 69745 in Robigus. The hub genes present in the Robigus network were upregulated at 48 and 96 hours post-inoculation and they code for hydroxycinnamoyl-CoA:shikimate hydroxycinnamoyltransferase 2 (hst2), receptor-like kinase/carbohydrate-binding protein, and late embryogenesis abundant protein. The latter plays a role in the cellulose synthase complex, part of the cell wall organization pathway. Pathway enrichment analysis indicated the following as the topmost significant pathways enriched in the Robigus network: catalytic activity, chitinase activity, catabolic and metabolic processes of cell wall macromolecule, aminoglycan and chitin. The hub genes in the Hereward network, interestingly, were all downregulated (except for a hexosyltransferase). The hub genes include Cytochrome P450, translocase of chloroplast 159, potassium transporters, glycosyltransferases, NADPH:quinone oxidoreductase, among others. Energy related pathways, including ATP and nucleoside binding, phosphorylation, phosphorus/phosphate metabolic process, phosphotransferase activity, and amino acid metabolism, were largely enriched in the susceptible interaction. 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 Tar Spot susceptibility.