Wheat blast, caused by Pyricularia oryzae Triticum lineage, is a major constraint to wheat production, mainly in the tropics of Brazil, where severe epidemics have been more frequent. We analyzed disease and wheat yield data from 42 uniform field trials conducted over 9 years (2012 to 2020) to assess whether the percent control and yield response were influenced by fungicide type, region (tropical or subtropical), and year. Six treatments were selected, all evaluated in at least 19 trials. Two fungicides were applied as solo active ingredients (MANCozeb, and TEBUconazole), and four were premixes (AZOXystrobin plus TEBU, TriFLoXystrobin plus PROThioconazole, TFLX plus TEBU, and PYRAclostrobin plus EPOXiconazole). Percent control, calculated from back-transforming estimates by a meta-analysis network model fitted to the log of the means, ranged from 43 to 58%, with all but PYRA plus EPOX showing efficacy >52% on average, not differing among them. The variation in both efficacy and yield response was explained by region, and all but TEBU performed better in the subtropics than in the tropics. Yield response from using three sequential sprays was approximately two times greater in the subtropics (319 to 532 kg/ha) than in the tropics (149 to 241.3 kg/ha). No significant decline in fungicide efficacy or yield response was observed in 9 years of study for any of the fungicides. These results reinforce the need to improve control by adopting an integrated management approach in the tropics given poorer performance and lower profitability, especially for the premixes, than in the subtropics.

Fusarium head blight (FHB), caused mainly by Fusarium graminearum, is best controlled with demethylation inhibitor (DMI) fungicides during flowering. However, the use of premixes of DMI and quinone outside inhibitor (QoI) fungicides to control FHB has increased in Brazil. Data on FHB severity and wheat yields measured in field experiments conducted in Brazil were gathered from both peer- and nonpeer-reviewed sources published from 2000 to 2018. After selection criteria were applied, 73 field trials from 35 bibliographic sources were identified, among which 50% of the data were obtained from cooperative network trials conducted after 2011. To be included in the analysis, DMI plus QoI premixes or tebuconazole were tested in at least 14 trials and 3 years. Four premixes met the criteria. Estimates of percent control (and respective 95% confidence intervals) by a network model fitted to the log of the treatment means ranged from 44.1% (pyraclostrobin plus metconazole applied once; 32.4 to 53.7) to 64.3% (pyraclostrobin plus metconazole; 58.4 to 69.3); the latter did not differ from tebuconazole (59.9%; 53.6 to 65.3). Yield response was statistically similar for pyraclostrobin plus metconazole (532.1 kg/ha; 441 to 623) and trifloxystrobin plus prothioconazole (494.9 kg/ha; 385 to 551), and both differed statistically from a group composed of tebuconazole (448.2 kg/ha; 342 to 554), trifloxystrobin plus tebuconazole (468.2 kg/ha; 385 to 551), azoxystrobin plus tebuconazole (462.4 kg/ha; 366 to 558), and pyraclostrobin plus metconazole applied once (413.7 kg/ha; 308 to 518). The two categories of FHB index (7% cutoff) and yield (3,000 kg/ha cutoff), both in the nontreated check, did not explain the heterogeneity in the estimates. Considering only the fungicide effects on yield, two sequential sprays of tebuconazole or one spray of pyraclostrobin plus metconazole as management choices are likely more profitable than DMI plus QoI premixes sprayed twice during flowering.

Pyrenophora tritici-repentis (Ptr), the causal agent of tan spot, is a necrotrophic fungus that represents a significant threat to wheat production worldwide. The development of resistant cultivars is limited by an incomplete understanding of wheat defence responses against Ptr. Here, weighted gene co-expression network analysis (WGCNA) was applied to RNA-seq data from resistant (Robigus) and susceptible (Hereward) wheat lines before and after Ptr infection to identify coordinated host responses. Eight co-expression modules were identified, three of which were linked to either resistance, susceptibility, or Ptr infection. The resistance-associated module was enriched with chloroplast ribosomal machinery genes (e.g., 50S ribosome-binding GTPase, L28, L6), and transcriptional regulators. This suggested that maintaining chloroplast function, coupled with large-scale transcriptional reprogramming, was important for resistance. The susceptibility-associated module indicated the high expression of post-transcriptional modifiers, including SGS3, RBX1, and SENPs. The Ptr-responsive module showed common responses in both genotypes and included several defence-related genes (nucleotide-binding domain leucine-rich repeat R-genes [NLRs], chitinases, beta-1,3-glucanases) and metabolic pathways, such as phenylpropanoid biosynthesis and nitrogen metabolism (phenylpropanoid ammonia lyase [PAL], cytochrome P450s, glutamine synthase, and ammonium transporters). These results define distinct and shared molecular networks that are linked to resistance and susceptibility, providing valuable candidate genes for functional validation that could ultimately be exploited to enhance wheat resilience against necrotrophic fungal pathogens.

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.