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Summary: The fungal pathogen, Magnaporthe oryzae Triticum pathotype, causing wheat blast disease was first identified in South America and recently spread across continents to South Asia and Africa. Here, we studied the genetic relationship among isolates found on the three continents.Magnaporthe oryzae strains closely related to a South American field isolate B71 were found to have caused the wheat blast outbreaks in South Asia and Africa. Genomic variation among isolates from the three continents was examined using an improved B71 reference genome and whole‐genome sequences.We found strong evidence to support that the outbreaks in Bangladesh and Zambia were caused by the introductions of genetically separated isolates, although they were all close to B71 and, therefore, collectively referred to as the B71 branch. In addition, B71 branch strains carried at least one supernumerary mini‐chromosome. Genome assembly of a Zambian strain revealed that its mini‐chromosome was similar to the B71 mini‐chromosome but with a high level of structural variation.Our findings show that while core genomes of the multiple introductions are highly similar, the mini‐chromosomes have undergone marked diversification. The maintenance of the mini‐chromosome and rapid genomic changes suggest the mini‐chromosomes may serve important virulence or niche adaptation roles under diverse environmental conditions. [ABSTRACT FROM AUTHOR]

Wheat blast, caused by the Pyricularia oryzae Triticum lineage (PoT), first emerged in Brazil and quickly spread to neighboring countries. Its recent appearance in Bangladesh and Zambia highlights a need to understand the disease's population biology and epidemiology so as to mitigate pandemic outbreaks. Current knowledge is mostly based on characterizations of Brazilian wheat blast isolates and comparison with isolates from non-wheat, endemic grasses. These foregoing studies concluded that the wheat blast population lacks host specificity and, as a result, undergoes extensive gene flow with populations infecting nonwheat hosts. Additionally, based on genetic similarity between wheat blast and isolates infecting Urochloa species, it was proposed that the disease originally emerged via a host jump from this grass and that Vrochloa likely plays a central role in wheat blast epidemiology owing to its widespread use as a pasture grass. However, due to inconsistencies with broader phylogenetic studies, we suspected that these seminal studies had not actually sampled the populations normally found on endemic grasses and, instead, had repeatedly isolated members of PoT and the related Lolium pathogen lineage (PoLl). Re-analysis of the Brazilian data as part of a comprehensive, global, phylogenomic dataset that included a small number of South American isolates sampled away from wheat confirmed our suspicion and identified four new P. oryzae lineages on grass hosts. As a result, the conclusions underpinning current understanding in wheat blast's evolution, population biology, and epidemiology are unsubstantiated and could be equivocal. [ABSTRACT FROM AUTHOR]

Resistance to wheat spike blast (WSB), caused by the Magnaporthe oryzae triticum pathotype (MoT), has relied upon a single major source: the 2NvS translocation introgressed from the wild relative Aegilops ventricosa Tausch. However, this resistance is partial and recently partially overcome by newer MoT races. To characterize potential novel loci conferring resistance to WSB, we conducted a genome‐wide association study (GWAS) using a diverse panel of 384 wheat genotypes phenotyped under three controlled‐environment conditions using MoT isolates T‐25 (301 genotypes), B‐71 (87 genotypes), and 008 (49 genotypes). Genotyping‐by‐sequencing identified 13,175 single nucleotide polymorphisms (SNPs) after filtering. Principal components analysis (PCA) identified two clusters based on the presence or absence of the 2NvS translocation, and the first three PCAs explained 13% of the genetic variation. Three individual analyses were performed (full [all genotypes combined], 2NvS genotypes only, and non‐2NvS genotypes only) using a linear mixed model and a threshold of significance of false discovery rate at 5%. Association analysis detected 25 significant SNPs for the full GWAS with isolate T‐25, in which 21 were mapped on chromosome 2A in the same physical position as the 2NvS translocation. Highly significant linkage disequilibrium among these SNPs suggested they might tag the same quantitative trait locus (QTL). No significant associations were identified with isolates B‐71 and 008, likely due to the small sample size. A QTL pyramiding analysis showed that the combination of multiple QTL was not statistically different from the individual effect of the 2A QTL. Further validation of these genomic regions can aid breeding for broad spectrum and durable WSB resistance. [ABSTRACT FROM AUTHOR]

Newly emerged wheat blast disease is a serious threat to global wheat production. Wheat blast is caused by a distinct, exceptionally diverse lineage of the fungus causing rice blast disease. Through sequencing a recent field isolate, we report a reference genome that includes seven core chromosomes and mini-chromosome sequences that harbor effector genes normally found on ends of core chromosomes in other strains. No mini-chromosomes were observed in an early field strain, and at least two from another isolate each contain different effector genes and core chromosome end sequences. The mini-chromosome is enriched in transposons occurring most frequently at core chromosome ends. Additionally, transposons in mini-chromosomes lack the characteristic signature for inactivation by repeat-induced point (RIP) mutation genome defenses. Our results, collectively, indicate that dispensable mini-chromosomes and core chromosomes undergo divergent evolutionary trajectories, and mini-chromosomes and core chromosome ends are coupled as a mobile, fast-evolving effector compartment in the wheat pathogen genome. [ABSTRACT FROM AUTHOR]

This is a response to a recent Letter to the Editor of Phytopathology, in which Gupta et al. (2019) caution against the indiscriminate use of the MoT3 diagnostic assay that distinguishes isolates of Magnaporthe oryzae in the Triticum lineage from those that do not cause aggressive wheat blast. We confirm that the assay does reliably distinguish between wheat and rice isolates from Bangladesh and worldwide, as described in the original paper by Pieck et al. (2017). We have been unable to reproduce the equally intense amplification of WB12 and WB 12-like sequences reported in Figure 1 of the Letter. Other data presented by Gupta et al. (2019) support the specificity of the MoT3 assay. Therefore, cautions beyond those always associated with accurate reproduction of diagnostic assays are unwarranted. [ABSTRACT FROM AUTHOR]

• We quantified the yield benefits of fungicide to wheat using plot and survey data. • Fungicide yield benefits (7.8 ± 15 %) were greater in wetter growing seasons. • Susceptible genotypes benefited more from fungicides (17 %) than resistant ones (6 %). • Fungicides improved stability and modified environment-adaptability of genotypes. • Fungicide yield benefits were greater (31 %) in the survey data. Foliar fungicides can account for a large portion of the yield gap in winter wheat (Triticum aestivum L.); however, their impacts on yield have been inconsistent in rainfed environments. We compiled a database of replicated field experiments and producer-reported fungicide and yield data from commercial fields to quantify the effects of fungicide application on winter wheat yield and yield stability. The database of field experiments (i.e., canopy level) included 56 non-inoculated environments spanning 12 growing seasons in eight Kansas locations, and was restricted to field experiments with direct comparisons between a foliar fungicide between Zadoks 40–55 and a side-by-side untreated control, resulting in 393 mean yield comparisons resulting from 3226 yield observations. The producer survey included genotype and fungicide management data from 654 commercial Kansas wheat fields cultivated across three growing seasons. Grain yield and weather conditions in the experimental and producer-reported database were similar, with seasonal precipitation ranging from ˜150 to 1035 mm and average grain yield of ˜3900 kg ha−1 with a ˜7000 kg ha−1 range. Foliar fungicide application resulted in 7.8 % average yield gain in the canopy-level data, ranging from −27 % to +97 %. Yield differences due to fungicide were strongly related to precipitation and to the ratio of precipitation and reference evapotranspiration (WS:WD) during the spring in the experimental data. Grain yield responsiveness to fungicide associated with the responsiveness of green canopy cover, kernel weight, biomass, and harvest index. Analysis of covariance suggested that grain yield usually decreased with increases in disease susceptibility in the absence of foliar fungicides; however, yield-disease relationships were either neutral or positive in the presence of fungicides. Average yield gain for resistant varieties was ˜166 kg ha−1 (5.6 %), which was lower than for intermediate (˜199 kg ha−1; 6.9 %) or susceptible genotypes (˜598 kg ha−1; 16.9 %). Foliar fungicides increased yield stability across genotypes at the canopy level and at the commercial field level. In the commercial-field level data, 53 % of the fields received foliar fungicide, with higher frequency in growing seasons with greater WS:WD (which were also higher yielding). The use of foliar fungicides was associated with improved yields and interacted with genotype's resistance level to stripe rust and with growing seasons' WS:WD. This work quantified and explained the yield benefits of foliar fungicide, and characterized its dependency on genotype-specific disease resistance and environmental conditions both at the canopy- and commercial field-levels. [ABSTRACT FROM AUTHOR]