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The virulence of 57 Australian isolates of Pyrenophora tritici‐repentis (Ptr), a necrotrophic fungal pathogen responsible for the major wheat disease tan spot, was assessed through plant infection assays. Isolates collected from the northern, southern, and western wheat‐cropping regions of Australia were evaluated against 16 Australian bread wheat cultivars under controlled growth conditions. Following infection, the wheat panel displayed varying disease symptoms ranging from tiny necrotic specks to spreading chlorotic and necrotic lesions. Analysis of variance indicated that the wheat cultivar exhibited a greater effect on the disease response, explaining 62.7% of the variation, in comparison to the isolate (10.4%). The interaction between the cultivar and the isolate was statistically significant and was attributed to 9.8% of the total variation. All Ptr isolates examined were able to cause disease, but did not display a clear distinction in virulence on the wheat panel investigated, instead showing subtle differences in aggressiveness. Based on the disease responses, there was no obvious pattern between isolate aggressiveness and cropping region. Some cultivars, such as Hydra, exhibited an effective level of resistance in relation to the panel of isolates tested. All 57 Ptr isolates were found to possess the ToxA effector gene and lack the ToxB effector gene. The gene expression level of ToxA was up‐regulated at 3 days postinfection in both ToxA‐sensitive and ‐insensitive cultivars, independent of ToxA–Tsn1 recognition. [ABSTRACT FROM AUTHOR]

Objectives: The assembly of fungal genomes using short-reads is challenged by long repetitive and low GC regions. However, long-read sequencing technologies, such as PacBio and Oxford Nanopore, are able to overcome many problematic regions, thereby providing an opportunity to improve fragmented genome assemblies derived from short reads only. Here, a necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr) isolate 134 (Ptr134), which causes tan spot disease on wheat, was sequenced on a MinION using Oxford Nanopore Technologies (ONT), to improve on a previous Illumina short-read genome assembly and provide a more complete genome resource for pan-genomic analyses of Ptr. Results: The genome of Ptr134 sequenced on a MinION using ONT was assembled into 28 contiguous sequences with a total length of 40.79 Mb and GC content of 50.81%. The long-read assembly provided 6.79 Mb of new sequence and 2846 extra annotated protein coding genes as compared to the previous short-read assembly. This improved genome sequence represents near complete chromosomes, an important resource for large scale and pan genomic comparative analyses. [ABSTRACT FROM AUTHOR]

Abstract Objectives The fungus Pyrenophora tritici-repentis is a major pathogen of wheat worldwide, causing the leaf spotting disease tan spot. To best inform approaches for plant genetic resistance, an understanding of the biology and pathogenicity mechanisms of this fungal pathogen is essential. Here, intracellular and extracellular proteins of P. tritici-repentis were extracted, and peptides analysed via high-resolution mass spectrometry. Our objective was to generate a useful proteomics resource for P. tritici-repentis. A survey of proteins secreted by the pathogen into culture filtrate is especially useful, as these are likely to come in direct contact with the wheat host and may play important roles in infection/pathogenicity. The peptide data presented herein, has also been used to successfully verify and refine in silico predicted P. tritici-repentis gene annotations, through the validation of alternative splicing and reading frame shifts. Data description The data sets presented consist of peptide spectra of the extracellular and intracellular proteomes of three P. tritici-repentis isolates. Peptide matches to translated transcripts of the North American reference isolate Pt-1C-BFP are also provided.

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable.

Here, we evaluate the expression of the proteinaceous effectors ToxA and ToxB, produced by the necrotrophic fungal pathogen Pyrenophora tritici-repentis , which confer tan spot disease susceptibility on wheat. These necrotrophic effectors were expressed in two heterologous systems: Escherichia coli and Pichia pastoris. The E. coli SHuffle system was demonstrated to be superior to P. pastoris in generating high-levels of recombinant proteins that were soluble and stable. In addition, protein extracts from P. pastoris induced non-specific chlorosis on wheat, postulated to be caused by co-purified glucanases secreted by the host. Up to 79.6 μg/ml of ToxB was obtained using the SHuffle system in the absence of the native signal peptide, whilst the ToxA yield was considerably lower at 3.2 μg/ml. Results indicated that a histidine tag at the ToxA C-terminus interfered with effector functionality. Heterologously expressed ToxA and ToxB were tested on a panel of Australian cereals, including 122 varieties of bread wheat, 16 durum, 20 triticale and 5 barley varieties, as well as common plant model species including tobacco and Arabidopsis thaliana. A varying degree of effector sensitivities was observed, with a higher ToxB sensitivity and prevalence in the durum and triticale varieties. ToxB-induced chlorosis was also detected on barley. The heterologous expression of effectors that are easily scalable, will facilitate effector-assisted selection of varieties in wheat breeding programs as well as the investigation of P. tritici-repentis effectors in host and non-host interactions. [ABSTRACT FROM AUTHOR]

The necrotrophic fungal pathogen Pyrenophora tritici‐repentis (Ptr) causes the major wheat disease tan spot, and produces multiple necrotrophic effectors that contribute to virulence. The proteinaceous effector ToxA induces necrosis in wheat genotypes possessing the Tsn1 gene, although the importance of the ToxA–Tsn1 interaction itself in varietal disease development has not been well studied. Here, 40 Australian spring wheat varieties were assessed for ToxA sensitivity and disease response to a race 1 wildtype Ptr isolate and ToxA‐deleted strain at both seedling and tillering growth stages. ToxA sensitivity was generally associated with disease susceptibility, but did not always predict spreading necrotic symptoms. Whilst the majority of Tsn1 varieties exhibited lower disease scores following toxa mutant infection, several exhibited no distinct differences between wildtype and toxa symptoms. This implies that ToxA is not the major determinant in tan spot disease development in some host backgrounds and indicates the presence of additional effectors. Unexpectedly, several tsn1 varieties exhibited a reduction in disease severity following toxa mutant inoculation, which may suggest an indirect role for ToxA in pathogen fitness. Additionally, increased chlorosis was observed following toxa mutant infection in three varieties, and further work is required to determine whether this is likely to be due to ToxA epistasis of ToxC symptoms. Taken together, these observations demonstrate that Ptr interacts with the host in a complex and intricate manner, leading to a variety of disease reactions that are dependent or independent of the ToxA–Tsn1 interaction. [ABSTRACT FROM AUTHOR]

Objectives: The fungus Pyrenophora tritici-repentis is a major pathogen of wheat worldwide, causing the leaf spotting disease tan spot. To best inform approaches for plant genetic resistance, an understanding of the biology and pathogenicity mechanisms of this fungal pathogen is essential. Here, intracellular and extracellular proteins of P. triticirepentis were extracted, and peptides analysed via high-resolution mass spectrometry. Our objective was to generate a useful proteomics resource for P. tritici-repentis. A survey of proteins secreted by the pathogen into culture filtrate is especially useful, as these are likely to come in direct contact with the wheat host and may play important roles in infection/pathogenicity. The peptide data presented herein, has also been used to successfully verify and refine in silico predicted P. tritici-repentis gene annotations, through the validation of alternative splicing and reading frame shifts. Data description: The data sets presented consist of peptide spectra of the extracellular and intracellular proteomes of three P. tritici-repentis isolates. Peptide matches to translated transcripts of the North American reference isolate Pt- 1C-BFP are also provided. [ABSTRACT FROM AUTHOR]

This work was done to demonstrate the opportunities provided by application of meta-analysis in plant pathology. It was a case study used to determine the effectiveness of foliar fungicides in minimising yield loss from a complex of yellow spot ( Pyrenophora tritici- repentis) and septoria nodorum blotch ( Stagonospora nodorum, teleomorph: Phaeosphaeria nodorum) (YS-SNB disease complex) on wheat in the northern grain-belt of Western Australia. Forty-seven datasets of experimental results from 14 growing seasons, using 18 varieties sprayed one to three times, predominantly with tebuconazole or propiconazole fungicides, were analysed. Across the datasets, the wheat yield gain from fungicide application was 297 kg ha with a 95 % confidence interval of 11.6 kg ha. Significant yield gains resulted from single or multiple applications of fungicides. Both propiconazole and tebuconazole, increased yield of wheat affected by the YS-SNB disease complex, with yield gain from propiconazole being greater than that from tebuconazole. Yield response varied significantly among crop growing seasons. Meta-analysis was able to aggregate a large number of experimental results and answer important questions related to the variables that influenced those results; in this case the effectiveness of fungicides in minimising yield loss from the YS-SNB disease complex on wheat. It also identified areas where further research needs to be done. It is concluded that meta-analysis has the potential to contribute to similar analyses in other crop disease systems. [ABSTRACT FROM AUTHOR]

Abstract: Tan spot, caused by Pyrenophora tritici-repentis (Died.) Drechs., is an important constraint to wheat (Triticum aestivum L.) yield in many countries. Since the inheritance of field resistance to tan spot is poorly understood, this study was conducted to determine the genetic control of resistance in the field. Resistance was measured as disease severity caused by P. tritici-repentis race 1 in four crosses involving five wheat parents: parent 1 (P1)=catbird; parent 2 (P2)=Milan/Shanghai-7; parent 3 (P3)=Alondra/Coc//Ures; parent 4 (P4)=Bcb//Dundee/Gul/3/Gul); parent 5 (P5)=ND/VG9144//Kal/BB/3/Yaco/4/Chil. P1, P2 and P3 were resistant and P4 was moderately resistant, whereas P5 was susceptible to tan spot. The F2-derived F3 families and the parents were field evaluated at El Batán, Mexico, in 1996. When all the plants within a F3 family expressed low levels of disease severity similar to that of the resistant parent it was classified resistant (R), otherwise the progeny was classified as susceptible (S). The progeny of the three crosses of the susceptible parent with the resistant and moderately resistant parents P2, P3, and P4 segregated as 3R:13S whereas the progeny in the cross with P1 showed a segregation ratio of 1R:15S. This suggests that each resistant parent possessed two genes conditioning resistance to tan spot severity caused by P. tritici-repentis race 1. Information on the inheritance of resistance measured as disease severity on adult plants under field conditions is of practical importance for wheat breeding programs seeking improvement in tan spot resistance. [Copyright &y& Elsevier]

The incidence of wheat head infection by Pyrenophora tritici-repentis (Ptr), the etiological agent of tan spot disease, was evaluated during grain development in a glasshouse experiment. Heads artificially inoculated with a Ptr spore suspension developed widespread brown spots across the spikelets, and mycelia and conidophores were observed on glumes and awns. Seeds of heavily infected heads were darkened and shrivelled, but no red smudge symptoms were apparent. The recovery rate of Ptr isolates from the inoculated wheat heads was low, and colonies that were re-isolated displayed an irregular morphology with reddish mycelia when grown on agar plates. The presence of Ptr on inoculated wheat heads was assessed directly via PCR detection, and a limitation of Ptr hyphae to proliferate beyond the point of contact of spore inoculum on floret tissues was observed. The systemic transmission of Ptr from infected seeds was minimal; however, saprophytic growth of the pathogen occurred on the senescing leaves of wheat plants grown from inoculated seeds. Thus, even though Ptr seed infection is not as common as foliar infection, infected seeds are still a source of disease inoculum and screening for pathogen contamination is advisable. [ABSTRACT FROM AUTHOR]

Objectives: The necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr) is the causal agent of tan spot a major disease of wheat. We have generated a new genome resource for an Australian Ptr race 1 isolate V1 to support comparative 'omics analyses. In particular, the V1 PacBio Biosciences long-read sequence assembly was generated to confirm the stability of large-scale genome rearrangements of the Australian race 1 isolate M4 when compared to the North American race 1 isolate Pt-1C-BFP. Results: Over 1.3 million reads were sequenced by PacBio Sequel small-molecule real-time sequencing (SRMT) cell to yield 11.4 Gb for the genome assembly of V1 (285X coverage), with median and maximum read lengths of 8959 bp and 72,292 bp respectively. The V1 genome was assembled into 33 contiguous sequences with a of total length 40.4 Mb and GC content of 50.44%. A total of 14,050 protein coding genes were predicted and annotated for V1. Of these 11,519 genes were orthologous to both Pt-1C-BFP and M4. Whole genome alignment of the Australian long-read assemblies (V1 to M4) confirmed previously identified large-scale genome rearrangements between M4 and Pt-1C-BFP and presented small scale variations, which included a sequence break within a race-specific region for ToxA, a well-known necrotrophic effector gene. [ABSTRACT FROM AUTHOR]