Pyrenophora tritici-repentis Pt-1C-BFP
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ABSTRACT:
PROVIDER: PRJNA18815 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| AAXI01.dat.gz | Other | |||
| AAXI01.fasta.gz | Fasta.gz | |||
| AAXI01.master.dat | Other | |||
| AAXI01.dat.gz | Other |
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Similar Datasets
Project description:Pyrenophora tritici-repentis Genome sequencing and assembly
| PRJNA315205 | ENA
Project description:Tan spot is a destructive foliar wheat disease worldwide and caused by the ascomycete fungus Pyrenophora tritici-repentis (Ptr); it has become more frequent in Tunisia over the last decade. In this study, the virulence of 73 single-spore isolates, collected from durum and bread wheat fields during 2017-2018 growing season, was evaluated on four differential wheat genotypes. This was followed by polymerase chain reaction tests with specific primers for the effector genes ToxA, ToxB, and toxb (ToxB-homolog). Sequence analysis to validate the identity of the amplified genes was followed, and ToxA amplicons from a subset of 22 isolates were analyzed to determine its haplotype identity. Ptr isolates from Tunisia were grouped in races 2, 4, 5, and 7, and 44% of the tested isolates did not fit under any known race, and were denoted here as atypical. These atypical isolates induced the same symptoms as race 7 isolates, extensive necrosis, and chlorosis on susceptible genotypes, but lacked the ToxA gene. ToxA is the only identified necrosis-inducing effector in Ptr, and was amplified in 51% of tested isolates, and shared identical sequence to previously identified haplotype (H15). ToxB and its homolog toxb were present in 97% and 93% of tested isolates, respectively. Ptr in Tunisia lacked Ptr ToxC activity, and none of the tested isolates induced the specific symptoms of that effector. Race 7 and the atypical isolates dominated the Tunisian Ptr population, while races 2, 4, and 5 were found at low percentages. In conclusion, ToxB and its homolog were the most dominant genes in Ptr from Tunisia, and the majority of the isolates induced necrosis and chlorosis on Ptr ToxA and Ptr ToxB susceptible wheat genotypes. However, only about half of that necrosis can be attributed to ToxA presence, this result necessitates further research to investigate the prevalence of additional necrotic effector(s). Terminology: in this paper, Pyrenophora tritici-repentis abbreviated as Ptr, the effectors are referred to by Ptr ToxA, Ptr ToxB and Ptr ToxC, and the genes coding for them are written in italic as ToxA, ToxB, and ToxC, respectively.
| S-EPMC6930679 | biostudies-literature
Project description:Pyrenophora tritici-repentis, the causal agent of tan spot disease of wheat, mediates disease by the production of host-selective toxins (HST). The known toxins are recognized in an 'inverse' gene-for-gene manner, where each is perceived by the product of a unique locus in the host and recognition leads to disease susceptibility. Given the importance of HSTs in disease development, we would predict that the loss of any of these major pathogenicity factors would result in reduced virulence and disease development. However, after either deletion of the gene encoding the HST ToxA or, reciprocally, heterologous expression of ToxA in a race that does not normally produce the toxin followed by inoculation of ToxA-sensitive and insensitive wheat cultivars, we demonstrate that ToxA symptom development can be epistatic to other HST-induced symptoms. ToxA epistasis on certain ToxA-sensitive wheat cultivars leads to genotype-specific increases in total leaf area affected by disease. These data indicate a complex interplay between host responses to HSTs in some genotypes and underscore the challenge of identifying additional HSTs whose activity may be masked by other toxins. Also, through mycelial staining, we acquire preliminary evidence that ToxA may provide additional benefits to fungal growth in planta in the absence of its cognate recognition partner in the host.
| S-EPMC4386829 | biostudies-literature
Project description:Tan Spot (TS), causal agent Pyrenophora tritici-repentis (Ptr), is a major threat to wheat production due to the lack of resistant cultivars. In our previous work, we identified MAGIC population parental lines exhibiting TS resistance and susceptibility, namely Robigus and Hereward, respectively. To understand the mechanisms underlying these phenotypes, we performed RNA-seq analysis of leaves before and during Ptr interaction. When comparing mock- and Ptr-inoculated samples, differentially expressed genes (DEGs) were identified with DESeq2, leading to the targeting of 15193 DEGs. Functional annotation showed the pathways enzyme classification, solute transport, RNA biosynthesis, protein modification and homeostasis represented 49.5% of DEGs in Robigus. Cellular metabolism pathways were induced, as well as vesicle trafficking, actin polymerization and cellulose. The upregulation of these cell wall related genes along with microscopic data suggested that barrier defence is a major feature of TS resistance in Robigus. Conversely, photosynthesis was the top fifth pathway in Hereward, totalling 389 repressed genes (12.63%). Photosynthesis collapse was linked to the activation of oligosaccharide metabolism and suppression of glycolysis, TCA cycle and amino acids degradation. This may reflect mobilization of host nutrients to Ptr. Our observations could inform wheat-breeding programmes targeting TS resistance.
2022-06-30 | GSE202986 | GEO
Project description:The ToxA effector is a major virulence gene of Pyrenophora tritici-repentis (Ptr), a necrotrophic fungus and the causal agent of tan spot disease of wheat. ToxA and co-located genes are believed to be the result of a recent horizontally transferred highly conserved 14kb region a major pathogenic event for Ptr. Since this event, monitoring isolates for pathogenic changes has become important to help understand the underlying mechanisms in play. Here we examined ToxA in 100 Ptr isolates from Australia, Europe, North and South America and the Middle East, and uncovered in isolates from Denmark, Germany and New Zealand a new variation, a novel 166 bp insertion element (PtrHp1) which can form a perfectly matched 59 bp inverted repeat hairpin structure located downstream of the ToxA coding sequence in the 3' UTR exon. A wider examination revealed PtrHp1 elements to be distributed throughout the genome. Analysis of genomes from Australia and North America had 50-112 perfect copies that often overlap other genes. The hairpin element appears to be unique to Ptr and the lack of ancient origins in other species suggests that PtrHp1 emerged after Ptr speciation. Furthermore, the ToxA UTR insertion site is identical for different isolates, which suggests a single insertion event occurred after the ToxA horizontal transfer. In vitro and in planta-detached leaf assays found that the PtrHp1 element insertion had no effect on ToxA expression. However, variation in the expression of ToxA was detected between the Ptr isolates from different demographic locations, which appears to be unrelated to the presence of the element. We envision that this discovery may contribute towards future understanding of the possible role of hairpin elements in Ptr.
| S-EPMC6209302 | biostudies-literature
Project description:OBJECTIVES:Tan spot is a yield-reducing disease that affects wheat and is caused by the fungus Pyrenophora tritici-repentis (Ptr). Eight races of Ptr have been identified based upon production of the effectors Ptr ToxA, Ptr ToxB, and Ptr ToxC. Wheat cultivars have also been characterized by their resistance and susceptibility to races of Ptr and sensitivity to the effectors. The objective of this research was to assess differences in gene expression between Ptr resistant and susceptible wheat cultivars when either inoculated with Ptr race 2 spores or directly infiltrated with Ptr ToxA. DATA DESCRIPTION:A greenhouse experiment was used to assess wheat-Ptr interaction. Wheat seedlings were grown for two weeks prior to the experiment under greenhouse conditions. Four treatments were used: (1) spray-inoculation with a suspension of Ptr spores (3000 spores/mL) (2) spray inoculation with water as a control (3) needleless syringe injection with Ptr ToxA, and (4) needleless syringe injection with water as a control. Plants were transferred to a humidity chamber and leaf sample were taken at 0, 8, and 16 h. After RNA extraction and sequencing, 48 RNA datasets are reported. This data will be useful in understanding how resistant wheat responds to Ptr compared to susceptible wheat.
| S-EPMC6670118 | biostudies-literature
Project description:Pathogenic fungus that causes tan spot of wheat
| PRJNA18823 | ENA
Project description:BackgroundThe necrotrophic fungal pathogen Pyrenophora tritici-repentis (Ptr) causes tan (syn. yellow) spot of wheat and accounts for significant yield losses worldwide. Understanding the molecular mechanisms of this economically important crop disease is crucial to counteract the yield and quality losses of wheat globally. Substantial progress has been made to comprehend the race structure of this phytopathogen based on its production of necrotrophic effectors and genomic resources of Ptr. However, one limitation for studying Ptr in a laboratory environment is the difficulty to isolate high spore numbers from vegetative growth with mycelial contamination common. These limitations reduce the experimental tractability of Ptr.ResultsHere, we optimized a multitude of parameters and report a sporulation method for Ptr that yields robust, high quality and pure spores. Our methodology encompasses simple and reproducible plugging and harvesting techniques, resulting in spore yields up to 1500 fold more than the current sporulation methods and was tested on multiple isolates and races of Ptr as well as an additional seven modern Australian Ptr isolates. Moreover, this method also increased purity and spore harvest numbers for two closely related fungal pathogens (Pyrenophora teres f. maculata and f. teres) that cause net blotch diseases in barley (Hordeum vulgare), highlighting the usability of this optimized sporulation protocol for the wider research community.ConclusionsLarge-scale spore infection and virulence assays are essential for the screening of wheat and barley cultivars and combined with the genetic mapping of these populations allows pinpointing and exploiting sources of host genetic resistance. We anticipate that improvements in spore numbers and purity will further advance research to increase our understanding of the pathogenicity mechanisms of these important fungal pathogens.
| S-EPMC8136220 | biostudies-literature
Project description:The fungus Pyrenophora tritici-repentis (Ptr) causes tan spot, a destructive foliar disease of wheat worldwide. The pathogen produces several necrotrophic effectors, which induce necrosis or chlorosis on susceptible wheat lines. Multiple races of Ptr have been identified, based on their ability to produce one or more of these effectors. Ptr has a wide host range of cereal and non-cereal grasses, but is known to cause damage only on wheat. Previously, we showed that Ptr can interact specifically with cultivated barley (Hordeum vulgare ssp. vulgare), and that the necrotrophic effector Ptr ToxB induces mild chlorosis in a highly selective manner when infiltrated into certain barley genotypes. In the present study, a barley doubled-haploid (DH) population was evaluated for reaction to Ptr race 5, a Ptr ToxB-producer. Then a comprehensive genetic map composed of 381 single nucleotide polymorphism (SNP) markers was used to map the locus conditioning this chlorosis. The F1 seedlings, and 92 DH lines derived from a cross between the resistant Japanese malting barley cultivar Haruna Nijo and the susceptible wild barley (H. vulgare ssp. spontaneum) OUH602 were inoculated with a conidial suspension of Ptr race 5 isolate at the two-leaf stage. The seedlings were monitored daily for symptoms and assessed for chlorosis development on the second leaf, 6 days after inoculation. All tested F1 seedlings exhibited chlorosis symptoms similar to the susceptible parent, and the DH lines segregated 1:1 for susceptible:resistant phenotypes, indicating the involvement of a single locus. Marker-trait linkage analysis based on interval mapping identified a single locus on the distal region of the short arm of chromosome 2H. We designate this locus Susceptibility to P. tritici-repentis1 (Spr1). The region encompassing this locus has 99 high confidence gene models, including membrane receptor-like kinases (RLKs), intracellular nucleotide-binding, leucine-rich repeat receptors (NLRs), and ankyrin-repeat proteins (ANKs). This shows the involvement of a dominant locus conferring susceptibility to Ptr in barley. Further work using high-resolution mapping and transgenic complementation will be required to identify the underlying gene.
| S-EPMC7059616 | biostudies-literature
Project description: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.
| S-EPMC6778365 | biostudies-literature