Generation of a <i><scp>ToxA</scp></i> knockout strain of the wheat tan spot pathogen <i><scp>P</scp>yrenophora tritici‐repentis</i>

Moffat, Caroline S.; See, Pao Theen; Oliver, Richard P.

doi:10.1111/mpp.12154

Cited by 45 publications

(38 citation statements)

References 46 publications

(75 reference statements)

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“…However, ToxA epistasis is not apparent in inoculations of the cultivar ‘Glenlea’, where in the absence of ToxA, BFP induces only small necrotic lesions and disease severity is limited ( Fig 3 ). Moffat and colleagues [ 41 ] also inoculated race1Δ toxA isolates on ‘Katepwa’ and ‘Glenlea’, with similar results, although the spreading chlorosis that we visualize in ‘Katewpa’ is not as evident and the extent of disease is reduced in their inoculations. The difference in the appearance of the spreading chlorosis could be because the isolates used in the two studies differ, and therefore are likely to have different suites of HSTs.…”

Section: Discussionsupporting

confidence: 63%

“…In this study, the large-linear fragment approach appears to have resulted in at least one recombinant with multiple fragments inserted, which suggests that the split-marker approach may be best for this organism/genome. A fusion PCR approach was also successfully used to generate a ToxA replacement construct for transformation of an Australian Ptr field isolate, although a different antibiotic was used for selection [ 41 ]. The ability to ‘knockout’ single and ‘silence’ multicopy genes [ 42 , 43 ] are important tools for studying tan spot as both single and multi-copy genes are known to impact virulence [ 44 , 45 ] and others are predicted to play a major role in disease establishment [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

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Necrotrophic Effector Epistasis in the Pyrenophora tritici-repentis-Wheat Interaction

Manning

Ciuffetti

2015

PLoS ONE

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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.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Necrotrophic Effector Epistasis in the Pyrenophora tritici-repentis-Wheat Interaction

Manning

Ciuffetti

2015

PLoS ONE

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“…We have previously examined the degree of correlation between the effector sensitivities of current cultivars of West Australian cultivars and their reported field resistance ( Tan et al, 2014 ). Unlike the tan spot system for which there is a clear dominance of one effector/recogniser interaction (ToxA/ Tsn1 ; Moffat et al, 2014 ), no single effector had a similarly dominating role in SNB. One consideration was that all the current cultivars were sensitive to at least one of these three effectors SnToxA, 1 or 3.…”

Section: Introductionmentioning

confidence: 89%

Functional redundancy of necrotrophic effectors – consequences for exploitation for breeding

et al. 2015

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Necrotrophic diseases of wheat cause major losses in most wheat growing areas of world. Tan spot (caused by Pyrenophora tritici-repentis) and septoria nodorum blotch (SNB; Parastagonospora nodorum) have been shown to reduce yields by 10–20% across entire agri-ecological zones despite the application of fungicides and a heavy focus over the last 30 years on resistance breeding. Efforts by breeders to improve the resistance of cultivars has been compromised by the universal finding that resistance was quantitative and governed by multiple quantitative trait loci (QTL). Most QTL had a limited effect that was hard to measure precisely and varied significantly from site to site and season to season. The discovery of necrotrophic effectors has given breeding for disease resistance new methods and tools. In the case of tan spot in West Australia, a single effector, PtrToxA and its recogniser gene Tsn1, has a dominating impact in disease resistance. The delivery of ToxA to breeders has had a major impact on cultivar choice and breeding strategies. For P. nodorum, three effectors – SnToxA, SnTox1, and SnTox3 – have been well characterized. Unlike tan spot, no one effector has a dominating role. Genetic analysis of various mapping populations and pathogen isolates has shown that different effectors have varying impact and that epistatic interactions also occur. As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex. We have deleted the three effectors in a strain of P. nodorum and measured effector activity and disease potential of the triple knockout mutant. The culture filtrate causes necrosis in several cultivars and the strain causes disease, albeit the overall levels are less than in the wild type. Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate. This indicates that one or more further effectors are secreted into the culture filtrate. We conclude that the in vitro-secreted necrotrophic effectors explain a very large part of the disease response of wheat germplasm and that this method of resistance breeding promises to further reduce the impact of these globally significant diseases.

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“…Yellow spot is a leaf disease that reduces the active photosynthetic area of plants by the formation of necrosis and/or extensive chlorosis. Yield reduction can reach up to 48% (Moffat et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Silicon dioxide and Bacillus subtilis applied in controlling wheat diseases

Telaxka

Faria

Maia

et al. 2019

Agraria

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Wheat is a crop that has high production; however, one of the limitations in planting is the presence of diseases, with the gibberella (Gibberella zeae) and yellow spot (Drechslera tritici-repentis) among them. Thus, the objective of this study was to evaluate the potential of fungicides based on strobilurins, silicon dioxide (SiO 2) and B. subtilis in controlling these diseases in wheat. The used treatments for all the experiments were: T1-SiO 2 ; T2-B. subtilis; T3-SiO 2 + B. subtilis; T4-trifloxystrobin + prothioconazole/trifloxystrobin + tebuconazole; T5-Control. For the field experiment, conducted in two locations, evaluations of the incidence of gibberella and yellow spot severity, crop agronomic characteristics and polyphenoloxidase (PPO) and phenylalanine ammonia-lyase (PAL) activities were carried out. According to the obtained results, the fungicides based on strobilurins and SiO 2 reduced the severity of the yellow spot, increasing, on average, 10 g the weight of a thousand grains (WTG) and the activity of the PPO and PAL enzymes in both municipalities. Hence, SiO 2 possibly activated the defense mechanisms of these plants disease severity.

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Generation of a ToxA knockout strain of the wheat tan spot pathogen Pyrenophora tritici‐repentis

Cited by 45 publications

References 46 publications

Necrotrophic Effector Epistasis in the Pyrenophora tritici-repentis-Wheat Interaction

Necrotrophic Effector Epistasis in the Pyrenophora tritici-repentis-Wheat Interaction

Functional redundancy of necrotrophic effectors – consequences for exploitation for breeding

Silicon dioxide and Bacillus subtilis applied in controlling wheat diseases

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