Pathogenic variation of Pyrenophora teres f. teres in Australia

Fowler, Ryan; Platz, G. J.; Bell, Kerry L.; Fletcher, S.; Franckowiak, J. D.; Hickey, Lee T.

doi:10.1007/s13313-017-0468-1

Cited by 23 publications

(41 citation statements)

References 53 publications

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“…Oxford (NB2016-045 and NB2016-047) or were shown to be virulent in pathotype tests (data not shown). NB2016-045 also showed virulence on the cultivar Skiff, which is common in South Australia and the eastern states and absent from WA where that cultivar has not been grown (Fowler et al, 2017). Following removal of the 2016 isolates from the PCA analysis, six (NB2015-20, NB2015-29, NB2015-30, NB2015-35, NB2015-36 and NB2015-42) were still juxtaposed with isolates from a different regional genetic group.…”

Section: Discussionmentioning

confidence: 99%

“…PTT populations are capable of adapting to cultivars common in particular regions leading to changes in their pathotype composition (Tekauz, 1990;Liu et al, 2012;Akhavan et al, 2016a;Fowler et al, 2017). In addition, PTT can mutate to acquire resistance to fungicides.…”

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confidence: 99%

“…Several studies have examined pathotype variation in Western Australia (WA; Khan & Boyd, 1969;Khan, 1982;Gupta & Loughman, 2001;Fowler et al, 2017), a region where barley cultivation is relatively recent and geographically isolated. However, data for PTT genetic variation in WA has so far been limited to a wide-scale study involving nine WA isolates collected over a 32-year period by Lehmensiek et al (2010) and 19 isolates by Serenius et al (2007).…”

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confidence: 99%

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Genetic variation of Pyrenophora teres f. teres isolates in Western Australia and emergence of a Cyp51A fungicide resistance mutation

et al. 2018

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Genome‐wide, unlinked, simple sequence repeat markers were used to examine genetic variation and relationships within Pyrenophora teres f. teres, a common pathogen of barley, in Western Australia. Despite the region's geographic isolation, the isolates showed relatively high allelic variation compared to similar studies, averaging 7.11 alleles per locus. Principal component, Bayesian clustering and distance differentiation parameters provided evidence for both regional genotypic subdivision together with juxtaposing of isolates possessing different genetic backgrounds. Genotyping of fungicide resistant Cyp51A isolates indicated a single mutation event occurred followed by recombination and long‐distance regional dispersal over hundreds of kilometres. Selection of recently emergent favourable alleles such as the Cyp51A mutation and a cultivar virulence may provide an explanation, at least in part, for juxtaposed genotypes. Factors affecting genotypic composition and the movement of new genotypes are discussed in the context of grower practices and pathogen epidemiology, together with the implications for resistance breeding.

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Section: Discussionmentioning

confidence: 99%

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Genetic variation of Pyrenophora teres f. teres isolates in Western Australia and emergence of a Cyp51A fungicide resistance mutation

et al. 2018

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“…P. teres f. maculata has become more prevalent in North Dakota (Liu and Friesen, ) and Idaho, USA (Marshall et al , ) and Victoria, Australia (McLean et al , ), but this likely depends on the susceptibility of the predominant cultivars planted in each region. Multiple differential barley sets have been proposed to classify global pathotypes of P. teres f. teres (Afanasenko et al , , ; Fowler et al , ) and P. teres f . maculata isolates in local populations (McLean et al , , ).…”

Section: Introductionmentioning

confidence: 99%

“…Multiple studies have shown that different virulence profiles exist within P. teres populations around the globe (Akhavan et al , ; Arabi et al , ; Cromey and Parkes, ; Fowler et al , ; Gupta and Loughman, ; Harrabi and Kamel, ; Jalli and Robinson, ; Jonsson et al , ; Khan and Boyd, ; Liu et al , ; McLean et al , ; Robinson and Jalli, ; Sato and Takeda, ; Steffenson and Webster, ; Tekauz, ; Wu et al , ). Virulence variation among isolates on different barley lines appears to originate from their segregating effector repertoire, many of which are now believed to be proteinaceous in nature (Liu et al , ; Richards et al , ).…”

Section: Introductionmentioning

confidence: 99%

Research advances in the Pyrenophora teres–barley interaction

Clare

Wyatt

Brueggeman

et al. 2019

Molecular Plant Pathology

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Summary Pyrenophora teres f. teres and P. teres f. maculata are significant pathogens that cause net blotch of barley. An increased number of loci involved in P. teres resistance or susceptibility responses of barley as well as interacting P. teres virulence effector loci have recently been identified through biparental and association mapping studies of both the pathogen and host. Characterization of the resistance/susceptibility loci in the host and the interacting effector loci in the pathogen will provide a path for targeted gene validation for better‐informed release of resistant barley cultivars. This review assembles concise consensus maps for all loci published for both the host and pathogen, providing a useful resource for the community to be used in pathogen characterization and barley breeding for resistance to both forms of P. teres.

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Workflows for detecting fungicide resistance in net form and spot form net blotch pathogens

Knight,

Adhikari,

Dodhia

et al. 2024

Pest Management Science

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BACKGROUNDFungicide resistance in Pyrenophora teres f. maculata and P. teres f. teres has become an important disease management issue. Control of the associated barley foliar diseases, spot form and net form net blotch, respectively, relies on three major groups of fungicides, demethylation inhibitors (DMI), succinate dehydrogenase inhibitors (SDHI) and quinone outside inhibitors (QoI). However, resistance has been reported for the DMI and SDHI fungicides in Australia. To enhance detection of different resistance levels, phenotyping and genotyping workflows were designed.RESULTSThe phenotyping workflow generated cultures directly from lesions and compared growth on discriminatory doses of tebuconazole (DMI) and fluxapyroxad (SDHI). Genotyping real‐time PCR assays were based on alleles associated with sensitivity or resistance to the DMI and SDHI fungicides. These workflows were applied to spot form and net form net blotch collections from 2019 consisting predominantly of P. teres f. teres from South Australia and P. teres f. maculata from Western Australia. For South Australia the Cyp51A L489‐3 and SdhC‐R134 alleles, associated with resistance to tebuconazole and fluxapyroxad, respectively, were the most prevalent. These alleles were frequently found in single isolates with dual resistance. This study also reports the first detection of a 134 base pair insertion located at position −66 (PtTi‐6) in the Cyp51A promoter of P. teres f. maculata from South Australia. For Western Australia, the PtTi‐1 insertion was the most common allele associated with resistance to tebuconazole.CONCLUSIONThe workflow and PCR assays designed in this study have been demonstrated to efficiently screen P. teres collections for both phenotypic and genetic resistance to DMI and SDHI fungicides. The distribution of reduced sensitivity and resistance to DMI and SDHI fungicides varied between regions in south‐western Australia, suggesting the emergence of resistance was impacted by both local pathogen populations and disease management programs. The knowledge of fungicide resistance in regional P. teres collections will be important for informing appropriate management strategies.This article is protected by copyright. All rights reserved.

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Pathogenic variation of Pyrenophora teres f. teres in Australia

Cited by 23 publications

References 53 publications

Genetic variation of Pyrenophora teres f. teres isolates in Western Australia and emergence of a Cyp51A fungicide resistance mutation

Genetic variation of Pyrenophora teres f. teres isolates in Western Australia and emergence of a Cyp51A fungicide resistance mutation

Research advances in the Pyrenophora teres–barley interaction

Workflows for detecting fungicide resistance in net form and spot form net blotch pathogens

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