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

Ellwood, Simon R.; Piscetek, V.; Mair, Wesley J.; Lawrence, Julie; Lopez‐Ruiz, Francisco J.; Rawlinson, C. J.

doi:10.1111/ppa.12924

Cited by 22 publications

(24 citation statements)

References 45 publications

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“…Model-based genetic structuring analysis of 188 P. teres f. teres isolates indicated that the most likely number of clusters is two. This is the same number of K groups as identified by Ellwood et al (2019) using isolates from Western Australia only. An association between the clusters and some of the phenotypic assessments of the isolates was observed with most of the isolates virulent on Beecher, Maritime, and Prior clustering in one group and those showing greater infection rates on Herta and Skiff clustering in group 2.…”

Section: Discussionmentioning

confidence: 62%

Genomic Regions Associated with Virulence in Pyrenophora teres f. teres Identified by Genome-Wide Association Analysis and Biparental Mapping

Martin

Moolhuijzen

Tao³

et al. 2020

Phytopathology®

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Net form net blotch (NFNB), caused by the fungal pathogen Pyrenophora teres f. teres, is an important foliar disease present in all barley-producing regions of the world. This fungus is a hemibiotrophic and heterothallic ascomycete, where sexual recombination can lead to changes in disease expression in the host. Knowledge of the genetic architecture and genes involved in virulence is vital to increase the durability of NFNB resistance in barley cultivars. We used a genome-wide association mapping approach to characterize P. teres f. teres genomic regions associated with virulence in Australian barley cultivars. One hundred eighty-eight P. teres f. teres isolates collected across five Australian states were genotyped using Diversity Arrays Technology sequence markers and phenotyped across 20 different barley genotypes. Association mapping identified 14 different genomic regions associated with virulence, with the majority located on P. teres f. teres chromosomes 3 and 5 and one each present on chromosomes 1, 6, and 9. Four of the regions identified were confirmed by quantitative trait loci (QTL) mapping. The QTL regions are discussed in the context of their genomic architecture together with examination of their gene contents, which identified 20 predicted effectors. The number of QTL shown in this study at the population level clearly illustrates a complex genetic basis of P. teres f. teres virulence compared with pure necrotrophs, such as the wheat pathogens Parastagonospora nodorum and Parastagonospora tritici-repentis.

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Section: Discussionmentioning

confidence: 62%

Genomic Regions Associated with Virulence in Pyrenophora teres f. teres Identified by Genome-Wide Association Analysis and Biparental Mapping

Martin

Moolhuijzen

Tao³

et al. 2020

Phytopathology®

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“…This represents a contrast with the situation reported in Ptt where all mutant strains had an identical Cyp51A sequence and the F489L (F495L) substitution was always associated with the same single nucleotide polymorphism, c1467a for codon TTA (Mair, Deng, et al 2016). A subsequent study using microsatellite markers suggested that this polymorphism most likely arose in Ptt from a single mutational event that subsequently recombined into different genetic backgrounds and spread through the pathogen population (Ellwood et al 2019). By comparison, in this study the mutation F489L (F495L) was caused by three different single nucleotide polymorphisms and each of these three SNPs were found in a distinct Cyp51A haplotype.…”

Section: Discussionmentioning

confidence: 63%

Parallel evolution of multiple mechanisms for demethylase inhibitor fungicide resistance in the barley pathogenPyrenophora teresf. sp.maculata

Mair

Thomas

Dodhia

et al. 2019

Preprint

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The demethylase inhibitor (DMI) or group 3 fungicides are the most important class of compounds for the control both of plant and human fungal pathogens. The necrotrophic fungal pathogen Pyrenophora teres f. sp. maculata (Ptm), responsible for spot form of net blotch (SFNB), is currently the most significant disease of barley in Australia, and a disease of increasing concern worldwide. The main basis for management of SFNB is by fungicide application, and in Australia the DMIs predominate. Although reduced sensitivity to DMI fungicides has recently been described in the closely related pathogen P. teres f. sp. teres (Ptt), the mechanisms of DMI resistance have not thus far been described for Ptm. In this study, several different levels of sensitivity to DMI fungicides were identified in Western Australian strains of Ptm from 2016 onwards, and reduced sensitivity phenotypes were correlated with a number of distinct mutations in both the promoter region and coding sequence of the DMI target gene encoding cytochrome P450 sterol 14α-demethylase (Cyp51A). Five insertions elements of 134-base pairs in length were found at different positions within the upstream regulatory region of Cyp51A in both highly DMI-resistant (HR) and select moderately DMI-resistant (MR1) Ptm isolates. The five insertion elements had at least 95% sequence identity and were determined to be Solo-LTR (Long Terminal Repeat) elements, all deriving from Ty1/Copia-family LTR Retrotransposons. The 134-bp elements contained a predicted promoter sequence and several predicted transcription factor binding sites, and the presence of an insertion element was correlated with constitutive overexpression of Cyp51A. The substitution of phenylalanine by leucine at position 489 of the predicted amino acid sequence of CYP51A was found in both HR and select moderately DMI-resistant (MR2) Ptm isolates. The same F489L amino acid substitution has been previously reported in Western Australian strains of Ptt, where it has also been associated with reduced sensitivity to DMI fungicides. In Ptm, the F489L amino acid change was associated with either of three different single nucleotide polymorphisms in codon 489. This suggests that, in contrast to Ptt, in Ptm the F489L mutation has emerged as a result of three distinct mutational events. Moderately DMI-resistant isolates had one or the other of the F489L substitution or a promoter insertion mutation, whereas highly DMI-resistant isolates were found to have combinations of both mechanisms together. Therefore, multiple mechanisms acting both alone and in concert were found to contribute to the observed phenomena of DMI fungicide resistance in Ptm. Moreover, these mutations have apparently emerged repeatedly and independently in Western Australian Ptm populations, by a process of convergent or parallel evolution.

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“…As Ptt is dispersed on infected seed, phylogenetic similarities may also be related to cultivation of historic cultivars, for example the American cultivar Beecher in Western Australia. Alternatively, as the genotypes in Australia appear to represent a subset of USA and European diversity, and with recent population studies confirming two groups occur in Australia [33,35], the genotypes present in Australia may represent chance incursions.…”

Section: Pyrenophora Whole Genome Comparative Analysismentioning

confidence: 99%

Expansion and Conservation of Biosynthetic Gene Clusters in Pathogenic Pyrenophora spp.

Moolhuijzen

Muria-Gonzalez

Syme

et al. 2020

Toxins

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Pyrenophora is a fungal genus responsible for a number of major cereal diseases. Although fungi produce many specialised or secondary metabolites for defence and interacting with the surrounding environment, the repertoire of specialised metabolites (SM) within Pyrenophora pathogenic species remains mostly uncharted. In this study, an in-depth comparative analysis of the P. teres f. teres, P teres f. maculata and P. tritici-repentis potential to produce SMs, based on in silico predicted biosynthetic gene clusters (BGCs), was conducted using genome assemblies from PacBio DNA reads. Conservation of BGCs between the Pyrenophora species included type I polyketide synthases, terpene synthases and the first reporting of a type III polyketide synthase in P teres f. maculata. P. teres isolates exhibited substantial expansion of non-ribosomal peptide synthases relative to P. tritici-repentis, hallmarked by the presence of tailoring cis-acting nitrogen methyltransferase domains. P. teres isolates also possessed unique non-ribosomal peptide synthase (NRPS)-indole and indole BGCs, while a P. tritici-repentis phytotoxin BGC for triticone production was absent in P. teres. These differences highlight diversification between the pathogens that reflects their different evolutionary histories, host adaption and lifestyles.

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

Cited by 22 publications

References 45 publications

Genomic Regions Associated with Virulence in Pyrenophora teres f. teres Identified by Genome-Wide Association Analysis and Biparental Mapping

Genomic Regions Associated with Virulence in Pyrenophora teres f. teres Identified by Genome-Wide Association Analysis and Biparental Mapping

Parallel evolution of multiple mechanisms for demethylase inhibitor fungicide resistance in the barley pathogenPyrenophora teresf. sp.maculata

Expansion and Conservation of Biosynthetic Gene Clusters in Pathogenic Pyrenophora spp.

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