Characterizing the <i>Pyrenophora teres</i> f. <i>maculata</i>–Barley Interaction Using Pathogen Genetics

Carlsen, Steven A.; Neupane, Anjan; Wyatt, Nathan A.; Richards, Jonathan; Faris, Justin D.; Xu, Steven S.; Brueggeman, Robert; Friesen, Timothy L.

doi:10.1534/g3.117.043265

Cited by 24 publications

(32 citation statements)

References 36 publications

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“…In both interactions, host resistance is complex with numerous quantitative gene resistances effective at seedling, adult and all stages across the barley genome ( McLean et al, 2009 ; Liu et al, 2011 ). Pathogen virulence involves different QTL of varying effect, however, stronger differential responses to PTT occur and virulence in PTM is more quantitative and additive ( Shjerve et al, 2014 ; Carlsen et al, 2017 ; Koladia et al, 2017 ). Host resistance to PTM also appears to be characterized by quantitative minor gene resistance only.…”

Section: Discussionmentioning

confidence: 99%

“…Limited periods of co-evolution of PTR and PTM with their crop hosts, the complexity of their genetic interactions and shared ancestry may explain their smaller genomes alongside P. semeniperda . Disease is primarily governed by just three effectors in PTR ( Ciuffetti et al, 2010 ) and by iterative minor effect QTL in PTM ( Carlsen et al, 2017 ). In recently invaded crops, a formerly marginal host (one that is not normally susceptible to a pathogen but with occasional susceptible genotypes) may lead to partial suppression of basal resistance ( Niks and Marcel, 2009 ).…”

Section: Discussionmentioning

confidence: 99%

“…A genetic map of isolate FGOB10Ptm-1 was developed based on a restriction site-associated genotype-by-sequencing (RAD-GBS) approach ( Carlsen et al, 2017 ). The resulting genetic map consisted of 488 filtered SNP markers, with 16 linkage groups and a total map size of 1807 cM.…”

Section: Methodsmentioning

confidence: 99%

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Transposable Element Genomic Fissuring in Pyrenophora teres Is Associated With Genome Expansion and Dynamics of Host–Pathogen Genetic Interactions

et al. 2018

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Pyrenophora teres, P. teres f. teres (PTT) and P. teres f. maculata (PTM) cause significant diseases in barley, but little is known about the large-scale genomic differences that may distinguish the two forms. Comprehensive genome assemblies were constructed from long DNA reads, optical and genetic maps. As repeat masking in fungal genomes influences the final gene annotations, an accurate and reproducible pipeline was developed to ensure comparability between isolates. The genomes of the two forms are highly collinear, each composed of 12 chromosomes. Genome evolution in P. teres is characterized by genome fissuring through the insertion and expansion of transposable elements (TEs), a process that isolates blocks of genic sequence. The phenomenon is particularly pronounced in PTT, which has a larger, more repetitive genome than PTM and more recent transposon activity measured by the frequency and size of genome fissures. PTT has a longer cultivated host association and, notably, a greater range of host–pathogen genetic interactions compared to other Pyrenophora spp., a property which associates better with genome size than pathogen lifestyle. The two forms possess similar complements of TE families with Tc1/Mariner and LINE-like Tad-1 elements more abundant in PTT. Tad-1 was only detectable as vestigial fragments in PTM and, within the forms, differences in genome sizes and the presence and absence of several TE families indicated recent lineage invasions. Gene differences between P. teres forms are mainly associated with gene-sparse regions near or within TE-rich regions, with many genes possessing characteristics of fungal effectors. Instances of gene interruption by transposons resulting in pseudogenization were detected in PTT. In addition, both forms have a large complement of secondary metabolite gene clusters indicating significant capacity to produce an array of different molecules. This study provides genomic resources for functional genetics to help dissect factors underlying the host–pathogen interactions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Transposable Element Genomic Fissuring in Pyrenophora teres Is Associated With Genome Expansion and Dynamics of Host–Pathogen Genetic Interactions

et al. 2018

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“…Ptt, by contrast, has a lengthy association with barley that may go beyond the earliest written records of leaf diseases. Ptt produces both necrotrophic effectors, characteristic of pure necrotrophs, and avirulence genes, characteristic of biotrophs, and is notable for complex host-pathogen genetic interactions [12,41,42] compared to Ptr, where three main effectors explain most of the disease [43], and Ptm where minor effect QTL condition disease [44]. In general, the phylogeny presented supports the diversification of Ptt and recent divergence of Ptm and Ptr [11,30].…”

Section: Pyrenophora Whole Genome Comparative Analysismentioning

confidence: 60%

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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“…Globally, NFNB results in regular yield losses of between 10 and 40% with the potential for complete losses in environmental settings favorable to the pathogen, namely, susceptible cultivars with high sustained humidity and the absence of fungicides ( Mathre et al 1997 ; Liu et al 2011 ). Several studies have investigated the genetics of this host–pathogen interaction, utilizing biparental mapping populations of both the host and pathogen as well as genome-wide association studies (GWAS) in the host ( Liu et al 2011 ; Shjerve et al 2014 ; Carlsen et al 2017 ; Koladia et al 2017a ; Richards et al 2017 ). These studies have been critical in developing hypothetical models for this pathosystem.…”

mentioning

confidence: 99%

Reference Assembly and Annotation of the Pyrenophora teres f. teres Isolate 0-1

Wyatt

Richards

Brueggeman

et al. 2018

G3 Genes|Genomes|Genetics

Self Cite

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Pyrenophora teres f. teres, the causal agent of net form net blotch (NFNB) of barley, is a destructive pathogen in barley-growing regions throughout the world. Typical yield losses due to NFNB range from 10 to 40%; however, complete loss has been observed on highly susceptible barley lines where environmental conditions favor the pathogen. Currently, genomic resources for this economically important pathogen are limited to a fragmented draft genome assembly and annotation, with limited RNA support of the P. teres f. teres isolate 0-1. This research presents an updated 0-1 reference assembly facilitated by long-read sequencing and scaffolding with the assistance of genetic linkage maps. Additionally, genome annotation was mediated by RNAseq analysis using three infection time points and a pure culture sample, resulting in 11,541 high-confidence gene models. The 0-1 genome assembly and annotation presented here now contains the majority of the repetitive content of the genome. Analysis of the 0-1 genome revealed classic characteristics of a “two-speed” genome, being compartmentalized into GC-equilibrated and AT-rich compartments. The assembly of repetitive AT-rich regions will be important for future investigation of genes known as effectors, which often reside in close proximity to repetitive regions. These effectors are responsible for manipulation of the host defense during infection. This updated P. teres f. teres isolate 0-1 reference genome assembly and annotation provides a robust resource for the examination of the barley–P. teres f. teres host–pathogen coevolution.

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Characterizing the Pyrenophora teres f. maculata–Barley Interaction Using Pathogen Genetics

Cited by 24 publications

References 36 publications

Transposable Element Genomic Fissuring in Pyrenophora teres Is Associated With Genome Expansion and Dynamics of Host–Pathogen Genetic Interactions

Transposable Element Genomic Fissuring in Pyrenophora teres Is Associated With Genome Expansion and Dynamics of Host–Pathogen Genetic Interactions

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

Reference Assembly and Annotation of the Pyrenophora teres f. teres Isolate 0-1

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