Comparative genomics of the wheat fungal pathogen Pyrenophora tritici-repentis reveals chromosomal variations and genome plasticity

Abstract

BackgroundPyrenophora tritici-repentis (Ptr) is a necrotrophic fungal pathogen that causes the major wheat disease, tan spot. We set out to provide essential genomics-based resources in order to better understand the pathogenicity mechanisms of this important pathogen.ResultsHere, we present eight new Ptr isolate genomes, assembled and annotated; representing races 1, 2 and 5, and a new race. We report a high quality Ptr reference genome, sequenced by PacBio technology with Illumina paired-end data support and optical mapping. An estimated 98% of the genome coverage was mapped to 10 chromosomal groups, using a two-enzyme hybrid approach. The final reference genome was 40.9 Mb and contained a total of 13,797 annotated genes, supported by transcriptomic and proteogenomics data sets.ConclusionsWhole genome comparative analysis revealed major chromosomal segmental rearrangements and fusions, highlighting intraspecific genome plasticity in this species. Furthermore, the Ptr race classification was not supported at the whole genome level, as phylogenetic analysis did not cluster the ToxA producing isolates. This expansion of available Ptr genomics resources will directly facilitate research aimed at controlling tan spot disease.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4680-3) contains supplementary material, which is available to authorized users.

The identification and deletion of the polyketide synthase‐nonribosomal peptide synthase gene responsible for the production of the phytotoxic triticone A/B in the wheat fungal pathogen Pyrenophora tritici‐repentis

“…It has been well established that small molecular weight compounds can contribute to phytopathogenicity in fungal systems (Möbius and Hertweck, ; Horbach et al ., ; Pusztahelyi et al ., ) and surveys of the Ptr genome by Manning () and Moolhuijzen (), elicited in excess of 20 biosynthetic gene clusters, none of which have been characterized for product or function. Given the prevalence of secondary metabolites involved in pathogenicity, it is not unreasonable to surmise one or more products from these biosynthetic gene clusters may contribute to virulence.…”

“…It has been well established that small molecular weight compounds can contribute to phytopathogenicity in fungal systems (Möbius and Hertweck, 2009;Horbach et al, 2011;Pusztahelyi et al, 2015) and surveys of the Ptr genome by Manning (2013) and Moolhuijzen (2018), elicited in excess of 20 biosynthetic gene clusters, none of which have been characterized for product or function.…”

Genome mining of the citrus pathogenElsinoë fawcettii; prediction and prioritisation of candidate effectors, cell wall degrading enzymes and secondary metabolite gene clusters

“…of scaffolds = 108) [117], Pyrenophora tritici-repentis (accession GCA_003231415.1, no. of scaffolds = 3964) [118], S. sclerotiorum (accession GCF_000146945.2, no. of scaffolds = 37) [119] and Z. tritici (accession GCA_900184115.1, no.…”

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

“…Previous PacBio genome sequencing projects for Ptr, Ptt and Ptm [28][29][30][31][32] have provided an opportunity to explore the genetic capacity of these taxa to produce specialised metabolites and explore gene cluster conservation within the three different species. To date, whole genome-based comparative investigation into specialised metabolite BGCs in Ptr, Ptt and Ptm has not been undertaken.…”

“…To date, whole genome-based comparative investigation into specialised metabolite BGCs in Ptr, Ptt and Ptm has not been undertaken. Initial investigations into Ptr found that not all backbone biosynthetic genes were conserved between the different races of Ptr [28,29]. In Ptt, a genome expansion of low complexity (low GC) regions and NRPS genes was identified when comparatively analysed to Ptm and Ptr, and many predicted NRPSs were found to be non-canonical, with some of their main enzymatic domains missing (e.g., adenylation, peptidyl carrier protein, condensation and/or thioesterase domains) [30].…”