Biology subjects

Gourlie, R.

Publications and source records attributed to Gourlie, R..

3 recordsLinked to original sources

bioRxiv2026

GENOME ASSEMBLIES FOR 28 PHAEOSPHAERIACEAE ISOLATES FROM CANADA

Glume blotch and Septoria Tritici Blotch (STB) are destructive crop diseases caused by fungal pathogens formerly classified under the genus Septoria. Recent taxonomical revisions have led to the reclassification and renaming of these fungi, some of which are now under the genus Parastagonospora, family Phaeosphaeriaceae, order Pleosporales, and class Dothideomycetes. In this study, we performed whole genome sequencing and assembly for 28 Phaeosphaeriaceae isolates from Canada. Sequencing was performed using a combination of Oxford Nanopore Technologies (ONT) long-read and Illumina short-read sequencing platforms. Most of the genomes were very complete, BUSCO >99%, with the genomes assemblies derived from ONT sequencing having very few contigs that likely encompass entire chromosomes or chromosome arms. To determine the relationship between these isolates and similar fungi that have been previously characterized, we performed whole genome alignments to 2,668 other Dothidiomycete genomes obtained from NCBI using NUCmer. Comparative genomic analysis revealed that 27 of the isolates clustered discretely with either Parastagonospora nodorum, or Parastagonospora pseudonodorum (Parastagonospora avenae f. sp. tritici), with one genome having no other similar genome in NCBI which we hypothesize to be the first genome assembly of Phaeosphaeria pontiformis. Both P. nodorum and P. pseudonodorum species were isolated from wheat and barley and only the latter was isolated from durum, while the P. pontiformis was isolated from wheat. In summary, we sequenced and assembled the genomes of 28 isolates of Phaeosphaeriaceae spp. from Canada and the genomes add to our foundational knowledge of these plant pathogens and efforts to better understand their diversity.

microbiology↗

bioRxiv2025

The virulence gene ToxB is both amplified and disrupted by transposons in the wheat pathogen Pyrenophora tritici-repentis

O_LIMechanisms that drive virulence gene duplication in plant pathogenic fungi remain poorly understood. In Pyrenophora tritici-repentis (Ptr), responsible for tan spot of wheat, ToxB is a multicopy virulence gene encoding a proteinaceous necrotrophic effector. ToxB exhibits a virulence dosage effect, where higher copy numbers are associated with increased disease severity. In this work, we sought to resolve a 25-year old question as to what drove the proliferation of ToxB within Ptr. C_LIO_LITo investigate this, 23 long-read assemblies were generated and analyzed from a collection of globally distributed isolates with various ToxB copy numbers, with a specific focus on regions containing ToxB. C_LIO_LIExtensive comparative alignments identified a Helitron-like element, ToxB-HLE, that appears to be driving the duplication of ToxB in an accessory region of chromosome 4. This region is entirely absent in isolates lacking ToxB or its nonfunctional homolog toxb. In addition to gene amplification by transposons, multiple independent transposon insertion events were identified in several isolates that disrupted the ToxB open reading frame creating inactive toxb haplotypes. C_LIO_LIThis study provides strong evidence supporting the hypothesis that transposons play dual roles in the rapid evolution of fungal pathogenicity by both amplifying and disrupting a key virulence gene in a globally distributed plant pathogen. C_LI

evolutionary biology↗

bioRxiv2022

Dissecting the Pyrenophora tritici-repentis (tan spot of wheat) pangenome

We sequenced the genome of a global collection (40 isolates) of the fungus Pyrenophora tritici-repentis (Ptr), a major foliar pathogen of wheat and model for the evolution of necrotrophic pathogens. Ptr exhibited an open-pangenome, with 43% of genes in the core set and 57% defined as accessory (present in only a subset of isolates), of which 56% were singleton genes (present in only one isolate). A clear distinction between pathogenic and non-pathogenic genomes was observed in size, gene content, and phylogenetic relatedness. Chromosomal rearrangements and structural organization, specifically around the effector coding genes, were explored further using the annotated genomes of two isolates sequenced by PacBio RS II and Illumina HiSeq. The Ptr genome exhibited major chromosomal rearrangements, including chromosomal fusion, translocation, and segment duplications. An intraspecies translocation of ToxA, the necrosis-inducing effector-coding gene, was facilitated within Ptr via a 143 kb Starship transposon (dubbed Horizon). Additionally, ToxB, the gene encoding the chlorosis-inducing effector, was clustered as three copies on a 294 kb transposable element in a ToxB-producing isolate. ToxB and its carrying transposon were missing from the ToxB non-coding reference isolate, but the homolog toxb and the transposon were both present in another non-coding isolate. The Ptr genome also appears to exhibit a one-compartment organization, but may still possess a two-speed genome that is facilitated by copy-number variation as reported in other fungal pathosystems. IMPORTANCEPtr is one of the most destructive wheat pathogens worldwide. Its genome is a mosaic of present and absent effectors, and serves as a model for examining the evolutionary processes behind the acquisition of virulence in necrotrophs and disease emergence. In this work, we took advantage of a diverse collection of pathogenic Ptr isolates with different global origins and applied short- and long-read sequencing technologies to dissect the Ptr genome. This study provides comprehensive insights into the Ptr genome and highlights its structural organization as an open pangenome with one-compartment. In addition, we identified the potential involvement of transposable elements in genome expansion and the movement of virulence factors. The ability of effector-coding genes to shuffle across chromosomes on large transposons was illustrated by the intraspecies translocation of ToxA and the multi-copy ToxB. In terms of gene contents, the Ptr genome exhibits a large percentage of orphan genes, particularly in non-pathogenic or weakly-virulent isolates.

genomics↗