|Goodwin, Stephen - Steve|
Submitted to: Genes, Genomes, Genetics
Publication Type: Peer reviewed journal
Publication Acceptance Date: 11/2/2012
Publication Date: 1/6/2013
Citation: Manning, V.A., Pandelova, I., Dhillon, B., Wilhelm, L.J., Goodwin, S.B., Berlin, A., Figueroa, M., Freitag, M., Hane, J.K., Henrissat, B. 2013. Comparative genomics of a plant-pathogenic fungus, Pyrenophora tritici-repentis, reveals transduplication and the impact of repeat elements on pathogenicity and population divergence. G3-Genes, Genomes, Genetics. 3:41-63. Interpretive Summary: Pyrenophora tritici-repentis is a fungal pathogen and causal agent of tan spot disease of wheat, which has increased significantly over the past few decades. Pathogenicity by this fungus is due to specific toxins that attack corresponding genes for susceptibility in the host to cause disease. Past research on the molecular interactions between P. tritici-repentis and wheat have made this pathosystem a model for the analysis of what is known as inverse gene-for-gene interactions. To better understand the mechanisms for the increased incidence of tan spot on wheat, genome sequences were obtained for three isolates of P. tritici-repentis. A wheat isolate was used to assemble a reference genome composed of 11 chromosomes that encode 12,141 predicted genes. A comparison of the genomes of two additional isolates to the reference genome indicated that a grass pathogen was more divergent compared to the wheat pathogens and identified numerous genes that may play a role in pathogenicity. A striking feature of the genome was that movement of mobile genetic elements appears to have contributed to the creation of novel genes, increased the number and diversity of specific proteins to increase pathogenicity, and has helped move pathogenicity-related genes within and between species of fungi. This information will be useful to fungal geneticists and evolutionary biologists to better understand the genetics and evolution of host specificity and speciation mechanisms in fungi. Plant pathologists and breeders may be able to use this information to design better strategies for disease management. Fungal geneticists can use the results to identify potential genes involved in toxin production and other important biological processes for future analyses of gene function.
Technical Abstract: Pyrenophora tritici-repentis is a necrotrophic fungal pathogen and causal agent of tan spot disease of wheat, which has increased significantly over the last few decades. Pathogenicity by this fungus is due to host-selective toxins. These toxins are recognized by their host plant in a genotype-specific manner that results in susceptibility and disease; therefore, this pathosystem has become a model for the study of inverse gene-for-gene interactions. To better understand the mechanisms for the increased incidence of tan spot, we sequenced the genomes of three P. tritici-repentis isolates. A wheat isolate was used to assemble a reference genome of approximately 40 Mb composed of 11 chromosomes that encode 12,141 predicted genes. A comparison of the genomes of two resequenced isolates to the reference genome indicated that a grass pathogen was more divergent compared to the wheat pathogens. Examination of shared gene-coding regions identified candidate pathogen-specific secreted proteins and secondary metabolite clusters and revealed some gene families that may play a role in necrotrophic pathogenicity. Analysis of transposable elements indicated that their presence in the genome of pathogenic isolates contributes to the creation of novel genes, copy number variation of pathogenesis-related proteins, effector diversification, and possible horizontal gene transfer events and provided the first example of transduplication by DNA transposable elements in fungi. Overall, comparative analyses of these genomes provided evidence that pathogenicity in this species arose through an influx of transposable elements, which created a genetically flexible genomic landscape that can easily respond to environmental changes.