Location: Cereal Crops ResearchTitle: Multiple host-specific toxins, lateral gene transfer and gene loss in the evolution of cereal Pleosporalean pathogens) Author
Submitted to: International Congress of Plant Pathology Abstracts and Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 11/15/2007
Publication Date: 8/24/2008
Citation: Oliver, R.P., Solomon, P.S., Hane, J., Ferguson-Hunt, M., Mcdonald, B.A., Faris, J.D., Friesen, T.L. 2008. Multiple host-specific toxins, lateral gene transfer and gene loss in the evolution of cereal Pleosporalean pathogens. International Congress of Plant Pathology Abstracts and Proceedings. Torino, Italy, August 24-29, 2008. Interpretive Summary:
Technical Abstract: We are analysing the wheat pathogen Stagonospora nodorum in order to determine the molecular basis of pathogenicity. The genome sequence of S. nodorum has been obtained and compared to the tan spot pathogen Pyrenophora tritici-repentis. Combined analyses of genome sequences, specific wheat populations segregating for susceptibility and pathogen population genetics have revealed a new model of pathogenicity in S. nodorum. In this model, the pathogen expresses at least 4 different host-specific toxins (HSTs). Each toxin interacts with a different host susceptibility gene. Interaction leads to necrosis which, unlike a classical gene-for-gene system, benefits fungal reproduction. The consequences of this model for disease control will be discussed. The evolutionary history of the toxin genes can be inferred by analysis of the genome sequences and by sampling geographically distinct pathogen populations. We have presented evidence that ToxA has been laterally transferred both into S. nodorum and from S. nodorum into P. tritici-repentis. The fate of the transferred DNA in P. tritici-repentis has been examined and evidence of gene duplication and gene loss was found. The history of twentieth-century emergence of plant disease is littered with examples of fungi related to S. nodorum and P. tritici-repentis, whose pathogenicity is determined by host-specific toxins. The idea that lateral transfer of the HST genes might be a common theme of these twentieth century diseases will be discussed.