Submitted to: Plant Journal
Publication Type: Peer reviewed journal
Publication Acceptance Date: 4/27/2007
Publication Date: 6/15/2007
Citation: Friesen, T.L., Meinhardt, S.W., Faris, J.D. 2007. The Stagonospora nodorum-wheat pathosystem involves multiple proteinaceous host-selective toxins and corresponding host sensitivity genes that interact in an inverse gene-for gene manner. Plant Journal. 51:681-692. Interpretive Summary: Stagonospora nodorum blotch (SNB) is an economically important fungal disease in most wheat growing regions worldwide. In this work, we partially purified a new toxin produced by the pathogen Stagonospora nodorum and designated the toxic component as SnTox2. The wheat population BR34 x Grandin (BG) was evaluated for toxin sensitivity by infiltration into seedlings. Evaluation of wheat populations showed that toxin sensitivity is conferred by a single dominant gene, which we designated as Snn2. We have identified this sensitivity gene to the short arm of chromosome 2D. Fungal inoculations were done on the BG RI population and QTL analysis was performed. The results indicated that Snn2 accounts for 58% of the disease phenotype. A second gene with less significance was detected at the Tsn1 locus, which confers sensitivity to SnToxA. These results indicate that both toxins are important in the development of SNB.
Technical Abstract: We recently showed that the wheat pathogen Stagonospora nodorum produces proteinaceous host-selective toxins (HSTs). These toxins include SnTox1 as well as SnToxA, a HST first identified from Pyrenophora tritici-repentis that was implicated in a very recent horizontal gene transfer event from S. nodorum to P. tritici-repentis. Compelling evidence implicating SnToxA and SnTox1 in disease development has been obtained. Here, we report the partial purification and characterization of a third host-selective toxin designated SnTox2, as well as the genetic characterization of the corresponding host-sensitivity gene. SnTox2 was protease sensitive and approximately 6.5 kDa in size. Sensitivity to SnTox2 was conferred by a single dominant gene designated Snn2, which mapped to the short arm of wheat chromosome 2D. Genetic analysis of reaction to conidial inoculations in a segregating wheat population indicated that both the Snn2-SnTox2 and the Tsn1-SnToxA interactions were involved in disease development, together accounting for 73% of the phenotypic variation. Therefore, S. nodorum produces multiple toxins that rely on specific interactions with host gene products to cause disease. The identification of multiple HST-host gene interactions important for disease development and the availability of the S. nodorum whole genome sequence points out the potential for this pathosystem to serve as a toxin-based, inverse gene-for-gene model.