Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/20/2007
Publication Date: 2/1/2008
Citation: Friesen, T.L., Zhang, Z., Solomon, P.S., Oliver, R.P., Faris, J.D. 2008. Genetic characterization of a novel wheat-Stagonospora nodorum host-selective toxin interaction and it role in disease susceptibility. Plant Physiology. 146:682-693 Interpretive Summary: We have previously shown that Stagonospora nodorum blotch, a highly destructive disease of common and durum wheat, is controlled by host-selective toxins (HSTs). Three toxins which we have identified as SnToxA, SnTox1, and SnTox2 have been shown to interact directly or indirectly with single wheat susceptibility genes (Tsn1, Snn1, and Snn2) to induce disease. Here we describe and characterize a new HST designated SnTox3, and the corresponding wheat susceptibility gene which we have designated Snn3. A compatible Snn3-SnTox3 interaction was shown to play a significant role in the development of disease caused by different isolates of S. nodorum, the fungal pathogen causing the disease. This work introduces a fourth HST produced by S. nodorum and builds on the notion that the disease S. nodorum blotch is largely based on the production of multiple toxins produced by the pathogen.
Technical Abstract: Recent work suggests that the S. nodorum-wheat pathosystem is controlled by host-selective toxins (HSTs) (SnToxA, SnTox1, SnTox2) that interact directly or indirectly with dominant host genes (Tsn1, Snn1, Snn2) to induce disease. Here we describe and characterize a novel HST designated SnTox3, and the corresponding wheat sensitivity /susceptibility gene identified on chromosome arm 5BS, which we designated as Snn3. SnTox3 is a proteinaceous necrosis-inducing toxin between 10 and 30 kDa in size. The S. nodorum isolates Sn1501 (SnToxA-, SnTox2+, SnTox3+), SN15 (SnToxA+, SnTox2+, SnTox3+), and SN15KO18, a strain of SN15 with a disrupted form of SnToxA, were evaluated on a population of wheat recombinant inbred lines. A compatible Snn3-SnTox3 interaction played a significant role in the development of disease caused by isolates Sn1501 and SN15KO18, with Snn2 being epistatic to Snn3. Snn3 was not significantly associated with disease caused by SN15 presumably due to the major effects observed for Snn2 and Tsn1, which were largely additive. This work introduces a fourth HST produced by S. nodorum and builds on the notion that the wheat-S. nodorum pathosystem is largely based on multiple host-toxin interactions that follow an inverse gene-for-gene scenario.