|Liu, Zhaohui - PLNT PATH, NDSU, FARGO ND|
|Hua, Ling - CHEM DEPT, NDSU, FARGO ND|
|Meinhardt, Steven - CHEM DEPT, NDSU, FARGO ND|
|Oliver, Richard P. - MURDOCH UNIV, AUSTRALIA|
|Rassmussen, Jack - PLANT PATH, NDSU, FARGO,|
Submitted to: Genome
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 16, 2006
Publication Date: October 15, 2007
Citation: Liu, Z., Friesen, T.L., Hua, L., Meinhardt, S.W., Oliver, R., Rassmussen, J.B., Faris, J.D. 2007. The tsn1-toxa interaction in the wheat-stagonospora nodorum pathosystem parallels that of the wheat-tan spot system. Genome. 49:1265-1273. Interpretive Summary: Stagonospora nodorum blotch (SNB) is a foliar disease of wheat caused by a fungal pathogen (Stagonospora nodorum). In previous research, we identified a major gene on the short arm of chromosome 1B associated with resistance to the fungus and designated the gene snn1. This gene also conferred insensitivity to a toxin produced by the SNB pathogen. Here, we evaluated a different segregating wheat population for reaction to SNB and the toxin. In this population, snn1 did not confer resistance/insensitivity. Instead, the tsn1 gene conferred insensitivity to the toxin and resistance to SNB. Tsn1 is on the long arm of chromosome 5B and is known to confer insensitivity to a toxin produced by a different pathogenic fungus. Therefore, our results suggest that Tsn1 can serve as a target for different toxins produced by different pathogenic fungi, and that the SNB toxin can utilize either Snn1 or Tsn1 to cause disease. In addition to tsn1, we also identified four putative genes with relatively minor resistance effects.
Technical Abstract: Stagonospora nodorum blotch (SNB) is an economically important foliar and glume disease in the major wheat growing areas of the world. We previously identified a host-selective toxin (SnTox1) produced by the isolate Sn2000 of S. nodorum and mapped the gene (Snn1) conditioning sensitivity to chromosome 1BS in the International Triticeae Mapping Initiative (ITMI) population. Here, we evaluated SnTox1 sensitivity and resistance to SNB caused by Sn2000 in a population of recombinant inbred lines (RILs) derived from a cross between Grandin and BR34. BR34 is insensitive to the SnTox1 and highly resistant to the fungus while Grandin is sensitive and highly susceptible. In the RIL population, sensitivity to partially purified SnTox1 mapped to the long arm of chromosome 5B and cosegregated with Tsn1, which confers sensitivity to Ptr ToxA produced by the tan spot fungus Pyrenophora tritici-repentis. The tsn1 locus underlied a major quantitative trait locus (QTL) for resistance to SNB and explained 62% of the phenotypic variation indicating that SnTox1 plays an important role in causing disease. In addition, minor QTL on chromosomes 1BS, 5AL, 5BL, and 6AS, and an interaction were detected. A multiple regression model explained 77% of phenotypic variation. These results suggest that SnTox1 can recognize multiple host genes to cause necrosis, and that the product of Tsn1 can serve as a target for proteinaceous toxins produced by different pathogenic fungi.