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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #201356
Title: The Stagonospora nodorum-wheat pathosystem is an inverse gene for gene system involving multiple proteinaceous host selective toxins

Author
item Friesen, Timothy
item Faris, Justin
item OLIVER, RICHARD - MURDOCH UNIV AUSTRALIA

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 9/28/2006
Publication Date: 1/14/2007
Citation: Friesen, T.L., Faris, J.D., Oliver, R. 2007. The Stagonospora nodorum-wheat pathosystem is an inverse gene for gene system involving multiple proteinaceous host selective toxins. Plant and Animal Genome VX Conference Abstracts. p. 179.

Interpretive Summary:

Technical Abstract: We have recently shown that Stagonospora nodorum produces multiple proteinaceous host selective toxins. These toxins include SnToxA, a host selective toxin first isolated from Pyrenophora tritici-repentis, which has been implicated in a very recent horizontal gene transfer event from S. nodorum to P. tritici-repentis. Strong evidence has implicated SnToxA, as well as SnTox1, SnTox2, and SnTox3 as significant factors in SNB disease. Each toxin has been shown to interact either directly or indirectly with single dominant host sensitivity genes designated as Tsn1 (SnToxA), Snn1 (SnTox1), Snn2 (SnTox2), and Snn3 (SnTox3). Using mapping populations segregating for multiple toxin sensitivities, disease significance for each toxin sensitivity gene has been shown to account for as much as 60% of the disease caused by S. nodorum isolates producing each toxin. Other than SnToxA and SnTox1, 2 and 3, at least three additional host selective toxins and their host sensitivity genes have been identified and disease significance data is being collected. This work shows that the S. nodorum pathosystem is a model inverse-gene-for-gene system where at least seven proteinaceous host selective toxins produced by the pathogen interact directly or indirectly with dominant sensitivity/susceptibility genes in the host to cause disease.