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    The Tsn1-ToxA interaction in the wheat-Stagonospora nodorum pathosystem parallels that of the wheat-tan spot system

    Access Status
    Fulltext not available
    Authors
    Liu, Z.
    Friesen, T.
    Ling, H.
    Meinhardt, S.
    Oliver, Richard
    Rasmussen, J.
    Faris, J.
    Date
    2006
    Type
    Journal Article
    
    Metadata
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    Citation
    LIU Z, FRIESEN TL, LING H, MEINHARDT SW, OLIVER RP, RASMUSSEN JB & FARIS JD (2006) The Tsn1-ToxA interaction in the wheat-Stagonospora nodorum pathosystem parallels that of the wheat-tan spot system. Genome 49 1265-1273
    DOI
    10.1139/G06-088
    Faculty
    Department of Environmental & Agriculture
    School of Agriculture and Environment
    Faculty of Science and Engineering
    Remarks

    A copy of this item may be available from Professor Richard Oliver

    Email: Richard.oliver@curtin.edu.au

    URI
    http://hdl.handle.net/20.500.11937/37482
    Collection
    • Curtin Research Publications
    Abstract

    The wheat tan spot fungus (Pyrenophora tritici-repentis) produces a well-characterized host-selective toxin (HST) known as Ptr ToxA, which induces necrosis in genotypes that harbor the Tsn1 gene on chromosome 5B. In previous work, we showed that the Stagonospora nodorum isolate Sn2000 produces at least 2 HSTs (SnTox1 and SnToxA). Sensitivity to SnTox1 is governed by the Snn1 gene on chromosome 1B in wheat. SnToxA is encoded by a gene with a high degree of similarity to the Ptr ToxA gene. Here, we evaluate toxin sensitivity and resistance to S. nodorum blotch (SNB) caused by Sn2000 in a recombinant inbred population that does not segregate for Snn1. Sensitivity to the Sn2000 toxin preparation cosegregated with sensitivity to Ptr ToxA at the Tsn1 locus. Tsn1-disrupted mutants were insensitive to both Ptr ToxA and SnToxA, suggesting that the 2 toxins are functionally similar, because they recognize the same locus in the host to induce necrosis. The locus harboring the tsn1 allele underlies a major quantitative trait locus (QTL) for resistance to SNB caused by Sn2000, and explains 62% of the phenotypic variation, indicating that the toxin is an important virulence factor for this fungus. The Tsn1 locus and several minor QTLs together explained 77% of the phenotypic variation. Therefore, the Tsn1–ToxA interaction in the wheat–S. nodorum pathosystem parallels that of the wheat–tan spot system, and the wheat Tsn1 gene serves as a major determinant for susceptibility to both SNB and tan spot.

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