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    Host specific toxins; effectors of necrotrophic pathogenicity

    Access Status
    Fulltext not available
    Authors
    Friesen, T.
    Faris, J.
    Solomon, P.
    Oliver, Richard
    Date
    2008
    Type
    Journal Article
    
    Metadata
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    Citation
    FRIESEN TL, FARIS JD, SOLOMON PS & OLIVER RP (2008) Host specific toxins; effectors of necrotrophic pathogenicity. Cellular Microbiology 10 1421-1428 (Front cover)
    DOI
    10.1111/j.1462-5822.2008.01153.x
    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/20.500.11937/44260
    Collection
    • Curtin Research Publications
    Abstract

    Host-specific toxins (HSTs) are defined as pathogen effectors that induce toxicity and promote disease only in the host species and only in genotypes of that host expressing a specific and often dominant susceptibility gene. They are a feature of a small but well-studied group of fungal plant pathogens. Classical HST pathogens include species of Cochliobolus, Alternaria and Pyrenophora. Recent studies have shown that Stagonospora nodorum produces at least four separate HSTs that interact with four of the many quantitative resistance loci found in the host, wheat. Rationalization of fungal phylogenetics has placed these pathogens in the Pleosporales order of the class Dothideomycetes. It is possible that all HST pathogens lie in this order. Strong evidence of the recent lateral gene transfer of the ToxA gene from S. nodorum to Pyrenophora tritici-repentis has been obtained. Hallmarks of lateral gene transfer are present for all the studied HST genes although definitive proof is lacking. We therefore suggest that the Pleosporales pathogens may have a conserved propensity to acquire HST genes by lateral transfer.

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