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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 #205702
Title: Stagonospora nodorum utilizes multiple proteinaceous host selective toxins which interact with dominant host sensitivity genes in wheat

Author
item Friesen, Timothy
item Faris, Justin
item OLIVER, RICHARD - MURDOCH UNIVERSITY

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2006
Publication Date: 3/20/2007
Citation: Friesen, T.L., Faris, J.D., Oliver, R.P. 2007. Stagonospora nodorum utilizes multiple proteinaceous host selective toxins which interact with dominant host sensitivity genes in wheat. Meeting Abstract. 24th Fungal Genetics Conference. p. 168.

Interpretive Summary:

Technical Abstract: Stagonospora nodorum has recently been shown to produce multiple proteinaceous host selective toxins that interact either directly or indirectly with dominant sensitivity genes in wheat. ToxA, a proteinaceous host selective toxin originally associated with Pyrenophora tritici-repentis, was recently identified in S. nodorum. The ToxA gene was convincingly shown to have moved from S. nodorum to P. tritici-repentis by a recent horizontal gene transfer event. SnTox1 has also been identified and shown to be highly associated with disease development. More recently we have identified and characterized two additional toxin interactions for their significance in disease. SnTox2 and SnTox3, which are produced by the majority of North American isolates tested, interact with the host sensitivity genes Snn2, located on wheat chromosome 2D, and Snn3 located on chromosome 5B, respectively. SnTox2 is a protein with an approximate size of 6.6 kDa whereas SnTox3 is a protein in the 10 to 30kDa range. By using wheat mapping populations segregating for Tsn1(ToxA sensitivity) Snn2 (Tox2 sensitivity), and Snn3 (Tox3 sensitivity), disease significance for each toxin sensitivity gene has been shown to account for as much as 60% of the disease phenotype caused by S. nodorum isolates producing each toxin. Several additional uncharacterized toxins have also been identified. The accumulation of work on the S. nodorum host pathogen system establishes it as a complex inverse gene-for-gene system where multiple host selective toxins interact with dominant host sensitivity gene products to induce disease.