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First published online December 7, 2007; 10.1104/pp.107.108761

Plant Physiology 146:682-693 (2008)
© 2008 American Society of Plant Biologists

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PLANTS INTERACTING WITH OTHER ORGANISMS

Characterization of the Interaction of a Novel Stagonospora nodorum Host-Selective Toxin with a Wheat Susceptibility Gene1,[W]

Timothy L. Friesen*, Zengcui Zhang, Peter S. Solomon, Richard P. Oliver and Justin D. Faris

United States Department of Agriculture-Agriculture Research Service Cereal Crops Research Unit, Northern Crop Science Laboratory, Fargo, North Dakota 58105 (T.L.F., J.D.F.); Department of Plant Sciences, North Dakota State University, Fargo, North Dakota 58105 (Z.Z.); and Australian Centre for Necrotrophic Fungal Pathogens, Western Australian State Agricultural Biotechnology Centre, Murdoch University, Western Australia 6150, Australia (P.S.S., R.P.O.)

Recent work suggests that the Stagonospora nodorum-wheat pathosystem is controlled by host-selective toxins (HSTs; SnToxA, SnTox1, and SnTox2) that interact directly or indirectly with dominant host genes (Tsn1, Snn1, and Snn2) to induce disease. Here we describe and characterize a novel HST designated SnTox3, and the corresponding wheat sensitivity/susceptibility gene identified on chromosome arm 5BS, which we designated as Snn3. SnTox3 is a proteinaceous necrosis-inducing toxin between 10 and 30 kD in size. The S. nodorum isolates Sn1501 (SnToxA–, SnTox2+, and SnTox3+), SN15 (SnToxA+, SnTox2+, and SnTox3+), and SN15KO18, a strain of SN15 with a disrupted form of SnToxA, were evaluated on a population of wheat recombinant inbred lines. A compatible Snn3-SnTox3 interaction played a significant role in the development of disease caused by isolates Sn1501 and SN15KO18, with Snn2 being epistatic to Snn3. Snn3 was not significantly associated with disease caused by SN15 presumably due to the major effects observed for Snn2 and Tsn1, which were largely additive. This work introduces a fourth HST produced by S. nodorum and builds on the notion that the S. nodorum-wheat pathosystem is largely based on multiple host-toxin interactions that follow an inverse gene-for-gene scenario.


1 This work was supported by the U.S. Department of Agriculture-Agriculture Research Service Current Research Information System (projects no. 5442–22000–043–00D and no. 5442–22000–030–00D).

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Timothy L. Friesen (timothy.friesen{at}ars.usda.gov).

[W] The online version of this article contains Web-only data.

www.plantphysiol.org/cgi/doi/10.1104/pp.107.108761

* Corresponding author; e-mail timothy.friesen{at}ars.usda.gov.

Received September 10, 2007; accepted November 30, 2007; published December 7, 2007.




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