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Quantitative Variation in Effector Activity of ToxA Isoforms from Stagonospora nodorum and Pyrenophora tritici-repentis

April 2012 , Volume 25 , Number  4
Pages  515 - 522

Kar-Chun Tan,1 Margo Ferguson-Hunt,2 Kasia Rybak,2 Ormonde D. C. Waters,1 Will A. Stanley,3 Charles S. Bond,4 Eva H. Stukenbrock,5 Timothy L. Friesen,6 Justin D. Faris,6 Bruce A. McDonald,7 and Richard P. Oliver1

1Environment and Agriculture, Curtin University, Bentley WA 6102, Australia; 2Health Science, Murdoch University, Murdoch, WA 6150, Australia; 3ARC Centre of Excellence in Plant Energy Biology and 4Biomedical, Biomolecular and Chemical Sciences, The University of Western Australia, Crawley 6009 WA, Australia; 5Max Planck Institute Marburg, Karl von Frisch Str. 10, D-35043 Marburg, Germany; 6United States Department of Agriculture–Agricultural Research Service Cereal Crops Research Unit, Red River Valley Agricultural Research Center, Fargo, ND 58105, U.S.A.; 7Plant Pathology Group, Institute of Integrative Biology, ETH Zurich, Universitätsstr 2, CH-8092 Zurich, Switzerland

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Accepted 12 December 2011.

ToxA is a proteinaceous necrotrophic effector produced by Stagonospora nodorum and Pyrenophora tritici-repentis. In this study, all eight mature isoforms of the ToxA protein were purified and compared. Circular dichroism spectra indicated that all isoforms were structurally intact and had indistinguishable secondary structural features. ToxA isoforms were infiltrated into wheat lines that carry the sensitivity gene Tsn1. It was observed that different wheat lines carrying identical Tsn1 alleles varied in sensitivity to ToxA. All ToxA isoforms induced necrosis when introduced into any Tsn1 wheat line but we observed quantitative variation in effector activity, with the least-active version found in isolates of P. tritici-repentis. Pathogen sporulation increased with higher doses of ToxA. The isoforms that induced the most rapid necrosis also induced the most sporulation, indicating that pathogen fitness is affected by differences in ToxA activity. We show that differences in toxin activity encoded by a single gene can contribute to the quantitative inheritance of necrotrophic virulence. Our findings support the hypothesis that the variation at ToxA results from selection that favors increased toxin activity.

© 2012 The American Phytopathological Society