Justin D. Faris and
Timothy L. Friesen
United States Department of Agriculture--Agricultural Research Service Cereal Crops Research Unit, Northern Crop Science Laboratory, 1307 18th Street North, Fargo, ND 58105.
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Accepted for publication 7 April 2009.
The wheat Tsn1 gene on chromosome 5B confers sensitivity to a host-selective toxin produced by the pathogens that cause tan spot and Stagonospora nodorum blotch (SNB) known as Ptr ToxA and SnToxA, respectively (hereafter referred to as ToxA). A compatible Tsn1--ToxA interaction is known to play a major role in conferring susceptibility of hexaploid (common) wheat to SNB. However, a recent study by another group suggested that the Tsn1--ToxA interaction was not relevant in conferring susceptibility of the tetraploid (durum) wheat cv. Langdon (LDN). Here, we reevaluated the role of the Tsn1--ToxA interaction in governing SNB susceptibility using the same mapping population and Stagonospora nodorum isolate (Sn2000) as were used in the previous study. Results of our quantitative trait locus analysis showed that the Tsn1 locus accounted for 95% of the variation in SNB. In addition, inoculation of the mapping population with two ToxA-knockout strains of Sn2000 revealed that the entire population was resistant. Furthermore, several LDN Tsn1-disrupted mutants were evaluated and found to be resistant to SNB. Together, these results prove unequivocally that Tsn1 is the only factor present along chromosome 5B that governs response to SNB in this population and that a compatible Tsn1--ToxA interaction is necessary for the manifestation of disease. Therefore, the results from the previous study are refuted.
Additional keywords:Phaeosphaeria nodorum, resistance, segregation distortion.
The American Phytopathological Society, 2009