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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 #245748
Title: Genetic Analysis of Disease Susceptibility Caused by Compatible Tsn1-SnToxA and Snn1-SnTox1 Interactions in the Wheat-Stagonospora Nodorum Pathosystem

Author
item CHU, CHENNGEN - North Dakota State University
item Faris, Justin
item Xu, Steven
item Friesen, Timothy

Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/30/2009
Publication Date: 1/22/2010
Citation: Chu, C.G., Faris, J.D., Xu, S.S., Friesen, T.L. 2010. Genetic Analysis of Disease Susceptibility Caused by Compatible Tsn1-SnToxA and Snn1-SnTox1 Interactions in the Wheat-Stagonospora Nodorum Pathosystem. Theoretical and Applied Genetics. 120:1451-1459

Interpretive Summary: Stagonospora nodorum blotch (SNB) is a leaf disease of wheat. Stagonospora nodorum, the pathogen that causes the disease, produces several toxins that increase the disease on wheat lines sensitive to the toxins. The objectives of this study were to dissect, quantify, and compare the effects of the compatible toxin-host interactions on SNB disease. Results indicated that both SnToxA and SnTox1 interactions were strongly associated with SNB susceptibility. The SnTox1 and SnToxA interactions explained 22 and 28% of the variation in disease, respectively, and together they explained 48% indicating that their effects are largely additive. The SnTox1 interaction accounted for 50% of the variation when the population was inoculated with an S. nodorum strain where the SnToxA gene has been mutated and thus eliminating the SnToxA interaction. These results support the theory that the wheat-S. nodorum pathosystem is largely based on multiple host-toxin interactions. The elimination of toxin sensitivities resulted in decreased susceptibility, but the elimination of both interactions was required to obtain resistance. We propose the use of molecular markers to select against the toxin sensitivity genes for SnTox1 sensitivity (Snn1), and SnToxA sensitivity (Tsn1), and other toxin sensitivity alleles to develop wheat varieties with high levels of SNB resistance.

Technical Abstract: Stagonospora nodorum is a foliar pathogen of wheat that produces several host-selective toxins (HSTs) and causes the disease Stagonospora nodorum blotch (SNB). The wheat genes Snn1 and Tsn1 confer sensitivity to the HSTs SnTox1 and SnToxA, respectively. The objectives of this study were to dissect, quantify, and compare the effects of compatible Snn1-SnTox1 and Tsn1-SnToxA interactions on susceptibility in the wheat-S. nodorum pathosystem. Inoculation of a wheat doubled haploid population that segregates for both Snn1 and Tsn1 with an S. nodorum isolate that produces both SnTox1 and SnToxA indicated that both interactions were strongly associated with SNB susceptibility. The Snn1-SnTox1 and Tsn1-SnToxA interactions explained 22 and 28% of the variation in disease, respectively, and together they explained 48% indicating that their effects are largely additive. The Snn1-SnTox1 interaction accounted for 50% of the variation when the population was inoculated with an S. nodorum strain where the SnToxA gene has been mutated and thus eliminating the Tsn1-SnToxA interaction. These results support the notion that the wheat-S. nodorum pathosystem is largely based on multiple host-toxin interactions that follow an inverse gene-for-gene scenario at the host-toxin interface, but disease is quantitatively inherited due to the additive nature of compatible interactions. The elimination of either Snn1 or Tsn1 toxin sensitivity alleles resulted in decreased susceptibility, but the elimination of both interactions was required to obtain resistance. We propose the use of molecular markers to select against Snn1, Tsn1, and other toxin sensitivity alleles to develop wheat varieties with high levels of SNB resistance.