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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 #347509

Title: Differential expression of the necrotrophic effector gene SnTox1 in the pathogen Parastagonospora nodorum

item PETERS, AMANDA - North Dakota State University
item Friesen, Timothy
item Faris, Justin

Submitted to: Plant and Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/2/2017
Publication Date: 1/13/2018
Citation: Peters, A.R., Friesen, T.L., Faris, J.D. 2018. Differential expression of the necrotrophic effector gene SnTox1 in the pathogen Parastagonospora nodorum. Plant and Animal Genome Conference XXVI. January 13-17, 2018, San Diego, CA. P1081.

Interpretive Summary:

Technical Abstract: Septoria nodorum blotch (SNB) is a major foliar disease on wheat, and is caused by the necrotrophic fungus Parastagonospora nodorum. The wheat-P. nodorum pathosystem involves the recognition of pathogen-produced necrotrophic effectors (NEs) by corresponding wheat NE sensitivity genes. Recognition leads to effector-triggered susceptibility and ultimately disease. In this study, we evaluated a recombinant inbred population that segregates for the NE sensitivity genes Snn1 and Tsn1, which recognize the P. nodorum NEs SnTox1 and SnToxA, respectively. The P. nodorum isolates Sn2000, which produces both SnTox1 and SnToxA, and Sn2000KO6-1, which is essentially identical to Sn2000 but harbors a disrupted SnToxA gene, were inoculated onto the population and disease was evaluated. For Sn2000, the Tsn1-SnToxA interaction explained 32.7% of the disease variation, with Snn1-SnTox1 explaining 7.1%. When Sn2000KO6 was inoculated onto plants, the Tsn1-SnToxA interaction was not significant and the Snn1-SnTox1 interaction explained 30.2% of the disease variation. Relative quantitative PCR experiments indicated that the level of SnTox1 expression was significantly higher at almost every time point in Sn2000KO6 compared to Sn2000, suggesting that the deletion of SnToxA resulted in increased SnTox1 expression in Sn2000. Differential expression of pathogen NE genes influences the overall importance of an interaction in its contribution to disease, providing another layer of complexity to this pathosystem.