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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 #335867

Research Project: Genetic Improvement of Durum and Spring Wheat for Quality and Resistance to Diseases and Pests

Location: Cereal Crops Research

Title: Quantification of disease expression conferred by three host gene-necrotrophic effector interactions in the wheat-Parastagonospora nodorum pathosystem

Author
item Peters, Amanda - North Dakota State University
item Friesen, Timothy
item Faris, Justin

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2016
Publication Date: 1/13/2017
Citation: Peters, A.R., Friesen, T.L., Faris, J.D. 2017. Quantification of disease expression conferred by three host gene-necrotrophic effector interactions in the wheat-Parastagonospora nodorum pathosystem [abstract]. Plant and Animal Genome Conference, January 14-18, 2017, San Diego, CA.

Interpretive Summary:

Technical Abstract: Septoria nodorum blotch (SNB), which is a major foliar disease on wheat is caused by the necrotrophic fungus Parastagonospora nodorum. The wheat-P. nodorum pathosystem involves the recognition of necrotrophic effectors (NEs) secreted by P. nodorum by corresponding wheat NE sensitivity genes. Recognition leads to effector-triggered susceptibility and ultimately disease. The objective of this project is to determine the effects of multiple host-NE interactions alone and in various combinations to determine the relative importance of these interactions in causing disease. A recombinant inbred wheat population was developed that segregates for the NE sensitivity genes Snn1, Snn3-B1, and Tsn1, which recognize the NEs SnTox1, SnTox3, and SnToxA, respectively. P. nodorum isolates that produce various combinations of the three NEs were used to quantify the level of disease explained by each interaction through spore inoculations and QTL analysis. When present, the Tsn1-SnToxA interaction accounted for 15-33% of the disease variation, and Snn3-B1-SnTox3 explained 19-25%. The Snn1-SnTox1 interaction explained as much as 31% of the variation, but the Snn3-B1-SnTox3 and Tsn1-SnToxA interactions were epistatic to the Snn1-SnTox1 interaction in some isolates as revealed through the analysis of knockout mutants. Currently, experiments to determine if NE expression is associated with disease susceptibility are being conducted. Results from this research will contribute to the understanding this pathosystem and provide researchers with knowledge for reducing losses to SNB.