Poster
Ashley Nelson
Ph.D. Candidate
Department of Plant Pathology, North Dakota State University, Fargo
Fargo, North Dakota, United States
Gayan Kariyawasam
Department of Entomology and Plant Pathology, University of Tennessee, Knoxville
Knoxville, Tennessee, United States
Michele C. Malvestiti
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
Zhaohui Liu
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
Justin Faris
Edward T. Schafer Agricultural Research Center, USDA-ARS
Fargo, North Dakota, United States
Timothy Friesen
Edward T. Schafer Agricultural Research Center, USDA-ARS
Fargo, North Dakota, United States
Parastagonospora nodorum is an economically important necrotrophic fungal pathogen that causes septoria nodorum blotch (SNB) of wheat. P. nodorum secretes a variety of necrotrophic effectors that interact directly or indirectly with host susceptibility genes. SnTox5 is a necrotrophic effector that indirectly interacts with the wheat susceptibility gene Snn5. Characterization using confocal microscopy showed that SnTox5 targets the wheat susceptibility gene Snn5 to induce programmed cell death (PCD) as well as facilitate mesophyll colonization, even in the absence of Snn5. Protein structural prediction showed that SnTox5 has high structural homology to SnTox3, which directly interacts with the wheat pathogenicity-related protein, TaPR-1-1. Given SnTox5’s predicted role in mesophyll colonization and its structural homology to SnTox3, we hypothesize that SnTox5 has a function in suppressing host defenses before induction of PCD. To understand the plant targets of SnTox5, we used a yeast two-hybrid assay to identify wheat proteins that directly interact with SnTox5. The identified wheat protein interactors targeted by SnTox5 will be discussed. Future experiments include multifaceted validation of interacting proteins of interest. This work will provide information on how necrotrophic effectors not only target host susceptibility pathways but also target other aspects of host defense to help complete the pathogen’s life cycle.