Poster
Gongjun Shi
North Dakota State University
Fargo, North Dakota, United States
Paula Moolhuijzen
Curtin University
Perth, Western Australia, Australia
Pao Theen See
Curtin University
Perth, Western Australia, Australia
Justin Faris
Edward T. Schafer Agricultural Research Center, USDA-ARS
Fargo, North Dakota, United States
Zhaohui Liu
Department of Plant Pathology, North Dakota State University
Fargo, North Dakota, United States
Pyrenophora tritici-repentis (Ptr) is the causal agent of tan spot, a significant foliar disease of wheat worldwide. Ptr ToxC, one of the necrotrophic effectors produced by Ptr, induces chlorosis on wheat lines carrying Tsc1. Ptr ToxC was partially characterized over 20 years ago as a secondary metabolite. We recently cloned a conserved hypothetical gene (ToxC1) that is required but insufficient for Ptr ToxC production. To identify additional genes for Ptr ToxC production and characterize its molecular function in compatible Ptr ToxC-Tsc1 interactions, a ToxC1-deleted mutant of a race 1 isolate was used along with the wild-type in an in-planta transcriptome analysis. Differential gene expression between the mutant and wild-type on a Ptr ToxC differential wheat line was profiled over four-time points: 0-, 1-, 3- and 5- day post inoculation. In the absence of ToxC1, the expression of Ptr genes involved in cellular iron and peptide uptake, and detoxification were perturbed. Three genes close to ToxC1 showed an upregulated expression and were further demonstrated to be required for the Ptr ToxC production through gene knockout experiments. On the host side, significant down-regulation of a potential Tsc1 candidate gene encoding a leucine-rich repeat and protein kinase (LRR-PK) was detected upon the infection of the ToxC1-deleted strain. Our findings provide further insight into molecular mechanisms governing Ptr ToxC production and host-pathogen interactions in wheat tan spot.