Molecular Genetic Characterization of Ptr ToxC-Tsc1 Interaction and Comparative Genomics of Pyrenophora tritici-repentis

Abstract

Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an economically important disease worldwide. The disease system is known to involve three pairs of interactions between fungal-produced necrotrophic effectors (NEs) and the wheat sensitivity genes, namely Ptr ToxA-Tsn1, Ptr ToxB-Tsc2 and Ptr ToxC-Tsc1, all of which result in susceptibility. Many lines of evidence also suggested the involvement of additional fungal virulence and host resistance factors. Due to the non-proteinaceous nature, Ptr ToxC, has not been purified and the fungal gene (s) controlling Ptr ToxC production is unknown. The objective for the first part of research is to map the fungal gene (s) controlling Ptr ToxC production. Therefore, A bi-parental fungal population segregating for Ptr ToxC production was first developed from genetically modified heterothallic strains of AR CrossB10 (Ptr ToxC producer) and 86-124 (Ptr ToxC non-producer), and then was genotyped and phenotyped. Using the data, the gene (s) was mapped to the distal end of chromosome 2 in the reference genome of Pt-1c-BFP. The objective for the second part of my research is to develop genomic and genetic resources for the fungal pathogen. A high quality of genome sequence for AR CrossB10 and the first P. tritici-repentis genetic linkage map was generated. The AR CrossB10 genome and genetic linkage map is highly comparable to newly published reference genome except some noticeable chromosomal structural variations (SVs). Comparison of the genome sequences between parental isolates and twenty progeny isolates also revealed some SVs including deletion, insertion and inversion were detected that likely occurred during the fungal sexual reproduction. The objective for the third of my research is to characterize genetic resistance in Nebraskan winter wheat cultivar ‘Wesley’ using QTL mapping in a recombinant inbred line population. The results showed that resistance in Wesley is largely due to the lack of susceptibility genes Tsc1 and Tsn1. My Ph.D. research provides a further understanding of the genetics of host-pathogen interaction in wheat tan spot and contributes knowledge and tools for breeding tan spot resistant cultivars.