Evolution, diversity, function, and marker-based elimination of the disease susceptibility geneSnn1in wheat

Abstract

AbstractSeptoria nodorum blotch (SNB), caused byParastagonospora nodorum,is a disease of durum and common wheat initiated by the recognition of pathogen-produced necrotrophic effectors (NEs) by specific wheat genes. The wheat geneSnn1encodes a wall-associated kinase that directly interacts with the NE SnTox1 leading to the development of SNB. Here, sequence analysis ofSnn1from 114 accessions including diploid, tetraploid and hexaploid wheat species revealed that some wheat lines possess two copies ofSnn1(designatedSnn1-B1andSnn1-B2) approximately 120 kb apart.Snn1-B2evolved relatively recently as a paralog ofSnn1-B1, and both genes have undergone diversifying selection. Three point mutations associated with the formation of the first SnTox1-sensitiveSnn1-B1allele from a primitive wild wheat were identified. Four subsequent and independent SNPs, three inSnn1-B1and one inSnn1-B2, converted the sensitive alleles to insensitive forms. Protein modeling indicated these four mutations could abolishSnn1-SnTox1 compatibility either through destabilization of the Snn1 protein or direct disruption of the protein-protein interaction. High-throughput markers were developed for the causal mutations and evaluated on panels of durum and common wheat. The markers were able to correctly identify 96.9 % of SnTox1-sensitive durum wheat accessions, and a marker for the null allele was 100% accurate at predicting SnTox1-insensitive lines in both durum and spring wheat. Results of this study increase our understanding of the evolution, diversity, and function ofSnn1-B1andSnn1-B2genes and will be useful for marker-assisted elimination of these genes for better host resistance.