Creating rust resistance in wheat via modification of host genes

Abstract

A major challenge to resistance breeding in bread wheat (Triticum aestivum L.) is limited genetic diversity. The traditional approach to combating this problem is introgression of resistant genes from other closely related species into elite but susceptible cultivars. This strategy is often associated with linkage drag. Moreover, pathogens continue to evolve into different and more virulent forms (races) that overcome these resistant genes in a process called resistance breakdown. A typical example is the outbreak of Ug99, a novel African stem rust pathotype that exhibited virulence against numerous stem rust resistance genes. Creating resistance within wheat's own genome is a panacea to the challenges surrounding the traditional method. Biotrophic plant pathogens such as wheat rusts are known to manipulate host genes as a means of overcoming host defense response and acquiring nutrients. Central to wheat-rust interactions is highly sophisticated immune repertoire consisting of diverse signal perception and intracellular signaling pathways which are regulated by transcriptional regulators and co-factors. Unfortunately, pathogen effector proteins also take advantage of host plant genes (so called pathogen susceptible host genes) including transcriptional mechanisms. Hence editing the genes targeted by these pathogens in wheat is a valuable means of creating host resistance that has been neglected. We conducted these studies to identify host genes targeted by rust pathogens through bioinformatics approaches including transcriptome analysis which showed that wheat NPR1 genes (transcriptional regulator) and MYC4 and MY21 (transcription factors) are negatively involved compatible wheat-rust interactions. Subsequently, when these genes were down regulated in susceptible Chinese Spring using Barley Mosaic Virus Induced Gene Silencing (BSMV) assay, the silenced plants became resistant to rust pathogens. Loss-of-function mutations created in these homeologs via Ethyl methanesulfonate mutagenesis conferred resistant to rust pathogens. Consequently, this study led to the development of new rust resistance germplasms.