Underlying mechanisms of FHB susceptibility and resistance in wheat: Insights from a transcriptome-based analysis

Abstract

Over the last two decades, several quantitative trait loci (QTLs) involved in Fusarium head blight (FHB) resistance have been identified and, in a few cases, resolved to the underlying genes. These results have not consistently translated into better FHB-resistant wheat (Triticum aestivum L.) cultivars, nor have they necessarily extended our understanding of how resistance to FHB can be achieved. Despite considerable efforts, FHB remains a serious disease in many wheat-growing regions. To gain insights into the underlying biology, we examined the wheat transcriptome at a key FHB developmental time point—the switch from the biotrophic to the necrotrophic phase—in both highly resistant (AAC Tenacious) and highly susceptible (Wilkin) spring wheat cultivars. Sequestering of deoxynivalenol (DON) does not appear to differentiate the resistant from the susceptible response. Instead, our findings suggest that true resistance to FHB requires the plant to downregulate or limit two pathways that are normally associated with disease resistance responses: programmed cell death (PCD) and the generation/accumulation of reactive oxygen species (ROS). Using a stringent RNA-Seq analysis targeting the transition period of the pathogen from its biotrophic phase to its necrotrophic phase, we show that susceptibility to FHB relies on the pathogen's ability to highjack the PCD response, consistent with other necrotrophs. In contrast, the resistance response to FHB relies on the plant's ability to suppress its PCD response and limit the ROS accumulation/production that is necessary for production of DON by the pathogen.