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.

Soybean cyst nematodes (SCN, Heterodera glycines Ichinohe) are a significant threat to soybean production globally, causing severe yield losses and necessitating the development of effective strategies to combat this devastating nematode disease. This study presents dual RNA-seq analyses of the three most common SCN-resistant lines (Plant Introduction (PI) 437654, 548402, and 88788) and the susceptible line Lee74 against the SCN HG type 1.2.5.7 to identify the mechanisms of resistance and virulence genes involved in resistance breakdown. Transcriptomic and pathway analyses reveal the activation of the phenylpropanoid pathway, MAPK signaling pathway, plant hormone signal transduction, and secondary metabolite pathways in the resistance mechanisms. PI 437654, which exhibited robust resistance (female index, FI=0%), demonstrated unique gene expression associated with cell wall reinforcement, oxidative enzymes, ROS scavengers, and Ca+2 sensors governing the salicylic acid (SA) biosynthesis process, indicating its key defense mechanism. Moreover, using different hosts with varying levels of immunity and a susceptible line provided insights into SCN pathogenesis and how H. glycine overcomes different layers of host immunity by modulating its virulence genes. This research provides novel insights into the molecular mechanisms underlying soybean-SCN interactions and identifies potential targets for developing strategies to manage this devastating nematode disease.