Fusarium head blight (FHB), mainly caused by Fusarium graminearum, is one of the most destructive fungal diseases of wheat (Triticum aestivum L.). Because of the quantitative nature of FHB resistance, its mechanism is poorly understood. We conducted a comparative transcriptome analysis to identify genes that are differentially expressed in FHB-resistant and FHB-susceptible wheat lines grown under field conditions for various periods after F. graminearum infection and determined the chromosomal distribution of the differentially expressed genes (DEGs). For each line, the expression in the spike (which exhibits symptoms in the infected plants) was compared with that in the flag leaves (which do not exhibit symptoms in the infected plants). We identified an island of 53 constitutive DEGs in a 140 kb region with high homology to the FhbL693b region on chromosome 3B. Of these genes, 13 were assigned to specific chloroplast-related pathways. Furthermore, one gene encoded inositol monophosphate (IMPa) and two genes encoded ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO). Our findings suggest that the temporary susceptibility in locally infected spikes results from the cross-talk between RuBisCO and IMPa, which blocks secondary signaling pathways mediated by salicylic acid and induces a systemic acquired resistance in the distant leaf tissue.

Fusarium head blight (FHB), mainly caused by Fusarium graminearum, is a destructive disease in wheat. A population consisting of 229 F and F plants derived from the cross PI 672538 × L661 was used to evaluate the reactions to FHB. The FHB resistance data distribution in the F population indicates that some quantitative trait loci (QTLs) were controlling the FHB resistance in PI 672538. We further detected two major QTLs (Qfhs-2B, Qfhs-3B) from analysis of the resistance data and the PCR-amplified results using WinQTLCart 2.5 software. Qfhs-2B, flanked by Xbarc55-2B and Xbarc1155-2B, explained more than 11.6% of the phenotypic variation of the percentage of diseased spikelets (PDS), and Qfhs-3B, flanked by Xwmc54-3B and Xgwm566-3B, explained more than 10% of the PDS phenotypic variation in the F population. In addition, Qfhs-3B was different from Fhb1 in terms of the pedigree, inheritance, resistance response, chromosomal location, and marker diagnosis. We also detected QTLs for other disease resistance indices, including the percentage of damaged kernels and 1,000-grain weight, in similar chromosomal regions. Therefore, the FHB resistance of PI 672538 was mainly controlled by two major QTLs, mapped on 2B (FhbL693a) and 3B (FhbL693b). PI 672538 could be a useful germplasm for improving wheat FHB resistance.