Fusarium head blight is a devastating disease of small grain cereals such as bread wheat (Triticum aestivum). The pathogen switches from a biotrophic to a nectrotrophic lifestyle in course of disease development forcing its host to adapt its defence strategies. Using a genetical genomics approach we illustrate genome-wide reconfigurations of genetic control over transcript abundances between two decisive time points after inoculation with the causative pathogen Fusarium graminearum. Whole transcriptome measurements have been recorded for 163 lines of a wheat doubled haploid population segregating for several resistance genes yielding 15 552 at 30 hours and 15 888 eQTL at 50 hours after inoculation. The genetic map saturated with transcript abundance-derived markers identified of a novel QTL on chromosome 6A, besides the previously reported QTL Fhb1 and Qfhs.ifa-5A. We find a highly different distribution of eQTL between time points with about 40% of eQTL being unique for the respective assessed time points. But also for more than 20% of genes governed by eQTL at either time point genetic control changes in time. These changes are reflected in the dynamic compositions of three major regulatory hotspots on chromosomes 2B, 4A and 5A. In particular control of defence-related biological mechanisms concentrated in the hotspot at 4A shift to hotspot 2B as the disease progresses. Hotspots do not colocalize with phenotypic QTL and within their intervals no higher than expected number of eQTL was detected. Thus, resistance conferred by either QTL is mediated by few or single genes.