Open AccessTime‐course expression QTL‐atlas of the global transcriptional response of wheat to Fusarium graminearum
Author(s) -
SamadZamini Mina,
Schweiger Wolfgang,
Nussbaumer Thomas,
Mayer Klaus F.X.,
Buerstmayr Hermann
Publication year - 2017
Publication title -
plant biotechnology journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.525
H-Index - 115
eISSN - 1467-7652
pISSN - 1467-7644
DOI - 10.1111/pbi.12729
Subject(s) - biology , quantitative trait locus , expression quantitative trait loci , genetics , doubled haploidy , fusarium , population , transcriptome , trichothecene , gene , gene expression profiling , genomics , genome , gene expression , genotype , single nucleotide polymorphism , demography , sociology
Summary 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 h and 15 888 eQTL at 50 h 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.