Abstract
SummaryFusarium head blight (FHB) resistance in wheat is considered to be polygenic in nature. Cell wall fortification is one of the best resistance mechanisms in wheat against Fusarium graminearum which causes FHB. Metabolomics approach in our study led to the identification of a wide array of resistance‐related (RR) metabolites, among which hydroxycinnamic acid amides (HCAAs), such as coumaroylagmatine and coumaroylputrescine, were the highest fold change RR metabolites in the rachis of a resistant near‐isogenic line (NIL‐R) upon F. graminearum infection. Placement of these metabolites in the secondary metabolic pathway led to the identification of a gene encoding agmatine coumaroyl transferase, herein referred to as TaACT, as a candidate gene. Based on wheat survey sequence, TaACT was located within a FHB quantitative trait loci on chromosome 2DL (FHB QTL‐2DL) between the flanking markers WMC245 and GWM608. Phylogenetic analysis suggested that TaACT shared closest phylogenetic relationship with an ACT ortholog in barley. Sequence analysis of TaACT in resistant and susceptible NILs, with contrasting levels of resistance to FHB, led to the identification of several single nucleotide polymorphisms (SNPs) and two inversions that may be important for gene function. Further, a role for TaACT in FHB resistance was functionally validated by virus‐induced gene silencing (VIGS) in wheat NIL‐R and based on complementation studies in Arabidopsis with act mutant background. The disease severity, fungal biomass and RR metabolite analysis confirmed TaACT as an important gene in wheat FHB QTL‐2DL, conferring resistance to F. graminearum.
Highlights
Fusarium head blight (FHB) is a worldwide wheat disease caused by Fusarium graminearum that significantly affects yield and grain quality (Bai and Shaner, 1994, 2004; Dexter et al, 1996; Steiner et al, 2004)
We identified several fold change differences in hydroxycinnamic acid amides (HCAAs) metabolites including coumaroylagmatine and coumaroylputrescine in FHB QTL-2DL NIL-R compared to the susceptible NIL (NIL-S)
The fungal biomass, estimated by measuring the relative transcript levels of the F. graminearum housekeeping gene Tri6 (Transcription factor regulating trichothecene biosynthesis) was significantly (P < 0.05) lower in NIL-R than in NIL-S (Figure 2c), confirming the discrimination of resistance based on disease severity
Summary
Fusarium head blight (FHB) is a worldwide wheat disease caused by Fusarium graminearum that significantly affects yield and grain quality (Bai and Shaner, 1994, 2004; Dexter et al, 1996; Steiner et al, 2004). There is an urgent need to identify the resistance genes underlying the QTL and to decipher the resistance mechanisms for their use in breeding programs. The functional characterization of mapped QTL using an alternative approach, such as metabolomics, is considered one of the best tools to decipher the resistance mechanisms and genes underlying FHB resistance (Kushalappa and Gunnaiah, 2013). Such an approach has led to the identification of several RR metabolites in barley (Bollina et al, 2010; Kumaraswamy et al, 2011) and wheat (Gunnaiah et al, 2012). The RR metabolites and their biosynthetic resistance genes were identified (Pushpa et al, 2013; Yogendra et al, 2014, 2015)
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