Abstract
Fusarium head blight (FHB), caused by the fungus Fusarium graminearum, represents one of the major wheat diseases worldwide, determining severe yield losses and reduction of grain quality due to the accumulation of mycotoxins. The molecular response associated with the wheat 2DL FHB resistance QTL was mined through a comprehensive transcriptomic analysis of the early response to F. graminearum infection, at 3 days post-inoculation, in spikelets and rachis. The analyses were conducted on two near isogenic lines (NILs) differing for the presence of the 2DL QTL (2-2618, resistant 2DL+ and 2-2890, susceptible null). The general response to fungal infection in terms of mRNAs accumulation trend was similar in both NILs, even though involving an higher number of DEGs in the susceptible NIL, and included down-regulation of the primary and energy metabolism, up-regulation of enzymes implicated in lignin and phenylpropanoid biosynthesis, activation of hormons biosynthesis and signal transduction pathways and genes involved in redox homeostasis and transcriptional regulation. The search for candidate genes with expression profiles associated with the 2DL QTL for FHB resistance led to the discovery of processes differentially modulated in the R and S NILs related to cell wall metabolism, sugar and JA signaling, signal reception and transduction, regulation of the redox status and transcription factors. Wheat FHB response-related miRNAs differentially regulated were also identified as putatively implicated in the superoxide dismutase activities and affecting genes regulating responses to biotic/abiotic stresses and auxin signaling. Altered gene expression was also observed for fungal non-codingRNAs. The putative targets of two of these were represented by the wheat gene WIR1A, involved in resistance response, and a gene encoding a jacalin-related lectin protein, which participate in biotic and abiotic stress response, supporting the presence of a cross-talk between the plant and the fungus.
Highlights
Fusarium head blight (FHB), caused by the filamentous ascomycete Fusarium graminearum Schwabe [telomorph Gibberella zeae (Schwein.) Petch], represents one of the major wheat diseases worldwide, resulting in yield losses because of kernel shriveling, reduction of grain quality due to a selective loss of albumin and gluten proteins in the seed endosperm, and accumulation of toxic fungal secondary metabolites known as mycotoxins including deoxynivalenol (DON) and its dereivatives 3-acetyl-deoxynivalenol and 15-acetyl-deoxynivalenol (Brown et al, 2010).The genetic bases of both FHB resistance type I and type II, have been largely studied and a number of major and minor FHB resistance quantitative trait locus (QTL) have been mapped in the wheat (Triticum aestivum) genome, supplying useful tools for breeding programs (Buerstmayr et al, 2009)
These data suggest some interaction between the resistance QTL and other genes present in the 2-2674 genetic background and reflect previous observations made by Long et al (2015) as in the S null 2-2890 the spreading of the infection occurred at greater extent compared to the R 2DL+ 2-2618, a finding in agreement with a type II resistance conferred by the 2DL FHB QTL
A comprehensive transcriptomic analysis of spikelets and rachis from two bread wheat near isogenic line (NIL), differing for the presence of the 2DL FHB resistance QTL, inoculated with F. graminearum at 3 dpi and mock, was performed to gain new insight in the molecular response associated with FHB tolerance
Summary
Fusarium head blight (FHB), caused by the filamentous ascomycete Fusarium graminearum Schwabe [telomorph Gibberella zeae (Schwein.) Petch], represents one of the major wheat diseases worldwide, resulting in yield losses because of kernel shriveling, reduction of grain quality due to a selective loss of albumin and gluten proteins in the seed endosperm, and accumulation of toxic fungal secondary metabolites known as mycotoxins including deoxynivalenol (DON) and its dereivatives 3-acetyl-deoxynivalenol and 15-acetyl-deoxynivalenol (Brown et al, 2010).The genetic bases of both FHB resistance type I (resistance to initial spikelet infection) and type II (resistance to the Transmission of FHB to other spikelets along the rachis), have been largely studied and a number of major and minor FHB resistance QTLs have been mapped in the wheat (Triticum aestivum) genome, supplying useful tools for breeding programs (Buerstmayr et al, 2009). The gene responsible for only one FHB resistance QTL, Fhb located on chromosome 3BS and conferring a durable broad-spectrum resistance, has been cloned and characterized. The type I Fhb resistance, derived from the wheat cultivar (cv) Sumai 3, is due to the action of a pore-forming toxin-like (PTF) gene which encodes a chimeric lectin with two agglutinin domains and one ETX/MTX2 toxin domain (Rawat et al, 2016). It has been proposed that the PFT protein may participate in the recognition of fungal carbohydrates and cause toxicity to the fungus, arresting its growth by interacting with the fungal wall (Rawat et al, 2016). Candidate genes were proposed for the Fhb QTL, located on chromosome 6BS and derived from Sumai 3, using an integrated large scale metabolo-transcriptomic
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