Functional Characterisation of Fhb5 QTL Controlling Resistance to Spikelets Infection Against Fusarium graminearum using Wheat NILs

Wheat (Triticum aestivum) is a staple and economically important crop. Fusarium head blight (FHB), caused by Fusarium graminearum Schwabe (Teleomorph: Gibberella zeae (Schwein) Petch), is one of the most destructive diseases of wheat. Besides yield loss, serious concern is the accumulation of mycotoxins in grains. The resistance in wheat to FHB is quantitative in nature and is generally classified as Type I (resistance to initial infection) and Type II (resistance to spread of the disease within spike).  The QTL (Qfhs.ifa-5A or Fhb5) on 5AS chromosome of wheat explained 36% of phenotypic variation for Type-I FHB resistance. The Fhb5 locus has been fine mapped to 0.3cM.  The metabolomics of wheat near isogenic lines (NILs) with contrasting alleles for resistance to FHB at Fhb5 locus revealed several resistance-related (RR) metabolites. The identified RR metabolites belonged to phenylpropanoid and flavonoid biosynthetic pathways.  Hydroxycinnamic acid amides (HCAA’s), like p-coumaroyl putrescine, caffeoylputrescine and feruloyl tyramine, were identified as resistant related induced (RRI) metabolites. These HCAA’s are well known phytoallexins with  antimicrobial properties, that also reduce pathogen movement through plant cellwall thickening. The plausible reason for non-detection of un-conjugated putrescine is due to its conjugation with flavonoids and conversion into pyrroline, hydrogen peroxide (H₂O₂), ammonia and reactive oxygen species (ROS) by copper-containing diamine oxidase (DAO) enzyme. The released H₂O₂ and ROS may play a role in suppressing the pathogenesis.  The genes coding for DAO and key enzymes that synthesize HCAAs are rate-limiting factors to confer the FHB resistance in wheat.