Omic characterisation of multi-component defences against the necrotrophic pathogen Pyrenophora tritici-repentis in wheat.

Abstract

Tan Spot disease is caused by the necrotrophic pathogen Pyrenophora tritici-repentis (Ptr) and poses a significant threat to global wheat production. Therefore, novel sources of resistance need to be identified, coupled with a fuller mechanistic understanding of host responses to Ptr. Herein, we characterise the interaction between a ToxA-positive Ptr strain and parental wheat lines from a multiparent advanced generation intercross (MAGIC) population. Genotypes displaying moderate resistance ('Robigus') or susceptibility ('Hereward') to Ptr challenge were identified and characterised through histological, metabolomic, and transcriptomic approaches. Histological investigations indicated the prominence of papilla-based defences in Robigus. Transcriptomic analyses could link this to the expression of barrier-related genes i.e. actin polymerisation, callose deposition, vesicle trafficking, and cellulose synthesis. Inhibiting actin polymerisation with cytochalasin E increased lesion numbers but did not augment lesion growth, suggesting the deployment of other defence mechanisms. These may be influenced by auxin, as its exogenous application exacerbated symptom development. Transcriptomic and metabolomic analyses in Hereward following challenge with Ptr suggested shifts in primary metabolism, affecting glycolysis, the TCA cycle, and the γ-aminobutyric acid (GABA) shunt. Activation of salicylic acid (SA)-associated genes, including NPR1 and WRKY33, was specific to Hereward, and exogenous SA increased susceptibility to Ptr in both genotypes. This study suggests barrier defences could be effective against Ptr as well as a lack of susceptibility factors like SA or the appropriate processing of IAA. These findings offer potential avenues for enhancing wheat resistance to Ptr.