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

<p>Supplementary data for a paper submission. The abstract is below.&nbsp;</p> <p>&nbsp;</p> <p><span><span>&middot;<span>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </span></span></span>Tan Spot disease is caused by the necrotrophic pathogen <em>Pyrenophora tritici-repentis</em> (<em>Ptr</em>) 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 <em>Ptr.</em></p> <p><span><span>&middot;<span>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </span></span></span>Herein, we characterise the interaction between <span>a <span>ToxA</span>-positive <em>Ptr</em> strain and parental wheat lines from a multiparent advanced generation intercross (MAGIC) population. Genotypes displaying moderate resistance (&lsquo;Robigus&rsquo;) or susceptibility (&lsquo;Hereward&rsquo;) to <em>Ptr </em>challenge were identified and characterised through histological, metabolomic, and transcriptomic approaches.</span></p> <p><span><span>&middot;<span>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </span></span></span><span>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. </span>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.</p> <p><span><span>&middot;<span>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </span></span></span>Transcriptomic and metabolomic analyses in Hereward following challenge with <em>Ptr</em> suggested shifts in primary metabolism, affecting glycolysis, the TCA cycle, and the &gamma;-<span>aminob</span>utyric acid (GABA) shunt. Activation of salicylic acid (SA)-associated genes, including NPR1 and WRKY33, was specific to Hereward, and exogenous SA increased susceptibility to <em><span>Ptr </span></em><span>in both genotypes</span>.</p> <p><span><span>&middot;<span>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </span></span></span>This study suggests <span>barrier defences </span>could be effective against <em><span>Ptr </span></em><span>as well as a lack of </span>susceptibility factors like SA or the appropriate processing of IAA. These findings offer potential avenues for enhancing wheat resistance to <em>Ptr</em>.</p>