| Summary: | Salicylic acid (SA) is a key defense hormone associated with wheat resistance against Fusarium head blight, which is a severe disease mainly caused by <i>Fusarium graminearum</i>. Although <i>F. graminearum</i> can metabolize SA, it remains unclear how this metabolic activity affects the wheat⁻<i>F. graminearum</i> interaction. In this study, we identified a salicylate hydroxylase gene (<i>FG05_08116</i>; <i>FgNahG</i>) in <i>F. graminearum</i>. This gene encodes a protein that catalyzes the conversion of SA to catechol. Additionally, FgNahG was widely distributed within hyphae. Disrupting the <i>FgNahG</i> gene (Δ<i>FgNahG</i>) led to enhanced sensitivity to SA, increased accumulation of SA in wheat spikes during the early infection stage and inhibited development of head blight symptoms. However, <i>FgNahG</i> did not affect mycotoxin production. Re-introducing a functional <i>FgNahG</i> gene into the Δ<i>FgNahG</i> mutant recovered the wild-type phenotype. Moreover, the expression of <i>FgNahG</i> in transgenic <i>Arabidopsis thaliana</i> decreased the SA concentration and the resistance of leaves to <i>F. graminearum</i>. These results indicate that the endogenous SA in wheat influences the resistance against <i>F. graminearum</i>. Furthermore, the capacity to metabolize SA is an important factor affecting the ability of <i>F. graminearum</i> to infect wheat plants.
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