Elicitor specific mechanisms of defence priming in oak seedlings against powdery mildew

Abstract

Defence priming sensitises plant defences to enable a faster and/or stronger response to subsequent stress. Various chemicals can trigger priming; however, the response remains unexplored in oak. Here, we characterise salicylic acid (SA)-, jasmonic acid (JA)-, and {beta}-aminobutyric acid (BABA)-induced priming of oak seedlings against the causal agent of powdery mildew (Erysiphe alphitoides, PM). Whilst JA had no effects, BABA and SA enhanced resistance by priming callose deposition and SA-dependent gene expression, respectively. Untargeted transcriptome and metabolome analyses revealed genes and metabolites uniquely primed by BABA, SA, and JA. Enrichment analyses demonstrated a limited number of pathways differentiating the three treatments or the resistance-inducing elicitors BABA and SA. However, a similar mode of action between BABA and JA was identified. Moreover, our analyses revealed a lack of crosstalk between SA and JA. Interestingly, priming by BABA was linked to alkaloid, lignan, phenylpropanoid, and indolitic compounds biosynthesis. Moreover, integration of the omics analyses revealed the role of ubiquitination and protein degradation in priming by BABA. Our results confirm the existence of chemical-induced priming in oak and has identified specific molecular markers associated with well-characterised elicitor.