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

Defense priming sensitises plant defenses to enable a faster and stronger response to subsequent stress. Various chemicals can trigger priming, however the response remains unexplored in oak. Following treatment with salicylic acid (SA), jasmonic acid (JA), or ß-aminobutyric acid (BABA), oak (Quercus robur) seedlings were infected with oak powdery mildew (Erysiphe alphitoides, PM). Whilst JA increased susceptibility to PM, BABA and SA enhanced resistance by priming callose deposition and SA-dependent gene expression, respectively. All three treatments had no impact on growth. To characterise molecular markers of priming, untargeted transcriptome and metabolome analyses were performed using RNAseq and LC-MS/MS. Differential gene expression analysis revealed around 2900, 1600, and 900 genes uniquely primed by each treatment BABA, SA, and JA, respectively. A limited number of enriched GO terms differentiated the three treatments. Meanwhile, metabolome analysis found roughly 340, 220, and 40 accumulated masses uniquely primed by BABA, SA, and JA, respectively. Pathway enrichment analysis linked BABA priming to alkaloids biosynthesis, whereas no specific pathways were identified for SA and JA priming. Our results confirm the existence of chemical-induced priming in oak and putatively identify associated molecular markers. Overall design: Examination of the trascriptome of leaves of Quercus robur (Forestart), from plants exposed to elicitors, including ß-aminobutyric (BABA), Salicylic acid (SA) and Jasmonic acid (JA), and then infected with the powdery mildew causal agent, Erysiphe alphitoides; along with water-treated and mock inoculated controls.