Distinct lipid and hormonal signatures reveal divergent responses to Erysiphe necator in resistant and susceptible grapevine genotypes

Background Powdery mildew, caused by the obligate biotroph Erysiphe necator, represents a major threat to grapevine production worldwide. Host-mediated resistance offers a sustainable alternative to chemical fungicides. To elucidate the role of plant membrane lipid modifications and oxylipin accumulation in pathogen perception and response, a controlled infection experiment was conducted comparing a resistant hybrid (NY_39) from the Edmund Mach Foundation germplasm collection with a susceptible variety (cv. ‘Teroldego’). Results A lipidomic approach was integrated with hormone profiling and lipoxygenase (LOX) gene expression analysis. Significant lipid modulation was observed following E. necator inoculation, highlighting the plasticity of membrane and storage lipids metabolism. A rapid decrease in triacylglycerol content was measured in NY_39 at 12 h post-inoculation (hpi), whereas the opposite trend occurred in ‘Teroldego’, suggesting divergent metabolic rearrangements. A fast galactolipids peroxidation occurred in NY_39, while a delayed accumulation of phosphatidic acid was observed in ‘Teroldego’ at 48 hpi. The resistant genotype exhibited higher constitutive levels of salicylic acid as well as the expression of the VviAMP1 defensin, a small cysteine-rich protein with broad-spectrum antifungal activity. VviPR10-s11 and VviWRKY51, related to the synthesis of lignin and stilbenoid phytoalexins, were induced at 12 hpi in both genotypes. Within the LOX family, significant up-regulation of the 9-LOX VviLOX1a and the 13-LOXs VviLOX9 and VviLOXO was specific to ‘Teroldego’ at 12 hpi, despite a higher constitutive level of VviLOX9 in NY_39. Conclusions This work identifies key metabolic, signalling and gene expression features in the selected hybrid that may be relevant for resistance. These include rapid triacylglycerols degradation, galactolipid peroxidation, constitutive higher SA level and expression of the defensin VviAMP1.