Stearic Acid in Grapevine Cuticular Wax Acts as a Chemical Stimulator of Erysiphe necator Conidial Germination

Cuticular wax metabolites on leaf surfaces function as chemical interfaces that modulate the pre-penetration development of phytopathogenic fungi. However, the specific monomeric constituents in grapevine leaf wax that regulate conidial germination and host recognition by grapevine powdery mildew caused by Erysiphe necator remain elusive. Here, we compared leaf cuticular wax characteristics between four susceptible Vitis vinifera cultivars and three resistant Chinese wild Vitis accessions. Scanning electron microscopy coupled with gravimetric analysis revealed that susceptible V. vinifera cultivars exhibited lower wax loads and lamellar crystals, whereas resistant Chinese wild Vitis accessions displayed higher wax accumulation with granular or blocky crystals. Gas chromatography–mass spectrometry profiling further demonstrated divergent compositional patterns: primary alcohols predominated among susceptible V. vinifera cultivars, while aldehydes and alkanes were enriched in resistant Chinese wild Vitis accessions. Paradoxically, in vitro conidial germination assays showed that wax extracts from all grapevines significantly promoted En. NAFU1 conidial germination, indicating that resistance in Chinese wild Vitis accessions is independent of direct wax-mediated inhibition of spore germination. Bioassays of representative monomers revealed that n-triacontane suppressed germination at high concentrations, whereas n-dotriacontanol and stearic acid stimulated it. Collectively, these findings demonstrate that specific cuticular wax monomers exert distinct biological effects on En. NAFU1 conidial germination. Given the ubiquitous presence and concentration-dependent stimulatory activity of stearic acid, we hypothesize that this monomer serves as a conserved chemical cue enabling initial host recognition by En. NAFU1, whereas the differential susceptibility among grapevine genotypes is governed by downstream physical and induced defense mechanisms rather than by variation in stearic acid levels.