Geraniol nanoemulsion primes systemic resistance in Panax notoginseng via HDA6-mediated activation of jasmonic acid and ethylene defenses

Fusarium solani is a major causative agent of root rot in Panax notoginseng , severely limiting its cultivation. This study investigated the physiological and molecular mechanisms by which geraniol nanoemulsion (GNE), an environmentally friendly immune inducer, regulates resistance against root rot in P. notoginseng . Foliar application of GNE significantly reduced disease severity, with an induced resistance efficacy of 56.3%. This process was accompanied by rapid accumulation of reactive oxygen species (ROS) and nitric oxide (NO), as well as increased phenylalanine ammonia-lyase (PAL) activity. Transcriptomic analysis revealed that GNE activated defense-related pathways, including glutathione metabolism and the plant MAPK signaling pathway. Mechanistically, GNE specifically suppressed the expression of histone deacetylase HDA6, leading to a global increase in histone H3 lysine 9 acetylation (H3K9ac) levels. ChIP-qPCR confirmed significant enrichment of H3K9ac at the promoter regions of key transcription factors in the jasmonic acid (JA) and ethylene (ET) signaling pathways and their downstream defense genes correlating with their transcriptional activation and promoting JA and ET accumulation. Experiments with exogenous hormones and inhibitors further demonstrated that JA and ET signaling pathways are essential for GNE-induced resistance. The negative regulatory role of HDA6 in disease resistance was validated using an Arabidopsis hda6 mutant. In summary, this study proposes that GNE triggers resistance via at least two parallel branches. One is an HDA6-dependent epigenetic branch, whereby HDA6 suppression drives H3K9ac enrichment, MYC2 and ERF1 transcription, and JA/ET accumulation, HDA6-mediated epigenetic regulation is an important node of, but not the exclusive pathway for, GNE-induced resistance. The other comprises HDA6-independent early defense branches marked by ROS, NO, PAL activity, and likely additional hormonal or secondary-metabolite pathways. This study provides a novel strategy for the green control of P. notoginseng diseases.