Synergistic action of abscisic acid and auxin in sweet potato defense against Sclerotium rolfsii

• Sweet potato counters S. rolfsii infection primarily through transcriptional activation, upregulating defense pathways and chitinase to degrade fungal cell walls. • Key roles for ethylene-responsive AP2/ERF transcription factors and core WRKY hubs (WRKY25, 46, and 70) in mediating sweet potato's defense against S. rolfsii . • Antagonistic ABA-IAA crosstalk as critical for antifungal immunity. The disease caused by the soil-borne fungus Sclerotium rolfsii poses a severe threat to sweet potato production. However, the molecular mechanisms underlying sweet potato defense against this devastating pathogen remain largely elusive. Here, we employed an integrated transcriptomic and metabolomic approach to characterize changes in sweet potato upon S. rolfsii infection. Metabolomic profiling revealed metabolic reprogramming, characterized by upregulation of phenolic and organic acids, synergistically modulate phytohormone signaling and membrane lipid metabolism. Further analysis highlighted that sweet potato counters S. rolfsii infection primarily through transcriptional activation, upregulating defense pathways (phenylpropanoid/flavonoid biosynthesis) and chitinase to degrade fungal cell walls. Conversely, the pathogen might secrete cell wall degrading enzymes increase to facilitate host tissue invasion. Functional enrichment and network analysis identified key roles for ethylene-responsive AP2/ERF transcription factors and core WRKY hubs (WRKY25, 46, and 70) in mediating sweet potato's defense against S. rolfsii . Collectively, this study uncovers the multidimensional defense mechanisms of sweet potato against S. rolfsii , providing novel insights for the development of disease-resistant varieties.