Dual RNA-Seq and Metabolomics Reveal the Interaction Mechanism Between Konjac and Southern Blight

Konjac (Amorphophallus muelleri) is widely cultivated in southwest China because of its high glucomannan content. Southern blight, caused by Athelia rolfsii (Ar), is one of the most devastating fungal diseases affecting konjac growth and development, for which no effective control methods are currently available. Therefore, this study aimed to elucidate the mechanisms underlying konjac–Ar interactions using dual RNA-seq and metabolomics. During the early stage of infection, hormone-related gene expression was altered and transcript levels of photosynthesis-associated genes were significantly reduced. At later stages, host responses were characterized by sustained activation of the phenylpropanoid biosynthetic pathway and a progressive decline in energy metabolism, consistent with a gradual loss of defense capacity as the infection advances. In the pathogen, Ar exhibited coordinated upregulation of carbohydrate metabolism pathways, including genes encoding glycoside hydrolase (GH) family proteins and other putative virulence-related genes, consistent with necrotrophic colonization and the exploitation of host carbohydrates. Notably, syringin, an infection-induced phenylpropanoid metabolite, inhibited Ar growth in vitro with an EC50 of 67–69 µM, indicating moderate antifungal activity. Collectively, these findings provide insights into the molecular and metabolic responses underlying the konjac–Ar interaction and establish a foundation for further investigation of konjac defense mechanisms.