Characterization of Enterobacter sp. C2 and its impact on ginger metabolism and defense

Ginger (Zingiber officinale Roscoe), a globally significant medicinal and culinary crop, is increasingly threatened by soil-borne diseases, leading to substantial yield losses and economic damage. Although multiple pathogens contribute to these diseases, the involvement of Enterobacter species remains poorly characterized. In this study, we isolated and characterized a novel Enterobacter sp., strain C2, from infected ginger rhizomes. Pathogenicity assays revealed that C2 predominantly colonizes stem tissue, followed by root and leaf tissues. Genomic analysis showed that the C2 genome comprises 4.58 Mb, encoding 4222 predicted proteins, with pan-genome analysis indicating that 65.73 % of these genes are core genes, including known virulence determinants. Integration of multiomic data demonstrated that C2 pathogenicity is mediated by adhesion mechanisms, regulatory gene networks, secretion systems, toxin biosynthesis, and host invasion strategies. In response to C2 infection, ginger activates a robust antioxidant defense system and undergoes significant metabolic reprogramming, particularly in nucleotide and tryptophan metabolism, ABC transporters, and photosynthesis (p < 0.01). Notably, C2 flagellin triggers the upregulation of defense-related genes in ginger, including the activation of the phenylpropanoid pathway and induction of a hypersensitive response, which collectively restrict bacterial proliferation. This study elucidates the molecular mechanisms underlying Enterobacter-mediated pathogenesis in ginger and reveals key host metabolic and defense perturbations caused by C2 infection. Our findings provide a foundation for developing targeted strategies to mitigate soil-borne diseases in ginger cultivation.