YgeP, a global regulator within the ETT2 pathogenicity island, coordinates motility-biofilm balance and negatively controls serum resistance in avian pathogenic Escherichia coli.
TL;DR
YgeP plays a central role in APEC pathogenesis by balancing two infection strategies: motility-mediated dissemination and colonization, and biofilm-mediated attachment and tolerance, and negatively regulates key virulence traits during the early stages of infection.
Abstract
Avian pathogenic Escherichia coli (APEC) is the primary pathogen causing avian colibacillosis, leading to significant economic losses in the global poultry industry. Its pathogenicity relies on a complex network of virulence factors, among which the type III secretion system 2 (ETT2) is a key component. However, unlike the classical T3SS, the ETT2 gene cluster in APEC commonly exhibits pseudogenization and deletions, suggesting that its function may have undergone adaptive remodeling. Notably, the YgeP gene located at the end of this pathogenicity island is highly conserved, implying that it may play an important role in the pathogenic process. To elucidate the function of YgeP, a member of this pathogenicity island, in APEC pathogenesis, a gene deletion mutant was constructed. The study confirmed that YgeP acts as a key global regulator, positively regulating bacterial motility by influencing the expression of flagellar synthesis-related genes. Conversely, YgeP negatively regulates biofilm formation and adhesion to chicken fibroblast cells. Additionally, YgeP differentially regulates bacterial tolerance to various environmental stresses, such as acid, alkali, heat, and oxidative stress. Mechanistically, YgeP negatively regulates serum resistance by inhibiting the Rcs phosphorelay system (manifested as upregulation of RcsA/B genes) and the expression of downstream capsular polysaccharide synthesis genes (e.g., wza, wzaA). Promoter activity assays further demonstrated that YgeP directly represses these target genes as a transcriptional repressor. Therefore, YgeP plays a central role in APEC pathogenesis by balancing two infection strategies: motility-mediated dissemination and colonization, and biofilm-mediated attachment and tolerance. Simultaneously, it negatively regulates key virulence traits, including serum resistance, during the early stages of infection.