flgK regulates food-related colonization and virulence potential of Vibrio mimicus in aquatic products.
TL;DR
It is demonstrated that flgK is indispensable for flagellar assembly, motility, and virulence in V. mimicus, and that its loss induces broad physiological adaptations that impair food-related persistence and host colonization, identifying flgK as a potential target for aquatic food safety interventions.
Abstract
Vibrio mimicus is a foodborne pathogen that contaminates aquatic products and causes gastroenteritis in humans. The flagellar protein FlgK is required for flagellar assembly and motility in several bacteria, but its role in V. mimicus remains unclear. In this study, we constructed an in-frame flgK deletion mutant and a complementary strain to investigate the biological functions of FlgK. Transmission electron microscopy revealed a complete loss of flagellar structures in the ΔflgK strain, which was restored upon complementation. Loss of flgK exerted no significant impact on bacterial growth yet abolished swimming motility entirely and diminished biofilm formation capacity. The ΔflgK strain exhibited significantly decreased adhesion to prawn, crayfish, plastic, glass, and stainless steel compared to the WT strain. Consistently, flgK deletion reduced colonization and pathogenicity in the prawn host. Transcriptomic analysis revealed extensive downregulation of flagellar biogenesis pathways accompanied by coordinated alterations in genes involved in transport processes and central metabolism in the ΔflgK strain. Collectively, these results demonstrate that flgK is indispensable for flagellar assembly, motility, and virulence in V. mimicus, and that its loss induces broad physiological adaptations that impair food-related persistence and host colonization, identifying flgK as a potential target for aquatic food safety interventions.