FucP mediates fucose to regulate T3SS in Edwardsiella piscicida and promotes intestinal colonization in Tilapia

Abstract

Edwardsiella piscicida (E. piscicida) is a common pathogen in freshwater and marine environments and an important intestinal pathogen of fish. Fucose large presence in the intestines could possibly regulate relevant genes to promote bacterial infectivity. In this study, the wild-type E. piscicida and the fucP gene-deleted strain ΔfucP were used to identify its virulence-regulating pathway and colonization. The results showed that the gene transcription levels of key FusKR and type III secretion system (T3SS) in E. piscicida were upregulated by different concentrations of fucose. Both the wild-type and the ΔfucP strain grew faster with 30 mM fucose added than that without fucose added. In addition, the penetration of the wild-type E. piscicida with fucose added was significantly stronger than that of both ΔfucP with fucose and the wild-type E. piscicida without fucose. Meanwhile, the gene transcription levels of T3SS-related genes eseB, eseC, eseD, eseE, and eseG in E. piscicida were significantly downregulated after the fucP gene mutant. Finally, tilapia infected with the wild-type strain showed a significant increase in the E. piscicida colonization compared to those infected with the mutant strain. All results indicate that FucP of E. piscicida mediated fucose to promote the growth, motility, and intestinal colonization in tilapia.