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.

爱德华氏菌（E. piscicida）是淡水和海洋环境中的常见病原体，也是鱼类的重要肠道病原体。肠道中大量存在岩藻糖可能会调节相关基因，从而促进细菌的感染性。在这项研究中，野生型大肠杆菌和fuc P基因缺失菌株Δfuc P用于确定其毒力调节途径和定殖。结果表明，在键FusKR的基因转录水平和类型III分泌系统（T3SS）E. piscicida是由不同浓度的岩藻糖的上调。野生型和Δfuc与未添加岩藻糖相比，添加30 mM岩藻糖的P菌株生长更快。此外，添加有岩藻糖的野生型大肠杆菌的穿透力明显强于有岩藻糖的Δfuc P和没有岩藻糖的野生型大肠杆菌。同时，T3SS相关基因的基因转录水平的ESE B，ESE C，ESE d，ESE E，和ESE G中E. piscicida的后显著下调FUC P基因突变体。最后，被野生型菌株感染的罗非鱼显示出大肠埃希氏菌的显着增加。与那些感染了突变菌株的人相比，细菌定植率更高。所有结果表明，FucP E. piscicida介导的岩藻糖，以促进生长，能动性和罗非鱼肠道定植。