AcfA is an essential regulator for pathogenesis of fish pathogen Vibrio alginolyticus.

Abstract

V. alginolyticus is an important opportunistic pathogen which causes vibriosis in aquatic animals. AcfA, as an accessory colonization factor, is hypothesized to be involved in the pathogenesis of infection. In this study, a mutant strain with an in-frame deletion removed nucleotides 86 to 561 of the acfA gene was constructed to reveal the role of AcfA in the physiology and virulence from V. alginolyticus. An acfA mutant showed a similar growth level, an obvious decrease in swarming motility and the activity of ECPase, a higher LDvalue by intraperitoneal injection of grouper fish compared to that of the wild-type. Furthermore, the deletion of acfA could enhance the level of biofilm formation and suppress the polar flagellum forming. The comparative proteomic analysis demonstrated the deletion mutation of acfA could up-regulate the expression of 4 proteins of p4alcd, deoD, phb and DctP, and down-regulate the expression of 8 proteins of Clp, hpV36980, ABCtp, pepD, arA, aggp, fla and ompA compared to that of the wild-type. The analysis of RT-qPCR showed the mRNA levels of DctP and deoD were significantly induced, and the mRNA levels of pepD, arA, fla and ompA were significantly reduced in acfA mutant compared with the wild-type. The results suggest that acfA may contribute to the overall success in the pathogenesis of V. alginolyticus by regulating the expression of some relevant genes.