Characterization of the role of ybgC in lysozyme resistance of Salmonella Enteritidis

Abstract The ybgC gene (encoding for acyl-CoA thioesterase) was shown to play a crucial role in the survival of Salmonella Enteritidis ( S . Enteritidis) in egg white in our previous study. In this study, the resistance mechanisms of S . Enteritidis wild-type, △ ybgC mutant, and △ ybgC -C complemented strains to lysozyme (a major antibacterial component of egg white) were explored by survival ability test, cell membrane characterization, and gene expression analysis. Our results showed that a 6-log reduction was observed with the △ ybgC mutant after incubation in egg white filtrate-lysozyme (FEW-LY) for 24 h, compared to the wild-type and △ ybgC -C complemented strains. Meanwhile, the △ ybgC mutant exhibited a significant increase in outer membrane permeability, along with the alteration from a rod to a spherical shape and the occurrence of cell lysis. Additionally, the amount of C14:0 and C17:0 cyclo fatty acids was decreased, while that of C18:1ω7c and C19:0 cyclo ω8c fatty acids was increased, respectively, in response to lysozyme by the deletion of ybgC . Genes responsible for the synthesis of fatty acids ( fadR , fabBDG , acpP , cfa , and tesAB ), phospholipid ( aas , plsB , and plsC ), and lipid A ( lpxA ) were up-regulated in the △ ybgC mutant after exposure to lysozyme. Taken together, these results indicate that deletion of ybgC induced the expression of membrane lipid composition-related genes probably contributing to alterations in fatty acid and phospholipid composition in S . Enteritidis, which resulted in an increase in outer membrane permeability conducing to a reduced resistance to lysozyme. Moreover, the ybgC gene has potential as a novel molecular target for controlling S . Enteritidis in eggs.