Functional Characterization of Triclosan-Resistant Enoyl-acyl-carrier Protein Reductase (FabV) in .

is extremely resistant to triclosan. Previous studies have shown that encodes a triclosan-resistant enoyl-acyl-carrier protein reductase (ENR), FabV, and that deletion of causes to be extremely sensitive to triclosan. In this report, we complemented a deletion strain with several triclosan-resistant ENR encoding genes, including and . All complemented strains restored triclosan resistance to the level of the wild-type strain, which confirmed that triclosan-resistant ENR allows to be extremely resistant to triclosan. Moreover, exhibits pleiotropic effects. Deletion of led to show attenuated swarming motility, decreased rhamnolipid, pyoverdine and acyl-homoserine lactones (AHLs) production. Complementation of the mutant with any one ENR encoding gene could restore these features to some extent, in comparison with the wild-type strain. Furthermore, we found that addition of exogenous AHLs could restore the mutant strain to swarm on semisolid plates and to produce more virulence factors than the mutant strain. These findings indicate that deletion of reduced the activity of ENR in , decreased fatty acid synthesis, and subsequently depressed the production of AHLs and other virulence factors, which finally may led to a reduction in the pathogenicity of . Therefore, should be an ideal target for the control of infectivity.