AUTHOR=Huang Yong-Heng , Lin Jin-Shui , Ma Jin-Cheng , Wang Hai-Hong 

TITLE=Functional Characterization of Triclosan-Resistant Enoyl-acyl-carrier Protein Reductase (FabV) in Pseudomonas aeruginosa

JOURNAL=Frontiers in Microbiology

VOLUME=7

YEAR=2016

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2016.01903

DOI=10.3389/fmicb.2016.01903

ISSN=1664-302X

ABSTRACT=<p><italic>Pseudomonas aeruginosa</italic> is extremely resistant to triclosan. Previous studies have shown that <italic>P. aeruginosa</italic> encodes a triclosan-resistant enoyl-acyl-carrier protein reductase (ENR), FabV, and that deletion of <italic>fabV</italic> causes <italic>P. aeruginosa</italic> to be extremely sensitive to triclosan. In this report, we complemented a <italic>P. aeruginosa fabV</italic> deletion strain with several triclosan-resistant ENR encoding genes, including <italic>Vibrio cholerae fabV, Bacillus subtilis fabL</italic> and <italic>Enterococcus faecalis fabK</italic>. All complemented strains restored triclosan resistance to the level of the wild-type strain, which confirmed that triclosan-resistant ENR allows <italic>P. aeruginosa</italic> to be extremely resistant to triclosan. Moreover, <italic>fabV</italic> exhibits pleiotropic effects. Deletion of <italic>fabV</italic> led <italic>P. aeruginosa</italic> to show attenuated swarming motility, decreased rhamnolipid, pyoverdine and acyl-homoserine lactones (AHLs) production. Complementation of the <italic>fabV</italic> 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 <italic>fabV</italic> mutant strain to swarm on semisolid plates and to produce more virulence factors than the <italic>fabV</italic> mutant strain. These findings indicate that deletion of <italic>fabV</italic> reduced the activity of ENR in <italic>P. aeruginosa</italic>, 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 <italic>P. aeruginosa</italic>. Therefore, <italic>fabV</italic> should be an ideal target for the control of <italic>P. aeruginosa</italic> infectivity.</p>