| dc.description.abstract | The genes acrA and acrB, first identified in Escherichia coli encode components
of a Resistance-Nodulation-Cell Division (RND) efflux system shown to be important
for resistance to multiple antimicrobials. In Pseudomonas chlororaphis 30-84,
transcriptional analysis demonstrated that the RpeA/RpeB two-component transduction
system differentially regulated two genes immediately adjacent to rpeA and rpeB
annotated as acrA and acrB. In the present study, I showed that constitutive expression
of the 30-84 acrA/acrB genes conferred acriflavine resistance to E. coli and enhanced
acriflavine resistance in 30-84 and also conferred resistance to tetracycline,
chloramphenicol, and carbenicillin. Importantly, constitutive expression of acrA/acrB
enhanced the growth of E. coli in the presence of ~300-800 μg of total phenazines
extracted from 30-84, demonstrating the function of AcrA and AcrB in phenazine
transport. Constitutive overexpression of the acrAB operon in trans in wild type 30-84
resulted in enhanced phenazine production and transport. Phenazine production by the
30-84 rpeB mutant was not rescued by overexpression of acrA/acrB unless other
RpeA/RpeB controlled traits involved in the regulation of phenazine biosynthesis such
as quorum sensing also were restored. Earlier and greater production and diffusion of
phenazines significantly increased the capacity of 30-84 to inhibit fungal growth. These
data indicated that acrA/acrB enhanced RND-type transporter activities and phenazine
transport. Based on the findings from this study, a model is proposed to illustrate how
phenazine transport and biosynthesis are related in 30-84 and whether transport may contribute to positive catabolic feedback regulation of phenazine biosysnthesis. | en |
