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Multidrug efflux systems contribute to antimicrobial resistance and pathogenicity in bacteria. Here, we report the identification and characterization of a transcriptional regulator AcrR controlling the yet uncharacterized multidrug efflux pump, AcrAB in  Acinetobacter nosocomialis. In silico  analysis revealed that the homologs of AcrR and AcrAB are reported in the genomes of many other bacterial species. We confirmed that the genes encoding the AcrAB efflux pump,  acrA  and  acrB  forms a polycistronic operon which is under the control of  acrR  gene upstream of  acrA . Bioinformatic analysis indicated the presence of AcrR binding motif in the promoter region of  acrAB  operon and the specific binding of AcrR was confirmed by electrophoretic mobility shift assay (EMSA). The EMSA data showed that AcrR binds to −89 bp upstream of the start codon of  acrA . The mRNA expression analysis depicted that the expression of  acrA  and  acrB  genes are elevated in the deletion mutant compared to that in the wild type confirming that AcrR acts as a repressor of  acrAB  operon in  A. nosocomialis . The deletion of  acrR  resulted in increased motility, biofilm/pellicle formation and invasion in  A. nosocomialis . We further analyzed the role of AcrR in  A. nosocomialis  pathogenesis  in vivo  using murine model and it was shown that  acrR  mutant is highly virulent inducing severe infection in mouse leading to host death. In addition, the intracellular survival rate of  acrR  mutant was higher compared to that of wild type. Our data demonstrates that AcrR functions as an important regulator of AcrAB efflux pump and is associated with several phenotypes such as motility, biofilm/pellicle formation and pathogenesis in  A. nosocomialis .

Local Repressor AcrR Regulates AcrAB Efflux Pump Required for Biofilm Formation and Virulence in Acinetobacter nosocomialis