AcrS Is a Potential Repressor of acrA Expression in Escherichia coli and Its Deletion Confers Increased Kanamycin Resistance in E. coli BW25113

AcrAB-TolC is a major efflux pump complex in the resistance nodulation-division family that is responsible for antibiotic resistance in Escherichia coli. Previous research has shown that deletion of the pump component protein, AcrA, leads to decreased drug resistance in E. coli. It is proposed that AcrS regulates the expression of AcrA, however, how acrA is regulated transcriptionally remains unknown. In this paper, the effect of acrS deletion on kanamycin resistance in E. coli was studied. Resistance to kanamycin in E. coli JW0452-3 (ΔacrA), E. coli JW3232-1 (ΔacrS) and E. coli BW25113 (wild-type) was compared using minimum inhibitory concentration (MIC) assays. MIC assay results showed that the ΔacrS strain had a higher resistance to kanamycin compared to both ΔacrA and the wild-type strain. These results suggest that AcrS might be a potential repressor of acrA in E. coli and the deletion of acrS leads to higher antibiotic resistance, possibly due to increased expression of AcrA, a critical component of AcrAB-TolC.