High hydrostatic pressure treatment impairs AcrAB-TolC pump resulting in differential loss of deoxycholate tolerance in Escherichia coli.
We reported previously that high hydrostatic pressure-injured stationary phase cells of Escherichia coli K-12 lost their intrinsic deoxycholate tolerance. The AcrAB-TolC multi-drug resistance pump driven by proton motive force has been argued to be responsible for the tolerance to deoxycholate. In this report, we tested the sensitivity of the AcrAB-TolC (three components) pump to high hydrostatic pressure treatment (HPT). E. coli K-12 treated with HPT became sensitive to AcrAB-TolC-specific drugs such as ethidium bromide, but not to tetracycline which is pumped out by a one-component transporter, Tet. Only E. coli K-12 overproducing both AcrAB and TolC exhibited restored tolerance to deoxycholate after HPT but not E. coli overproducing either TolC or AcrAB. These observations strongly suggest that three-component pumps such as AcrAB-TolC are more susceptible to HPT than one-component pumps such as Tet, resulting in the differential loss of deoxycholate tolerance in high hydrostatic pressure-injured E. coli cells.
Kawarai
Taketo
T
Department of Food Science and Technology, College of Bioresource Sciences, Nihon University, Fujisawa, Kanagawa, Japan.
Ogihara
Hirokazu
H
Furukawa
Soichi
S
Aono
Rikizo
R
Kishima
Mami
M
Inagi
Yoshinori
Y
Irie
Ayako
A
Ida
Akari
A
Yamasaki
Makari
M
D001426:Bacterial Proteins / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D003840:Deoxycholic Acid / Q000494:pharmacology*; D024881:Drug Resistance, Bacterial / Q000502:physiology; D048168:Escherichia coli K12 / Q000254:growth & development* / Q000378:metabolism*; D006874:Hydrostatic Pressure
C493251:AcrAB-TolC protein, Salmonella enterica; D001426:Bacterial Proteins; D002352:Carrier Proteins; D003840:Deoxycholic Acid