Open AccessEffects of sarA inactivation on the intrinsic multidrug resistance mechanism of Staphylococcus aureus
Author(s) -
O'Leary Jessica O.,
Langevin Mark J.,
Price Christopher T.D.,
Blevins Jon S.,
Smeltzer Mark S.,
Gustafson John E.
Publication year - 2004
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2004.tb09710.x
Subject(s) - staphylococcus aureus , mutant , fusidic acid , microbiology and biotechnology , ciprofloxacin , vancomycin , multiple drug resistance , biology , antibiotics , ethidium bromide , gene , chemistry , bacteria , genetics , dna
The sarA locus of Staphylococccus aureus regulates the synthesis of over 100 genes on the S. aureus chromosome. We now report the effects of sarA inactivation on intrinsic multidrug resistance expression by S. aureus . In a strain‐dependent fashion, sarA :: kan mutants of three unrelated strains of S. aureus demonstrated significantly increased susceptibility to five or more of the following substances: the antibiotics ciprofloxacin, fusidic acid, and vancomycin; the DNA‐intercalating agent ethidium; and four common household cleaner formulations. In addition, all three sarA :: kan mutants demonstrated significantly increased accumulation of ciprofloxacin and one sarA :: kan mutant demonstrated increased ethidium accumulation. Our data therefore indicate that sarA plays a role in the intrinsic multidrug resistance mechanism expressed by S. aureus , in part by regulating drug accumulation.