Plasticity of transcriptional regulation under antibiotic stress

ABSTRACT: Evolution of antibiotic resistance in microbes is frequently achieved by acquisition of spontaneous mutations during antimicrobial therapy. Here we demonstrate that inactivation of a central regulator of iron homeostasis (fur) facilitates laboratory evolution of ciprofloxacin resistance in Escherichia coli. To decipher the underlying molecular mechanisms, we first performed a global transcriptome analysis and demonstrated a substantial reorganization of the Fur regulon in response to antibiotic treatment. We hypothesized that the impact of Fur on evolvability under antibiotic pressure is due to the elevated intracellular concentration of free iron and the consequent enhancement of oxidative damage-induced mutagenesis. In agreement with expectations, over-expression of iron storage proteins

ORGANISM(S): Escherichia coli K-12

SUBMITTER: Balazs Bogos 

PROVIDER: E-GEOD-55662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress