Regulatory proteins control a transcriptional network in response to antibiotic stress

In a given bacterial population, antibiotic treatment kills a large portion of the population, while a small, tolerant subpopulation survives. Tolerant cells disrupt the efficacy of antibiotic treatment and increase the likelihood that a population gains antibiotic resistance. Antibiotic tolerance is different from resistance because tolerant cells cannot grow and replicate in the presence of the antibiotic, but when the antibiotic is removed, they begin to propagate. When a population becomes resistant, the antibiotic becomes ineffective, which is a major health concern. Since antibiotic tolerance often leads to antibiotic resistance, we have taken a systems biology approach to examine how regulatory networks respond to antibiotic stress so that cells can survive and recover after antibiotic treatment. We have compared gene expression with and without ampicillin in E. coli. RNA-sequencing from three different E. coli populations: (1) stationary phase cells and two populations incubated for three hours in fresh media (2) without ampicillin (untreated) and (3) with ampicillin at bactericidal concentrations (treated).