@article{93710,
  author = {Zhu J and Wang B and Pan M and Zeng Y and Rego H and Javid B},
  title = {Rifampicin can induce antibiotic tolerance in mycobacteria via paradoxical changes in rpoB transcription.},
  abstract = {<p>Metrics commonly used to describe antibiotic efficacy rely on measurements performed on bacterial populations. However, certain cells in a bacterial population can continue to grow and divide, even at antibiotic concentrations that kill the majority of cells, in a phenomenon known as antibiotic tolerance. Here, we describe a form of semi-heritable tolerance to the key anti-mycobacterial agent rifampicin, which is known to inhibit transcription by targeting the β subunit of the RNA polymerase (RpoB). We show that rifampicin exposure results in rpoB upregulation in a sub-population of cells, followed by growth. More specifically, rifampicin preferentially inhibits one of the two rpoB promoters (promoter I), allowing increased rpoB expression from a second promoter (promoter II), and thus triggering growth. Disruption of promoter architecture leads to differences in rifampicin susceptibility of the population, confirming the contribution of rifampicin-induced rpoB expression to tolerance.</p>},
  year = {2018},
  journal = {Nature communications},
  volume = {9},
  pages = {4218},
  month = {01/2018},
  issn = {2041-1723},
  url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6181997/pdf/41467_2018_Article_6667.pdf},
  doi = {10.1038/s41467-018-06667-3},
  language = {eng},
}