Post‐transcriptional deregulation of thetisB /istR ‐1toxin–antitoxin system promotesSOS ‐independent persister formation inEscherichia coli
Autor: | Daniel Edelmann, Markus Oberpaul, Bork A. Berghoff, Till F. Schäberle |
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Rok vydání: | 2020 |
Předmět: |
0303 health sciences
Messenger RNA 030306 microbiology Chemistry Escherichia coli Proteins Bacterial Toxins Mutant RNA Toxin-Antitoxin Systems medicine.disease_cause Toxin-antitoxin system Agricultural and Biological Sciences (miscellaneous) Anti-Bacterial Agents Cell biology 03 medical and health sciences Transcription (biology) Escherichia coli medicine Humans Antitoxin SOS response Escherichia coli Infections Ecology Evolution Behavior and Systematics 030304 developmental biology |
Zdroj: | Environmental Microbiology Reports. 13:159-168 |
ISSN: | 1758-2229 |
Popis: | Bacterial dormancy is a valuable strategy to endure unfavourable conditions. The term 'persister' has been coined for cells that tolerate antibiotic treatments due to reduced cellular activity. The type I toxin-antitoxin system tisB/istR-1 is linked to persistence in Escherichia coli, because toxin TisB depolarizes the inner membrane and causes ATP depletion. Transcription of tisB is induced upon activation of the SOS response by DNA-damaging drugs. However, translation is repressed both by a 5' structure within the tisB mRNA and by RNA antitoxin IstR-1. This tight regulation limits TisB production to SOS conditions. Deletion of both regulatory RNA elements produced a 'high persistence' mutant, which was previously assumed to depend on stochastic SOS induction and concomitant TisB production. Here, we demonstrate that the mutant generates a subpopulation of growth-retarded cells during late stationary phase, likely due to SOS-independent TisB accumulation. Cell sorting experiments revealed that the stationary phase-derived subpopulation contains most of the persister cells. Collectively our data show that deletion of the regulatory RNA elements uncouples the persister formation process from the intended stress situation and enables the formation of TisB-dependent persisters in an SOS-independent manner. |
Databáze: | OpenAIRE |
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