Post-transcriptional deregulation of the tisB/istR-1 toxin-antitoxin system promotes SOS-independent persister formation in Escherichia coli

© 2020 The Authors. Environmental Microbiology Reports published by Society for Applied Microbiology and John Wiley & Sons Ltd..

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.

Medienart:

E-Artikel

Erscheinungsjahr:

2021

Erschienen:

2021

Enthalten in:

Zur Gesamtaufnahme - volume:13

Enthalten in:

Environmental microbiology reports - 13(2021), 2 vom: 17. Apr., Seite 159-168

Sprache:

Englisch

Beteiligte Personen:

Edelmann, Daniel [VerfasserIn]
Oberpaul, Markus [VerfasserIn]
Schäberle, Till F [VerfasserIn]
Berghoff, Bork A [VerfasserIn]

Links:

Volltext

Themen:

Anti-Bacterial Agents
Bacterial Toxins
Escherichia coli Proteins
Journal Article
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 04.04.2022

Date Revised 05.04.2022

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1111/1758-2229.12919

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM319146855