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Post‐transcriptional deregulation of the tisB / istR ‐1 toxin–antitoxin system promotes SOS ‐independent persister formation in Escherichia coli
Author(s) -
Edelmann Daniel,
Oberpaul Markus,
Schäberle Till F.,
Berghoff Bork A.
Publication year - 2021
Publication title -
environmental microbiology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.229
H-Index - 69
ISSN - 1758-2229
DOI - 10.1111/1758-2229.12919
Subject(s) - sos response , escherichia coli , multidrug tolerance , antitoxin , biology , mutant , microbiology and biotechnology , transcription (linguistics) , rna , stringent response , gene , toxin , genetics , bacteria , biofilm , linguistics , philosophy
Summary 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.