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Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli

Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli

Published on: March 24, 2023

A general model for toxin-antitoxin module dynamics can explain persister cell formation in E. coli.

Lendert Gelens¹, Lydia Hill, Alexandra Vandervelde

¹Applied Physics Research Group APHY, Vrije Universiteit Brussel, Brussels, Belgium. lendert.gelens@vub.ac.be

Plos Computational Biology

|September 7, 2013

Summary

Toxin-antitoxin systems control cell survival during stress. Mathematical models reveal that toxin sequestration, not gene regulation, manages toxin levels, enabling persister cell formation through rare toxin spikes.

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Area of Science:

Molecular Biology
Systems Biology
Genetics

Background:

Toxin-antitoxin (TA) modules are genetic elements crucial for bacterial stress response and persister cell formation.
Their regulation involves conditional cooperativity to prevent premature toxin activation.

Purpose of the Study:

To develop mathematical models for TA module regulation using existing molecular and structural data.
To investigate the mechanisms controlling free toxin levels and persister cell generation.

Main Methods:

Mathematical modeling based on published data for F-plasmid ccdAB, bacteriophage P1 phd/doc, and E. coli relBE.
Analysis of toxin sequestration, stoichiometry, and gene regulation dynamics.

Main Results:

Free toxin levels are primarily controlled by sequestration into toxin-antitoxin complexes.
Toxin accumulation occurs when translation rates exceed a 2:1 ratio of toxin to antitoxin.
Conditional cooperativity and increased operator binding sites minimize metabolic load.
Persister cell formation is linked to stochastic spikes in free toxin levels.

Conclusions:

Toxin sequestration is the dominant mechanism regulating free toxin levels in TA systems.
Conditional cooperativity and specific binding dynamics facilitate persister cell formation.
Antitoxin degradation rates and bacterial growth rates influence persister cell populations under stress.