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Updated: Jan 21, 2026
Isolation and Identification of Waterborne Antibiotic-Resistant Bacteria and Molecular Characterization of their Antibiotic Resistance Genes
Published on: March 3, 2023
[Molecular Mechanisms of Non-Inherited Antibiotic Tolerance in Bacteria and Archaea]
T M Khlebodarova1,2, V A Likhoshvai1
1Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, 630090 Russia.
Abstract:
The phenomenon of bacterial persistence, also known as non-inherited antibiotic tolerance in a part of bacterial populations, was described more than 70 years ago. This type of tolerance contributes to the chronization of infectious diseases, including tuberculosis. Currently, the emergence of persistent cells in bacterial populations is associated with the functioning of some stress-induced molecular triggers, including toxin-antitoxin systems. In the presented review, genetic and metabolic peculiarities of persistent cells are considered and the mechanisms of their occurrence are discussed. The hypothesis of the origin of persister cells based on bistability, arising due to the non-linear properties of a coupled transcription-translation system, was proposed. Within this hypothesis, the phenomenon of the bacterial persistence of modern cells is considered as a result of the genetic fixation of the phenotypic multiplicity that emerged in primitive cells in the process of neutrally coupled co-evolution (genetic drift of multiple neutrally coupled mutations). Our hypothesis explains the properties of persister cells, as well as their origin and "ineradicable" nature.
Insights
Bacterial persistence, a non-inherited antibiotic tolerance, contributes to chronic infections. This review proposes a new hypothesis for persister cell origin, linking it to genetic drift and phenotypic multiplicity in primitive cells.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- Bacterial persistence, a non-inherited antibiotic tolerance, has been known for over 70 years.
- Persistent cells contribute to chronic infectious diseases like tuberculosis.
- Toxin-antitoxin systems are implicated in the emergence of bacterial persisters.
Purpose of the Study:
- To review the genetic and metabolic characteristics of persistent cells.
- To discuss the mechanisms underlying the formation of persister cells.
- To propose a novel hypothesis for the origin of bacterial persistence.
Main Methods:
- Review of existing literature on bacterial persistence.
- Analysis of genetic and metabolic data of persister cells.
- Theoretical modeling based on bistability and coupled transcription-translation systems.
Main Results:
- Persistent cells exhibit unique genetic and metabolic profiles.
- Bistability in coupled transcription-translation systems may drive persister formation.
- A hypothesis suggests genetic fixation of phenotypic multiplicity via neutral evolution explains persistence.
Conclusions:
- The proposed hypothesis offers a framework for understanding persister cell properties and origin.
- Bacterial persistence may stem from the evolutionary history of primitive cells.
- This perspective sheds light on the 'ineradicable' nature of persister cells.
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