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Microbiology

GhoSTly bacterial persisters

Nature Chemical Biology volume 8, pages 812–813 (2012)Cite this article

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Bacterial persisters consist of a phenotypic subpopulation that survives antibiotic treatment, prolonging infection. The GhoT toxin from the newly discovered ghoS-ghoT toxin-antitoxin system contributes to persistence, most likely by interfering with bacterial inner membrane integrity.

Modules of toxin and antitoxin genes, or toxin-antitoxin systems, are widespread in bacterial genomes. They are composed of a toxin gene closely linked to a specific antitoxin gene and participate in a variety of biological processes such as growth modulation, protection against mobile genetic elements and biofilm formation1. They are categorized into four classes depending on the nature and mode of action of the antitoxin, the toxin universally being a protein1. In type I and III systems, antitoxins are RNAs preventing either toxin synthesis (I) or inhibiting its activity (III). In type II and IV systems, antitoxins are proteins that either interact with the toxin (II) or with the toxin target (IV). Toxins inhibit essential physiological processes such as translation or cell wall synthesis or affect cell membrane permeability1. In this issue, Wang et al.2 present a new type of toxin-antitoxin system in which the antitoxin, GhoS, is a RNAse that specifically degrades the mRNA encoding its associated toxin, GhoT, thereby inhibiting its synthesis. In addition, the authors show that the ghoS-ghoT (ghoST) system is involved in persistence in E. coli.

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Figure 1: Model for persistence and possible interplay between the MqsR toxin and the ghoST system.

References

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Authors and Affiliations

  1. Laurence Van Melderen is in the Bacterial Genetic and Physiology Laboratory at the Université Libre de Bruxelles, Brussels, Belgium.,

    Laurence Van Melderen

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  1. Laurence Van Melderen
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Correspondence to Laurence Van Melderen.

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The author declares no competing financial interests.

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Van Melderen, L. GhoSTly bacterial persisters. Nat Chem Biol 8, 812–813 (2012). https://doi.org/10.1038/nchembio.1066

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