Toxin GhoT of the GhoT/GhoS toxin/antitoxin system damages the cell membrane to reduce adenosine triphosphate and to reduce growth under stress

Toxin/antitoxin (TA) systems perhaps enable cells to reduce their metabolism to weather environmental challenges although there is little evidence to support this hypothesis. Escherichia coli GhoT/GhoS is a TA system in which toxin GhoT expression is reduced by cleavage of its messenger RNA (mRNA) b...

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Bibliographic Details
Published in:Environmental microbiology 2014-06, Vol.16 (6), p.1741-1754
Main Authors: Cheng, Hsin‐Yao, Soo, Valerie W. C, Islam, Sabina, McAnulty, Michael J, Benedik, Michael J, Wood, Thomas K
Format: Article
Language:English
Subjects:
Adenosine
adenosine triphosphate
Adenosine Triphosphate - metabolism
Animal, plant and microbial ecology
Anti-Bacterial Agents - pharmacology
antimicrobial agents
antitoxins
Biological and medical sciences
Biphenyl Compounds - pharmacology
Carbenicillin - pharmacology
Cefoxitin - pharmacology
Cell Membrane - metabolism
cell membranes
Chloroquinolinols - pharmacology
Escherichia
Escherichia coli
Escherichia coli - drug effects
Escherichia coli - growth & development
Escherichia coli Proteins - physiology
fluorescence microscopy
Fundamental and applied biological sciences. Psychology
General aspects
Medical research
messenger RNA
metabolism
Microbial ecology
Microbial Sensitivity Tests
Microscopy
Protein Transport
Proton-Motive Force
RNA, Messenger - metabolism
transmission electron microscopy
weathering
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Summary:Toxin/antitoxin (TA) systems perhaps enable cells to reduce their metabolism to weather environmental challenges although there is little evidence to support this hypothesis. Escherichia coli GhoT/GhoS is a TA system in which toxin GhoT expression is reduced by cleavage of its messenger RNA (mRNA) by antitoxin GhoS, and TA system MqsR/MqsA controls GhoT/GhoS through differential mRNA decay. However, the physiological role of GhoT has not been determined. We show here through transmission electron microscopy, confocal microscopy and fluorescent stains that GhoT reduces metabolism by damaging the membrane and that toxin MqsR (a 5′‐GCU‐specific endoribonuclease) causes membrane damage in a GhoT‐dependent manner. This membrane damage results in reduced cellular levels of ATP and the disruption of proton motive force (PMF). Normally, GhoT is localized to the pole and does not cause cell lysis under physiological conditions. Introduction of an F38R substitution results in loss of GhoT toxicity, ghost cell production and membrane damage while retaining the pole localization. Also, deletion of ghoST or ghoT results in significantly greater initial growth in the presence of antimicrobials. Collectively, these results demonstrate that GhoT reduces metabolism by reducing ATP and PMF and that this reduction in metabolism is important for growth with various antimicrobials.
ISSN:1462-2912
1462-2920
DOI:10.1111/1462-2920.12373