Antibiotic stress drives protein transfer between bacteria via membrane vesicles, aiding persister cell survival
By
Christophe Herman
Summary
This article reports on a scientific discovery showing that antibiotic stress triggers protein exchange between neighboring bacteria through membrane-bound vesicles. Dormant "persister" cells, which normally shut down protein synthesis, are more likely to absorb these vesicles and use their contents to survive antibiotic treatment. This creates two transient cell states—donor and recipient cells—within an otherwise identical bacterial population, revealing a mechanism of bacterial adaptation and evolution under antibiotic stress.
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Key quotes
· 5 pulledAntibiotic stress triggers protein exchange between neighboring bacteria through membrane-bound vesicles.
Some bacteria, especially dormant 'persister' cells that normally turn off their protein synthesis, are more likely to take up these vesicles and use their contents to withstand antibiotic treatment.
This process creates two transient cell states within an otherwise identical population: donor cells that release proteins and recipient cells that take them up.
The exchange of biological matter between bacterial cells drives adaptation and evolution.
Whether bacteria can exchange functional proteins remains unclear.
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