Slow growth determines nonheritable antibiotic resistance in Salmonella enterica.

Slow growth determines nonheritable antibiotic resistance in Salmonella enterica. Sci Signal. 2019 Jul 30;12(592): Authors: Pontes MH, Groisman EA Abstract Bacteria can withstand killing by bactericidal antibiotics through phenotypic changes mediated by their preexisting genetic repertoire. These changes can be exhibited transiently by a large fraction of the bacterial population, giving rise to tolerance, or displayed by a small subpopulation, giving rise to persistence. Apart from undermining the use of antibiotics, tolerant and persistent bacteria foster the emergence of antibiotic-resistant mutants. Persister formation has been attributed to alterations in the abundance of particular proteins, metabolites, and signaling molecules, including toxin-antitoxin modules, adenosine triphosphate, and guanosine (penta) tetraphosphate, respectively. Here, we report that persistent bacteria form as a result of slow growth alone, despite opposite changes in the abundance of such proteins, metabolites, and signaling molecules. Our findings argue that transitory disturbances to core activities, which are often linked to cell growth, promote a persister state regardless of the underlying physiological process responsible for the change in growth. PMID: 31363068 [PubMed - in process]
Source: Science Signaling - Category: Biomedical Science Authors: Tags: Sci Signal Source Type: research

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