Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/32705
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dc.contributor.authorLevin, Bruce R
dc.contributor.authorMcCall, Ingrid C
dc.contributor.authorPerrot, Véronique
dc.contributor.authorWeiss, Howard
dc.contributor.authorOvesepian, Armen
dc.contributor.authorBaquero, Fernando
dc.date.accessioned2019-06-28T17:07:01Z-
dc.date.available2019-06-28T17:07:01Z-
dc.date.issued2017
dc.identifier.citationMBio.2017 02;(8)1:
dc.identifier.urihttps://hdl.handle.net/20.500.12530/32705-
dc.description.abstractWe postulate that the inhibition of growth and low rates of mortality of bacteria exposed to ribosome-binding antibiotics deemed bacteriostatic can be attributed almost uniquely to these drugs reducing the number of ribosomes contributing to protein synthesis, i.e., the number of effective ribosomes. We tested this hypothesis with Escherichia coli K-12 MG1655 and constructs that had been deleted for 1 to 6 of the 7 rRNA (rrn) operons. In the absence of antibiotics, constructs with fewer rrn operons have lower maximum growth rates and longer lag phases than those with more ribosomal operons. In the presence of the ribosome-binding "bacteriostatic" antibiotics tetracycline, chloramphenicol, and azithromycin, E. coli strains with 1 and 2 rrn operons are killed at a substantially higher rate than those with more rrn operons. This increase in the susceptibility of E. coli with fewer rrn operons to killing by ribosome-targeting bacteriostatic antibiotics is not reflected in their greater sensitivity to killing by the bactericidal antibiotic ciprofloxacin, which does not target ribosomes, but also to killing by gentamicin, which does. Finally, when such strains are exposed to these ribosome-targeting bacteriostatic antibiotics, the time before these bacteria start to grow again when the drugs are removed, referred to as the post-antibiotic effect (PAE), is markedly greater for constructs with fewer rrn operons than for those with more rrn operons. We interpret the results of these other experiments reported here as support for the hypothesis that the reduction in the effective number of ribosomes due to binding to these structures provides a sufficient explanation for the action of bacteriostatic antibiotics that target these structures.
dc.language.isoeng
dc.rightsopenAccess-
dc.subject.meshAnti-Bacterial Agents
dc.subject.meshEscherichia coli K12
dc.subject.meshMicrobial Viability
dc.subject.meshProtein Biosynthesis
dc.subject.meshRibosomes
dc.titleA Numbers Game: Ribosome Densities, Bacterial Growth, and Antibiotic-Mediated Stasis and Death.
dc.typeArtículo
dc.identifier.pubmedID28174311
dc.format.volume8
dc.identifier.e-issn2150-7511
dc.identifier.journalmBio
dc.identifier.doi10.1128/mBio.02253-16
dc.format.number1
dc.identifier.pmcPMC5296603
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, N.I.H., Extramural
dc.pubmedtypeResearch Support, Non-U.S. Gov't
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. U. Ramón y Cajal > Artículos

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