ArticleCurrent microbiology2012
SigB-dependent tolerance to protein synthesis-inhibiting antibiotics in Listeria monocytogenes EGDe.
Article in Current microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 12 citations in OpenAlex.
- Inhibition ofFood science & nutrition · 2022Article
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The alternative sigma factor SigB in food-borne pathogen Listeria monocytogenes was determined in this study to be required for tolerance to protein synthesis-inhibiting antibiotics. The minimum inhibitory concentrations of tetracycline HCl and gentamicin sulphate against EGDeΔsigB were two- and fourfold less than those for EGDe, respectively. The ability of EGDeΔsigB to overcome the growth arrest caused by erythromycin and rifampin was also weaker than that of EGDe. The transcription analysis of four genetic loci (known to be induced by rifampin in Bacillus subtili) kat, fri, ropB and rsbU in EGDe and EGDeΔsigB in the absence or presence of rifampin revealed that: (1) expression of kat and fri genes is σ (B) dependent, but only the former is inducible by rifampin stress; (2) the transcriptional level of rpoB gene was stable under all the experimental conditions, while that of rsbU in EGDeΔsigB was remarkably higher in the absence of rifampin and significantly increased in EGDe but reduced in EGDeΔsigB after rifampin application, when compared to those in EGDe and EGDeΔsigB control without antibiotic, respectively. These results suggest that complex physiological reactions to tolerance of the antibiotic stress are variably regulated in bacteria, and in contrast to B. subtilis, rsbU in EGDeΔsigB may compensate for the σ (B)-dependent genes that are necessary for tolerance to rifampin stress and therefore plays a role in overcoming the antibiotic-triggered growth arrest.
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