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Using DNA microarray analysis, mRNA levels from wild-type Yersinia pestis cells treated with the iron chelator 2,2′-dipyridyl were compared with those supplemented with excessive iron, and subsequent to this, gene expression in the fur mutant was compared with that in the wild-type strain under iron rich conditions. The microarray analysis revealed many iron transport or storage systems that had been induced in response to the iron starvation, which is mediated by the Fur protein, using the iron as a co-repressor. The iron–Fur complex also affected some genes involved in various non-iron functions (ribonucleoside-diphosphate reductase, membrane proteins, electron transport and oxidative defense, etc.). The Fur protein still participated in the regulation of genes involved in broad cellular processes (virulence factors, pesticin activity, haemin storage and many proteins with unknown functions) that were not affected by iron depletion conditions. In addition to its classical negative regulatory activities, the Fur protein activates gene transcription. Using bioinformatics tools, we were able to predict the Y. pestis Fur box sequence that was clearly the over-presented motif in the promoter regions of members of the iron–Fur modulon.

Plague is a deadly disease caused by Yersinia pestis. Human plague can be effectively controlled by timely antibiotic administration, chloramphenicol being a drug of choice. In this study, a DNA microarray was used to investigate the gene expression profile of Y. pestis in response to chloramphenicol. Seven hundred and fifty-five genes were differentially expressed on chloramphenicol treatment: 364 genes were up-regulated and 391 were down-regulated. In addition to a large number of genes encoding unknown or unassigned functions, genes encoding the components of the translation apparatus, cell envelope and transport/binding functions were strongly represented amongst the induced genes. Genes encoding proteins involved in energy metabolism and synthesis and modification of macromolecules were strongly represented amongst the down-regulated genes. A number of heat-shock genes were also repressed. These global transcriptional changes provide an insight into the mechanisms of action of chloramphenicol against Y. pestis.

Using DNA microarray analysis, mRNA levels from wild-type Yersinia pestis cells treated with the iron chelator 2,2'-dipyridyl were compared with those supplemented with excessive iron, and subsequent to this, gene expression in the fur mutant was compared with that in the wild-type strain under iron rich conditions. The microarray analysis revealed many iron transport or storage systems that had been induced in response to the iron starvation, which is mediated by the Fur protein, using the iron as a co-repressor. The iron-Fur complex also affected some genes involved in various non-iron functions (ribonucleoside-diphosphate reductase, membrane proteins, electron transport and oxidative defense, etc.). The Fur protein still participated in the regulation of genes involved in broad cellular processes (virulence factors, pesticin activity, haemin storage and many proteins with unknown functions) that were not affected by iron depletion conditions. In addition to its classical negative regulatory activities, the Fur protein activates gene transcription. Using bioinformatics tools, we were able to predict the Y. pestis Fur box sequence that was clearly the over-presented motif in the promoter regions of members of the iron-Fur modulon.

Plague, caused by Y ersinia pestis, is one of the most dangerous diseases that impressed a horror onto human consciousness that persists to this day. Cases of plague can be normally controlled by timely antibiotic administration. Streptomycin is the first-line antibiotic for plague treatment. In this study, a DNA microarray was used to investigate the changes in the gene expression profile of Y. pestis upon exposure to streptomycin. A total of 345 genes were identified to be differentially regulated, 144 of which were up-regulated, and 201 down-regulated. Streptomycin-induced transcriptional changes occurred in genes responsible for heat shock response, drug/analogue sensitivity, biosynthesis of the branched-chain amino acids, chemotaxis and mobility and broad regulatory functions. A wide set of genes involved in energy metabolism, biosynthesis of small macromolecules, synthesis and modification of macromoclecules and degradation of small and macro molecules were among those down-regulated. The results reveal general changes in gene expression that are consistent with known mechanisms of action of streptomycin and many new genes that are likely to play important roles in the response to streptomycin treatment, providing useful candidates for investigating the specific mechanisms of streptomycin action.