Global gene expression profile of <i>Yersinia pestis</i> induced by streptomycin

Qiu, Jingfu; Zhou, Dongsheng; Han, Yanping; Zhang, Ling; Tong, Zongzhong; Song, Yajun; Dai, Erfu; Li, Bei; Wang, Jin; Guo, Zhaobiao; Zhai, Jing; Du, Zongmin; Wang, Xiaoyi; Yang, Ruifu

doi:10.1016/j.femsle.2005.01.018

Cited by 23 publications

(30 citation statements)

References 46 publications

(59 reference statements)

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“…Several transcriptome studies have shown that higBA2 transcription is induced by various stress conditions, hypersaline shock, the presence of streptomycin or chloramphenicol, and amino acid starvation (19,20,41,42), or during the stationary growth phase (5). HigB2 may thus participate in the adaptation of Y. pestis to its environment (19).…”

Section: Discussionmentioning

confidence: 99%

The Yersinia pestis Chromosome Encodes Active Addiction Toxins

et al. 2010

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Toxin-antitoxin (TA) loci consist of two genes in an operon, encoding a stable toxin and an unstable antitoxin. The expression of toxin leads to cell growth arrest and sometimes bacterial death, while the antitoxin prevents the cytotoxic activity of the toxin. In this study, we show that the chromosome of Yersinia pestis, the causative agent of plague, carries 10 putative TA modules and two solitary antitoxins that belong to five different TA families (HigBA, HicAB, RelEB, Phd/Doc, and MqsRA). Two of these toxin genes (higB2 and hicA1) could not be cloned in Escherichia coli unless they were coexpressed with their cognate antitoxin gene, indicating that they are highly toxic for this species. One of these toxin genes (higB2) could, however, be cloned directly and expressed in Y. pestis, where it was highly toxic, while the other one (hicA1) could not, probably because of its extreme toxicity. All eight other toxin genes were successfully cloned into the expression vector pBAD-TOPO. For five of them (higB1, higB3, higB5, hicA2, and tox), no toxic activity was detected in either E. coli or Y. pestis despite their overexpression. The three remaining toxin genes (relE1, higB4, and doc) were toxic for E. coli, and this toxic activity was abolished when the cognate antitoxin was coexpressed, showing that these three TA modules are functional in E. coli. Curiously, only one of these three toxins (RelE1) was active in Y. pestis. Cross-interaction between modules of the same family was observed but occurred only when the antitoxins were almost identical. Therefore, our study demonstrates that of the 10 predicted TA modules encoded by the Y. pestis chromosome, at least 5 are functional in E. coli and/or in Y. pestis. This is the first demonstration of active addiction toxins produced by the plague agent.

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Section: Discussionmentioning

confidence: 99%

The Yersinia pestis Chromosome Encodes Active Addiction Toxins

et al. 2010

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“…Expression of these determinants has been shown in vitro to be regulated by temperature, pH, and divalent cation concentration. Recently, expression analysis has been used to map the transcriptional response of Y. pestis to individual environmental stresses in vitro, such as temperature, antibiotics, and osmotic stress (Han et al, 2004(Han et al, , 2005a(Han et al, , 2005bMotin et al, 2004;Qiu et al, 2005). Whereas the responses to these environmental stresses have been elucidated using in vitro systems, there has not been a comprehensive analysis of their expression within a host.…”

Section: Introductionmentioning

confidence: 99%

Expression Profiling ofYersinia pestisDuring Mouse Pulmonary Infection

Lawson

Lyons

Johnston

2006

DNA and Cell Biology

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Yersinia pestis, the causative agent of plague, can be transmitted by infected flea bite or inhaled aerosol. Both routes of infection have a high mortality rate, and pneumonic infections of Y. pestis represent a significant concern as a tool of bioterrorism. Understanding the transcriptional program of this pathogen during pulmonary infection should be valuable in understanding plague pathogenesis, as well as potentially offering insights into new vaccines and therapeutics. Toward this goal we developed a long oligonucleotide microarray to the plague bacillus and evaluated the expression profiles of Y. pestis in vitro and in the mouse pulmonary infection model in vivo. The in vitro analysis compared expression patterns at 27 versus 37 degrees C, as a surrogate of the transition from the flea to the mammalian host. The in vivo analysis used intranasal challenge to the mouse lung. By amplifying the Y. pestis RNA from individual mouse lungs we were able to map the transcriptional profile of plague at postinfection days 1 to 3. Our data present a very different transcriptional profile between in vivo and in vitro expression, suggesting Y. pestis responds to a variety of host signals during infection. Of note was the number of genes found in genomic regions with altered %GC content that are upregulated within the mouse lung environment. These data suggest these regions may provide particularly promising targets for both vaccines and therapeutics.

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“…Possibly, antibiotic-induced ribosome perturbation stimulates MexXY-OprM production in order to counter or alleviate some stress or adverse effect resultant from such perturbation. Transcriptomic and proteomic studies certainly confirm that agents that interfere with prokaryotic translation impact expression of a myriad of genes (1,3,15,28,37,47,49,54) including, in some instances, genes associated with stress responses (28,37,47,49). Recently, a gene, PA5471, encoding a conserved hypothetical protein has been shown to be induced by the same ribosome-disrupting antimicrobials as mexXY and to be required for antibiotic-inducible mexXY expression (36).…”

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confidence: 98%