Comparative transcriptomics in Yersinia pestis: a global view of environmental modulation of gene expression

Han, Yanping; Qiu, Jingfu; Guo, Zhaobiao; Gao, He; Song, Yajun; Zhou, Dongsheng

doi:10.1186/1471-2180-7-96

Cited by 30 publications

(35 citation statements)

References 77 publications

(73 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Beside the above iron assimilation genes, Table 1 still included the following genes: (i) genes whose transcription was affected by both DP treatment and the fur mutation, as shown by our previous microarray analysis (35) (these genes encode various non-iron functions), and (ii) several genes belonging to the iron uptake-associated gene cluster, as determined by the clustering analysis on the data of 25 microarray expression profiles of Y. pestis (in addition, EMSA has shown that the His-Fur binds to the upstream DNA region of these genes) (17).…”

Section: Resultsmentioning

confidence: 69%

The Iron-Responsive Fur Regulon in Yersinia pestis

et al. 2008

Self Cite

View full text Add to dashboard Cite

The ferric uptake regulator (Fur) is a predominant bacterial regulator controlling the iron assimilation functions in response to iron availability. Our previous microarray analysis on Yersinia pestis defined the iron-Fur modulon. In the present work, we reannotated the iron assimilation genes in Y. pestis, and the resulting genes in complementation with those disclosed by microarray constituted a total of 34 genome loci (putative operons) that represent the potential iron-responsive targets of Fur. The subsequent real-time reverse transcription-PCR (RT-PCR) in conjunction with the primer extension analysis showed that 32 of them were regulated by Fur in response to iron starvation. A previously predicted Fur box sequence was then used to search against the promoter regions of the 34 operons; the homologue of the above box could be predicted in each promoter tested. The subsequent electrophoretic mobility shift assay (EMSA) demonstrated that a purified His 6 tag-fused Fur protein was able to bind in vitro to each of these promoter regions. Therefore, Fur is a global regulator, both an activator and a repressor, and directly controls not only almost all of the iron assimilation functions but also a variety of genes involved in various non-iron functions for governing a complex regulatory cascade in Y. pestis. In addition, real-time RT-PCR, primer extension, EMSA, and DNase I footprinting assay were used to elucidate the Fur regulation of the ybt locus encoding a virulence-required iron uptake system. By combining the published data on the YbtA regulation of ybt, we constructed a concise Fur/YbtA regulatory network with a map of the Fur-promoter DNA interactions within the ybt locus. The data presented here give us an overview of the iron-responsive Fur regulon in Y. pestis.

show abstract

Section: Resultsmentioning

confidence: 69%

The Iron-Responsive Fur Regulon in Yersinia pestis

et al. 2008

Self Cite

View full text Add to dashboard Cite

show abstract

“…The transcription of the phd/doc genes was also induced in human plasma, suggesting that conditions mimicking the in vivo environment might be necessary to evidence the activity of Doc in Y. pestis. Moreover, the tox/Antitox gene locus has been shown to be upregulated under various stress conditions (19). The different types of regulations observed for these TA modules also suggest that they may act at different times during the Y. pestis life cycle.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, the overexpression of the antitoxin MazE was previously shown to resuscitate E. coli cells that overproduced the MazF toxin within a period of 6 h only (1), after which bacterial death started to occur. Since the relEB1 module was previously shown to be a stress-responsive operon (19), it is possible that this module is involved in the adaptation of Y. pestis to changes in host or environmental conditions. Interestingly, RelE1 is the toxin that had the most drastic effect on E. coli growth.…”

Section: Discussionmentioning

confidence: 99%

“…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%

“…HigB2 may thus participate in the adaptation of Y. pestis to its environment (19). Since antibodies to the HigA2 antitoxin have been detected in the serum of rabbits immunized with Y. pestis EV76 (27), this also suggests that the HigBA2 module is produced and plays a role during the in vivo step of the Y. pestis life cycle.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

The Yersinia pestis Chromosome Encodes Active Addiction Toxins

et al. 2010

View full text Add to dashboard Cite

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.

show abstract