Abstract

BackgroundEnvironmental modulation of gene expression in Yersinia pestis is critical for its life style and pathogenesis. Using cDNA microarray technology, we have analyzed the global gene expression of this deadly pathogen when grown under different stress conditions in vitro.ResultsTo provide us with a comprehensive view of environmental modulation of global gene expression in Y. pestis, we have analyzed the gene expression profiles of 25 different stress conditions. Almost all known virulence genes of Y. pestis were differentially regulated under multiple environmental perturbations. Clustering enabled us to functionally classify co-expressed genes, including some uncharacterized genes. Collections of operons were predicted from the microarray data, and some of these were confirmed by reverse-transcription polymerase chain reaction (RT-PCR). Several regulatory DNA motifs, probably recognized by the regulatory protein Fur, PurR, or Fnr, were predicted from the clustered genes, and a Fur binding site in the corresponding promoter regions was verified by electrophoretic mobility shift assay (EMSA).ConclusionThe comparative transcriptomics analysis we present here not only benefits our understanding of the molecular determinants of pathogenesis and cellular regulatory circuits in Y. pestis, it also serves as a basis for integrating increasing volumes of microarray data using existing methods.

Highlights

  • Environmental modulation of gene expression in Yersinia pestis is critical for its life style and pathogenesis

  • Comparative transcriptomics analysis presented here can be used to mine the regulatory information from these available microarray data, providing an opportunity to gain a global view on environmental modulation of gene expression in Y. pestis

  • Stress-responsive operons predicted from microarray expression data By using the criteria described in Methods, we identified 39 potential operons that consisted of 183 genes in Y. pestis (Table 1)

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Summary

Introduction

Environmental modulation of gene expression in Yersinia pestis is critical for its life style and pathogenesis. Yersinia pestis is the etiological agent of plague, alternatively growing in fleas or warm-blood mammals [1]. Fleas acquire this organism via blood meal from a bacteremic mammal, usually a rodent. To produce a transmissible infection, Y. pestis colonizes the flea midgut and forms a biofilm in the proventricular valve optimally at 20 to 26°C, blocking its normal blood feeding [2]. Y. pestis must experience a temperature shift during the transmission process between rodents, fleas, and humans. It is considered a facultative intracellular pathogen. Most of the organisms that invade the (page number not for citation purposes)

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