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      A Dilemma for Research on Yersinia Pestis, a Bioterrorism Agent

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          Abstract

          Yersinia pestis research requires biosafety level thee laboratory practices, which prevents many scientists from conducting research on this pathogen. However, for convenience, many laboratories employ avirulent pCD1-cured strains, such as KIM6+, to perform experiments to study the evolutionary and pathogenic mechanisms of Y. pestis. However, research, including the report by Zhou et al. in this issue, shows that some important Y. pestis phenotypes, including biofilm formation, are influenced by the presence of pCD1. This indicates that we should be prudent when drawing conclusions based on results obtained from plasmid-cured Y. pestis strains.

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          Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis.

          Plague, one of the most devastating diseases of human history, is caused by Yersinia pestis. In this study, we analyzed the population genetic structure of Y. pestis and the two other pathogenic Yersinia species, Y. pseudotuberculosis and Y. enterocolitica. Fragments of five housekeeping genes and a gene involved in the synthesis of lipopolysaccharide were sequenced from 36 strains representing the global diversity of Y. pestis and from 12-13 strains from each of the other species. No sequence diversity was found in any Y. pestis gene, and these alleles were identical or nearly identical to alleles from Y. pseudotuberculosis. Thus, Y. pestis is a clone that evolved from Y. pseudotuberculosis 1,500-20,000 years ago, shortly before the first known pandemics of human plague. Three biovars (Antiqua, Medievalis, and Orientalis) have been distinguished by microbiologists within the Y. pestis clone. These biovars form distinct branches of a phylogenetic tree based on restriction fragment length polymorphisms of the locations of the IS100 insertion element. These data are consistent with previous inferences that Antiqua caused a plague pandemic in the sixth century, Medievalis caused the Black Death and subsequent epidemics during the second pandemic wave, and Orientalis caused the current plague pandemic.
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            Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas.

            Yersinia pestis, the cause of bubonic plague, is transmitted by the bites of infected fleas. Biological transmission of plague depends on blockage of the foregut of the flea by a mass of plague bacilli. Blockage was found to be dependent on the hemin storage (hms) locus. Yersinia pestis hms mutants established long-term infection of the flea's midgut but failed to colonize the proventriculus, the site in the foregut where blockage normally develops. Thus, the hms locus markedly alters the course of Y. pestis infection in its insect vector, leading to a change in blood-feeding behavior and to efficient transmission of plague.
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              Hfq-dependent, co-ordinate control of cyclic diguanylate synthesis and catabolism in the plague pathogen Yersinia pestis.

              Yersinia pestis, the cause of the disease plague, forms biofilms to enhance flea-to-mammal transmission. Biofilm formation is dependent on exopolysaccharide synthesis and is controlled by the intracellular levels of the second messenger molecule cyclic diguanylate (c-di-GMP), but the mechanisms by which Y. pestis regulates c-di-GMP synthesis and turnover are not fully understood. Here we show that the small RNA chaperone Hfq contributes to the regulation of c-di-GMP levels and biofilm formation by modulating the abundance of both the c-di-GMP phosphodiesterase HmsP and the diguanylate cyclase HmsT. To do so, Hfq co-ordinately promotes hmsP mRNA accumulation while simultaneously decreasing the stability of the hmsT transcript. Hfq-dependent regulation of HmsP occurs at the transcriptional level while the regulation of HmsT is post-transcriptional and is localized to the 5' untranslated region/proximal coding sequence of the hmsT transcript. Decoupling HmsP from Hfq-based regulation is sufficient to overcome the effects of Δhfq on c-di-GMP and biofilm formation. We propose that Y. pestis utilizes Hfq to link c-di-GMP levels to environmental conditions and that the disregulation of c-di-GMP turnover in the absence of Hfq may contribute to the severe attenuation of Y. pestis lacking this RNA chaperone in animal models of plague. © 2012 Blackwell Publishing Ltd.
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                Author and article information

                Contributors
                Journal
                Infectious Diseases and Translational Medicine
                Infect. Dis. Transl. Med.
                Infect. Dis. Transl. Med.
                International Biological and Medical Journals Publishing House Co., Limited (Room E16, 3/f, Yongda Commercial Building, No.97, Bonham Stand (Sheung Wan), HongKong )
                2411-2917
                31 October 2017
                31 October 2017
                : 3
                : 2
                : 20-21 (pp. )
                Affiliations
                From Beijing Institute of Microbiology and Epidemiology, No. 20, Dongdajie, Fengtai District, Beijing 100071, China.
                Author notes
                Correspondence to: Ruifu Yang, Email: ruifuyang@gmail.com.
                Article
                10.11979/idtm.201702002
                b08aa68f-8f4e-4c82-a5c3-4b629000309f

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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                Figures: 0, Tables: 0, References: 14, Pages: 2
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                Medicine,Infectious disease & Microbiology
                Yersinia pestis,Plasmid-cured strain,pCD1,Biofilm formation

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