Genome sequence of Yersinia pestis, the causative agent of plague

Parkhill, Julian; Wren, Brendan W.; Thomson, Nicholas R.; Titball, Richard W.; Holden, Matthew T. G.; Prentice, Michael B.; Sebaihia, Mohammed; James, Keith; Churcher, Carol; Mungall, Karen; Baker, Stephen; Basham, D.; Bentley, Stephen D.; Brooks, Karen; Cerdeño-Tárraga, Ana; Chillingworth, Tracey; Cronin, Ann; Davies, Robert M.; Davis, Paul A.; Dougan, Gordon; Feltwell, Theresa; Hamlin, N.; Holroyd, S.; Jagels, Kay; Karlyshev, Andrey V.; Leather, S.; Moule, Sharon; Oyston, Petra C. F.; Quail, Michael A.; Rutherford, Kim; Simmonds, Mark; Skelton, Jason; Stevens, Kim; Whitehead, Sally; Barrell, Bart

doi:10.1038/35097083

Cited by 1,116 publications

(973 citation statements)

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“…Different genome sequences provide different snapshots of this process of evolution. For example, Y. pestis seems to be at the very early stages of evolution and has both lost and acquired genes during this process 38 . Mycobacterium leprae 39 and Rickettsia prowazekii 40 seem to have evolved solely by gene loss from a progenitor species 39 .…”

Section: Discussionmentioning

confidence: 99%

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

et al. 2005

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Francisella tularensis is one of the most infectious human pathogens known. In the past, both the former Soviet Union and the US had programs to develop weapons containing the bacterium. We report the complete genome sequence of a highly virulent isolate of F. tularensis (1,892,819 bp). The sequence uncovers previously uncharacterized genes encoding type IV pili, a surface polysaccharide and iron-acquisition systems. Several virulence-associated genes were located in a putative pathogenicity island, which was duplicated in the genome. More than 10% of the putative coding sequences contained insertion-deletion or substitution mutations and seemed to be deteriorating. The genome is rich in IS elements, including IS630 Tc-1 mariner family transposons, which are not expected in a prokaryote. We used a computational method for predicting metabolic pathways and found an unexpectedly high proportion of disrupted pathways, explaining the fastidious nutritional requirements of the bacterium. The loss of biosynthetic pathways indicates that F. tularensis is an obligate host-dependent bacterium in its natural life cycle. Our results have implications for our understanding of how highly virulent human pathogens evolve and will expedite strategies to combat them.

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Section: Discussionmentioning

confidence: 99%

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

et al. 2005

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“…The recently sequenced genome of Y. pestis (Parkhill et al, 2001) suggests that many of the genes that Yersinia uses during infection and invasion, including adhesins, secretion systems and insecticidal toxins, have been acquired from other bacteria and viruses. Furthermore, all three pathogenic species of Yersinia harbour an extrachromosomal plasmid of 70 kb that is essential for virulence (Portnoy and Martinez, 1985).…”

Section: Innate Immunity and Signallingmentioning

confidence: 99%

“…Recognition of Yersinia by M cells is mediated via b1 integrins on the M-cell plasma membrane and the invasin protein of Yersinia (Marra and Isberg, 1997;Clark et al, 1998). Once Yersinia has penetrated the M cells, it can localize in the lymphoid tissue of its host.The recently sequenced genome of Y. pestis (Parkhill et al, 2001) suggests that many of the genes that Yersinia uses during infection and invasion, including adhesins, secretion systems and insecticidal toxins, have been acquired from other bacteria and viruses. Furthermore, all three pathogenic species of Yersinia harbour an extrachromosomal plasmid of 70 kb that is essential for virulence (Portnoy and Martinez, 1985).…”

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confidence: 99%

Yersinia effectors target mammalian signalling pathways

2002

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SummaryAnimals have an immune system to fight off challenges from both viruses and bacteria. The first line of defence is innate immunity, which is composed of cells that engulf pathogens as well as cells that release potent signalling molecules to activate an inflammatory response and the adaptive immune system. Pathogenic bacteria have evolved a set of weapons, or effectors, to ensure survival in the host. Yersinia spp. use a type III secretion system to translocate these effector proteins, called Yops, into the host. This report outlines how Yops thwart the signalling machinery of the host immune system. Introduction Innate immunity and signallingInnate immunity is the first line of defence against bacterial and viral infection (for a review of innate immunity, see Medzhitov and Janeway, 2000). The cells involved in the immune response use a wide variety of signalling cascades to activate processes such as phagocytosis, cytokine production and release and production of reactive oxygen species. In addition to eliminating pathogens, the innate immune system activates the adaptive immune response through the presentation of foreign peptides to T cells.Phagocytosis is an essential component of the innate immune system (May and Machesky, 2001). Rearrangement of the actin cytoskeleton during phagocytosis is mediated by the recruitment of proteins that function in actin rearrangement; these include paxillin, p130Cas and focal adhesion kinase (FAK) (Greenberg et al., 1990;Allen and Aderem, 1996). These proteins may form through M cells (microfold cells), which are specialized cells that take up foreign antigens, in intestinal Peyer's patches (Autenrieth and Firsching, 1996). Recognition of Yersinia by M cells is mediated via b1 integrins on the M-cell plasma membrane and the invasin protein of Yersinia (Marra and Isberg, 1997;Clark et al., 1998). Once Yersinia has penetrated the M cells, it can localize in the lymphoid tissue of its host.The recently sequenced genome of Y. pestis (Parkhill et al., 2001) suggests that many of the genes that Yersinia uses during infection and invasion, including adhesins, secretion systems and insecticidal toxins, have been acquired from other bacteria and viruses. Furthermore, all three pathogenic species of Yersinia harbour an extrachromosomal plasmid of 70 kb that is essential for virulence (Portnoy and Martinez, 1985). This plasmid contains the genes of a type III secretion system, a translocation apparatus highly conserved among pathogenic Gram-negative bacteria (for a review, see Cornelis, 1998). This secretion system is responsible for the translocation of the Yersinia effectors, termed Yops, into the host cell. Once inside the host cell, Yops carry out disruption of signalling cascades that activate the processes of phagocytosis, cytokine release and respiratory burst. Six Yop effectors have been identified (YopH, YopE, YopJ/P, YpkA/YopO, YopT and YopM). Some of these effectors are known to function in the downregulation of critical signalling cascades of the immune system (Fig...

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“…The fully virulent Y. pestis strain CO92 37,38 and the variants CO92 ⌬F1 20 and CAC1 39 have been previously described. The ⌬F1 variant of Y. pestis CO92 carries a deletion of the caf1 gene, which encodes the F1 (Caf1) pilin subunit of plague bacteria.…”

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

Plague in Guinea Pigs and Its Prevention by Subunit Vaccines

Quenee

Ciletti

Berube

et al. 2011

The American Journal of Pathology

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Human pneumonic plague is a devastating and transmissible disease for which a Food and Drug Administration-approved vaccine is not available. Suitable animal models may be adopted as a surrogate for human plague to fulfill regulatory requirements for vaccine efficacy testing. To develop an alternative to pneumonic plague in nonhuman primates, we explored guinea pigs as a model system. On intranasal instillation of a fully virulent strain, Yersinia pestis CO92, guinea pigs developed lethal lung infections with hemorrhagic necrosis, massive bacterial replication in the respiratory system, and blood-borne dissemination to other organ systems. Expression of the Y. pestis F1 capsule was not required for the development of pulmonary infection; however, the capsule seemed to be important for the establishment of bubonic plague. The mean lethal dose (MLD) for pneumonic plague in guinea pigs was estimated to be 1000 colony-forming units. Immunization of guinea pigs with the recombinant forms of LcrV, a protein that resides at the tip of Yersinia type III secretion needles, or F1 capsule generated robust humoral immune responses. Whereas LcrV immunization resulted in partial protection against pneumonic plague challenge with 250 MLD Y. pestis CO92, immunization with recombinant F1 did not. rV10, a vaccine variant lacking LcrV residues 271-300, elicited protection against pneumonic plague, which seemed to be based on conformational antibodies directed against LcrV.

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Genome sequence of Yersinia pestis, the causative agent of plague

Cited by 1,116 publications

References 30 publications

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

Yersinia effectors target mammalian signalling pathways

Plague in Guinea Pigs and Its Prevention by Subunit Vaccines

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