The failure of different strains of Yersinia pestis to produce lipopolysaccharide O-antigen under different growth conditions is due to mutations in the O-antigen gene cluster

Prior, J

doi:10.1016/s0378-1097(01)00107-0

Cited by 23 publications

(33 citation statements)

References 23 publications

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“…Genes encoding uptake and transport functions are often inactivated, while central and intermediate metabolism genes remain largely intact. The derived strains also share phenotypic features, including expression of rough LPS (37,39,45) and limited capability to survive outside the host (1,14,35). A fundamental difference is that gene acquisition has played a fundamental role in the evolution of Y. pestis (12) but does not appear to have contributed significantly to Bordetella evolution.…”

Section: Fig 2 Phylogeny Ofmentioning

confidence: 99%

Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation

et al. 2004

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Pathogens of the bacterial genus Bordetella cause respiratory disease in humans and animals. Although virulence and host specificity vary across the genus, the genetic determinants of this diversity remain unidentified. To identify genes that may underlie key phenotypic differences between these species and clarify their evolutionary relationships, we performed a comparative analysis of genome content in 42 Bordetella strains by hybridization of genomic DNA to a microarray representing the genomes of three Bordetella species and by subtractive hybridization. Here we show that B. pertussis and B. parapertussis are predominantly differentiated from B. bronchiseptica by large, species-specific regions of difference, many of which encode or direct synthesis of surface structures, including lipopolysaccharide O antigen, which may be important determinants of host specificity. The species also exhibit sequence diversity at a number of surface protein-encoding loci, including the fimbrial major subunit gene, fim2. Gene loss, rather than gene acquisition, accompanied by the proliferation of transposons, has played a fundamental role in the evolution of the pathogenic bordetellae and may represent a conserved evolutionary mechanism among other groups of microbial pathogens.Bacteria of the genus Bordetella are important pathogens that cause respiratory disease in humans and animals. B. pertussis is the causative agent of whooping cough (8), which is responsible for up to 500,000 annual deaths worldwide in unvaccinated populations (52) and is increasing in incidence in some countries with established vaccination programs, including the United States (e.g., see references 15, 30, and 38). Although most Bordetella species can cause similar disease in the upper respiratory tract, their host specificities vary dramatically. B. pertussis infects only humans; B. parapertussis strains can be classified in two groups, one of which infects only humans and one of which infects only sheep (16,17,25); B. bronchiseptica causes respiratory infections in a wide variety of mammals and birds but only rarely in humans (22,41,51).These three Bordetella species are closely related at the nucleotide sequence level (4, 24), and their relatedness has been further established using a variety of common molecular strain typing techniques (reviewed in reference 29). Phylogenetic analyses of the genus Bordetella, using pulsed-field gel electrophoresis, multilocus enzyme electrophoresis (MLEE), and IS typing data, suggested that B. pertussis, human-derived B. parapertussis, and sheep-derived B. parapertussis arose independently from B. bronchiseptica-like ancestors (46, 47). Comparative genome sequencing of a representative strain of each species (33) confirmed that nucleotide sequence similarity is very high in conserved regions of the genome but demonstrated that B. pertussis and B. parapertussis evolved by genome decay from a B. bronchiseptica-like ancestor.Although a number of critical conserved virulence mechanisms have been identified in the bor...

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Section: Fig 2 Phylogeny Ofmentioning

confidence: 99%

Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation

et al. 2004

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“…pestis has rough LPS and lacks genes encoding synthesis of the O antigen present in the smooth LPS form (31,32,54,55,62,69), whereas the other human pathogenic yersiniae, Yersinia pseudotuberculosis and Yersinia enterocolitica, express O antigens that are important for bacterial colonization in infected mice (61). Pla-mediated proteolysis is sterically inhibited by the O antigen, and one of the selective advantages of the loss of the O antigen in Y. pestis is the ability to express high Pla-mediated proteolytic activity (39).…”

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confidence: 99%

Temperature-Induced Changes in the Lipopolysaccharide ofYersinia pestisAffect Plasminogen Activation by the Pla Surface Protease

Suomalainen

Lobo

Brandenburg³

et al. 2010

Infect Immun

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“…16 The third form of this disease, primary pneumonic plague, occurs by seeding of the lungs with the organism following spread from bubonic or septicemic disease. Secondary pneumonic plague occurs by spread of respiratory droplets through close contact with infected humans or animals.…”

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Current Trends in Plague Research: From Genomics to Virulence

Huang

Nikolich²,

Lindler³

2006

Clinical Medicine & Research

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Yersinia pestis is the causative agent of plague, which diverged from Yersinia pseudotuberculosis within the past 20,000 years. Although these two species share a high degree of homology at the DNA level (>90%), they differ radically in their pathogenicity and transmission. In this review, we briefly outline the known virulence factors that differentiate these two species and emphasize genetic studies that have been conducted comparing Y. pestis and Y. pseudotuberculosis.These comparisons have led to a better understanding of the genetic contributions to the differences in the virulence and pathogenicity between these two organisms and have generated information that can be applied in future diagnostic and vaccine development. Comparison of the genetic differences between Y. pestis and Y. pseudotuberculosis has also lent insight into the emergence of acute pathogens from organisms causing milder diseases.

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The failure of different strains of Yersinia pestis to produce lipopolysaccharide O-antigen under different growth conditions is due to mutations in the O-antigen gene cluster

Cited by 23 publications

References 23 publications

Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation

Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation

Temperature-Induced Changes in the Lipopolysaccharide ofYersinia pestisAffect Plasminogen Activation by the Pla Surface Protease

Current Trends in Plague Research: From Genomics to Virulence

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