5/14/2024 0 Comments Marek vimr facebookCircular genome map of IP32953 and comparison with Y. In all cases, experiments yielding negative results were repeated under the same conditions and also by using a lower annealing temperature in the event that the region in question had undergone divergence.įig. For the other pseudogenes, sequencing each PCR product was followed by multiple alignments of the sequences to identify wild-type versus mutant loci. Due to homologous recombination between IS elements, the alternative and sometimes expected result was a negative one (e.g., no PCR product when the IS in question underwent recombination, or in the event of a deletion removing at least one of the priming sites). For the insertion sequence (IS)-interrupted genes, primers were designed to amplify a 300- to 600-bp region of the WT gene or a 1- to 2.5-kb fragment that includes the interrupting IS element. Specifically, for the strain- or species-specific genes, primers were designed to amplify an ≈500-bp region within the gene (or gene portion) that was found to be missing from the other strains or species. Analysis of these strains was performed by screening PCR results, and, if necessary, sequencing the resulting products. The Yersinia strains studied came from the collection at the Institut Pasteur. pestis and may hold the key to the exceptional virulence of the plague bacillus. These comparisons reveal many of the molecular details that were involved in the speciation and emergence of Y. pseudotuberculosis IP32953 (serotype I) presented here provides the first opportunity, to our knowledge, to examine all differences in genome structure and at the nucleotide level. Although a microarray-based comparison of these two Yersinia species has been reported recently ( 18), the detailed comparison between the completed genomes of Y. strain, CO92 ( 16), and an M strain, KIM10+ ( 17), the mechanism(s) underlying the strikingly different clinical manifestations of Y. Despite many extensive studies of the plasmid-encoded virulence determinants induced during the infectious process, and the recent availability of the genome sequences of a Y. ![]() However, the presence of these plasmids by themselves cannot account for the remarkable increase in virulence observed in Y. pestis, termed pPCP1 (9.6 kb) and pMT1 (102 kb), play roles in tissue invasion ( 7, 8) and capsule formation ( 9), as well as infection of the plague flea vector ( 10, 11), respectively. ![]() pestis is the shared requirement of a virulence plasmid pCD1 (pYV in enteropathogenic Yersinia) that encodes a type III secretion system ( 4), which is responsible for injecting into host cells a number of cytotoxins and effectors ( Yersinia outer proteins) that inhibit bacterial phagocytosis and processes of innate immunity ( 5, 6). Of special importance to the pathogenic process of both Y. These results provide a sobering example of how a highly virulent epidemic clone can suddenly emerge from a less virulent, closely related progenitor. ![]() Extensive insertion sequence-mediated genome rearrangements and reductive evolution through massive gene loss, resulting in elimination and modification of preexisting gene expression pathways, appear to be more important than acquisition of genes in the evolution of Y. pseudotuberculosis genes no longer function in Y. pestis were detected, indicating that as many as 13% of Y. In contrast, 149 other pseudogenes (doubling the previous estimate) and 317 genes absent from Y. pestis acquired since the the divergence from Y. pestis-specific plasmids, to our knowledge, represent the only new genetic material in Y. pestis chromosomal genes that, together with the two Y. Analyses of identified differences across a panel of Yersinia isolates from around the world reveal 32 Y. pseudotuberculosis IP32953 and its use for detailed genome comparisons with available Y. Here, we report the complete genomic sequence of Y. ![]() Despite their close genetic relationship, they differ radically in their pathogenicity and transmission. Yersinia pestis, the causative agent of plague, is a highly uniform clone that diverged recently from the enteric pathogen Yersinia pseudotuberculosis.
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