January 12-16, 2002
Town & Country Convention Center
San Diego, CA
Poster: Microbial Sequencing and Genome Programs
There is mounting evidence that Yersinia pestis, the etiological agent of plague may have evolved recently from Y. pseudotuberculosis. While highly similar at the nucleotide level (~95%), and despite sharing at least one virulence plasmid and a number of chromosomally-encoded virulence-associated factors, Y. pseudotuberculosis causes a much milder enteric disease in humans; the reason for their dramatic difference in virulence remains unknown. We conducted whole genomic sequencing of Y. pseudotuberculosis IP32953 in order to provide in-depth information on the physiological capabilities of these two Yersinia species. Given their relatedness but their marked difference in clinical manifestations, understanding and contrasting the genetic complement of each organism may allow reconstruction of the evolution of pathogenicity in Yersinia (i.e., How does a mild chronic pathogen become such a deadly pathogen?). Preliminary analysis of the work in progress has confirmed the largely colinear nature of the two genomes. We have identified some potential genomic rearrangements as well as the complement of insertion elements most common to Yersinia. We have uncovered the presence of a novel 27 kb plasmid in Y. pseudotuberculosis IP32953, confirmed the presence of seven ribosomal RNA operons, and also discovered a small number of regions that are unique either to Y. pestis or Y. pseudotuberculosis. A more complete comparison of the whole genomes will most likely identify a set of genes whose function might have contributed to the different degree of pathogenicity and will shed light on the evolutionary process that led to the emergence of plague.