"Increased virulence of Yersinia pseudotuberculosis by two independent mutations." (1988)
Roland Rosqvist, Mikael Skurnik, and Hans Wolf-Watz
Abstract
A chromosomally encoded protein, which mediates invasion into HeLa cells was recently identified in Yersinia pseudotuberculosis. The role of this protein (invasin) in the virulence process was not, however, investigated. We show that mutation of the invasin gene in Y. pseudotuberculosis abolishes the ability of the bacteria to invade HeLa cells. When mice were challenged by intraperitoneal injection both the mutant and the wild-type strain produced infections of similar virulence but mutant showed a slower rate of infection after oral challenge. A double mutant, carrying an additional mutation in the gene coding for the Yop1 protein, was also constructed. The double mutant was significantly more virulent than either the wild-type or the corresponding single mutants. Y. pestis, in contrast to Y. pseudotuberculosis lacks the ability to express either invasin or Yop1, sequence analysis of the yopA gene from both Y. pestis and Y. pseudotuberculosis shows that the yopA gene of Y. pestis contains a point-mutation leading to a reading-frame shift. When the yopA+ gene was introduced into Y. pestis the virulence of this strain was reduced. These results may provide insight into the rise and fall of plague epidemics caused by Y. pestis.
"Reevaluation of the Virulence Phenotype of the inv yadA Double Mutants of Yersinia
Yiping W. Han and Virginia L. Miller
Abstract
Yersinia pseudotuberculosis and Yersinia enterocolitica are closely related human pathogens causing gastroenteritis.Invasin and YadA are two of the most extensively studied virulence factors of the Yersinia genus. Invasin is the primary invasion factor encoded by the inv gene on the chromosome and is required for the penetration of the epithelial cells. YadA is encoded by the yadA gene on the 70-kb virulence plasmid and has multiple functions. Previous studies indicate that an inv yadA double mutant of Y. enterocolitica is avirulent while an inv yadA mutant of Y. pseudotuberculosis is hypervirulent. In this study, we investigated this unexpected difference. New constructs of the inv yadA mutants of Y. pseudotuberculosis were made and tested in mice. These new constructs were not hypervirulent; rather, they maintained the same virulence as the wild-type strain. Further examination of the inv mutant used for the previous study revealed that it carries an aberrant inv phenotype and has an altered outer membrane profile and an altered colony morphology. Therefore, the mutants used previously were not isogenic to the parental wild-type strain, which may in part account for the difference in the results obtained.