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A Rationale for Repression and/or Loss of Motility by Pathogenic Yersinia in the Mammalian Host

  • Scott A. Minnich
  • Harold N. Rohde
Part of the Advances In Experimental Medicine And Biology book series (AEMB, volume 603)

Pathogenic yersiniae either repress flagella expression under host conditions (Yersinia enterocolitica and Yersinia pseudotuberculosis) or have permanently lost this capability by mutation (Yersinia pestis). The block in flagella synthesis for the enteropathogenic Yersinia centers on fliA (σF) repression. This repression ensures the downstream repression of flagellin structural genes which can be cross-recognized and secreted by virulence type III secretion systems. Y. pestis carries several flagellar mutations including a frame shift mutation in flhD, part of the flagellar master control operon. Repression of flagellins in the host environment may be critical because they are potent inducers of innate immunity. Artificial expression of flagellin in Y. enterocolitica completely attenuates virulence, supporting the hypothesis that motility is a liability in the mammalian host.

Keywords

Yersinia Enterocolitica Yersinia Pestis Flagellar Gene Flagellin Gene Yersinia Pseudotuberculosis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Scott A. Minnich
    • 1
  • Harold N. Rohde
    • 1
  1. 1.Department of Microbiology, Molecular Biology, and BiochemistryUniversity of IdahoMoscowUSA

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