Location: Cool and Cold Water Aquaculture ResearchTitle: Flagellar regulation in Yersinia ruckeri during infection Author
|Welch, Timothy - Tim|
Submitted to: European Association of Fish Pathologists
Publication Type: Abstract Only
Publication Acceptance Date: 5/12/2015
Publication Date: 9/7/2015
Citation: Snyder, A.K., Welch, T.J. 2015. Flagellar regulation in Yersinia ruckeri during infection [abstract]. European Association of Fish Pathologists. p. O-102.
Technical Abstract: The gram-negative Enterobacterium Yersinia ruckeri is the etiologic agent of enteric redmouth disease (ERM), a septicemia affecting primarily farmed rainbow trout (Oncorhynchus mykiss, Walbaum). Over the past decade, there has been an increase in the prevalence of non-motile variants of Y. ruckeri and the appearance of these variants has correlated to ERM outbreaks in previously vaccinated fish. Additional research demonstrated that this phenotype has evolved independently several times in the U.S. and Europe and has had no discernable effect on the virulence of this pathogen. Since flagellin, the structural component of the flagellum, is a potent immune stimulator it is plausible that inappropriate expression of the motility phenotype during the infection process could be deleterious due to flagellin-mediated host recognition. Therefore, mutational loss would ensure against inappropriate flagellin expression. Here, we use quantitative RT-PCR to demonstrate that expression of the flagellin locus fliC is repressed during the course of infection and subsequently up-regulated upon host mortality in a motile strain of Y. ruckeri. We hypothesize that the repression of flagellin expression during infection occurs in order to evade host recognition. Related bacterial flagellar secretion assembly, and thus motility, is often regulated in response to environmental stimuli through transcriptional regulators that act by modulating expression of the flagellar master regulator flhDC. Expression of flhDC in turn initiates a cascade of downstream flagellar biosynthetic gene activation. To confirm that flhDC regulates flagellar secretion in Y. ruckeri, we constructed an isogenic flhD knockout mutant. This mutation caused complete loss of the flagellar motility and secretion phenotypes when assessed in culture, suggesting that flhDC is an essential, positive regulator of flagellar assembly in Y. ruckeri. Further work is necessary to identify putative environmental response-regulator(s) necessary for host sensing and in vivo repression of flagellar motility during infection. This research will lead to a better understanding of how Y. ruckeri senses and responds adaptively to its host environment, and may lead to the identification of other virulence regulated genes.