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ARS Home » Southeast Area » Auburn, Alabama » Aquatic Animal Health Research » Research » Publications at this Location » Publication #312937
Title: Flavobacterium columnare type IX secretion system mutations result in defects in gliding motility and virulence

Author
item LI, NAN - University Of Wisconsin
item POWERS, JONATHON - University Of Wisconsin
item ROETS, JACK - University Of Wisconsin
item NIE, PIN - Chinese Academy Of Sciences
item Lafrentz, Benjamin
item HUNNICUTT, DAVID - University Of Wisconsin
item MCBRIDE, MARK - University Of Wisconsin

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/22/2014
Publication Date: 1/18/2015
Citation: Li, N., Powers, J., Roets, J., Nie, P., Lafrentz, B.R., Hunnicutt, D.W., Mcbride, M.J. 2015. Flavobacterium columnare type IX secretion system mutations result in defects in gliding motility and virulence [abstract]. Bacterial Locomotion and Signal Transduction. p.87.

Interpretive Summary:

Technical Abstract: Background: The gliding bacterium Flavobacterium columnare causes columnaris disease in wild and aquaculture-reared freshwater fish. The mechanisms responsible for columnaris disease are not known. The related bacterium Flavobacterium johnsoniae uses a type IX secretion system (T9SS) to secrete enzymes, adhesins, and proteins involved in gliding motility. F. columnare has all of the T9SS components, and this system may have a role in virulence. Genetic techniques were recently developed for F. columnare, including procedures to make in-frame deletions. We used these techniques to test the hypothesis that the T9SS is required for virulence. Methods: In-frame deletion mutations in the T9SS genes gldN and porV were constructed in F. columnare strain C#2. The mutants were examined for motility, secretion, and ability to kill zebrafish and yellow perch. Results: An F. columnare gldN deletion mutant was constructed. GldN is a core component of the F. johnsoniae T9SS and is required for secretion. gldN mutants are unable to secrete the motility adhesin SprB to the cell surface, and thus are also defective in gliding motility. The F. columnare gldN mutant was deficient in the secretion of several extracellular proteins and lacked gliding motility. The gldN mutant exhibited greatly reduced virulence on zebrafish and yellow perch, and complementation restored virulence. Cell-free spent media from cultures of wild type and complemented cells caused rapid mortality in zebrafish, while cell-free spent media from gldN mutant cells did not. F. johnsoniae PorV is required for secretion of a subset of proteins targeted to its T9SS and is not required for motility. A porV mutant of F. columnare was constructed to determine whether motility or secretion was associated with virulence. The porV mutant exhibited gliding motility but in preliminary tests it had decreased virulence similar to the gldN mutant. Conclusion: The F. columnare T9SS appears to be required for virulence. Future studies will identify the secreted proteins responsible for disease and test the efficacy of avirulent mutants as vaccine strains to prevent columnaris disease in aquaculture fish.