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ARS Home » Southeast Area » Auburn, Alabama » Aquatic Animal Health Research » Research » Publications at this Location » Publication #317676
Research Project: Pathogen Characterization, Host Immune Response and Development of Strategies to Reduce Losses to Disease in Aquaculture

Location: Aquatic Animal Health Research

Title: Flavobacterium columnare type IX secretion system mutations result in defects in gliding motility and loss of virulence

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

Submitted to: Flavobacterium Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 9/15/2015
Publication Date: 10/27/2015
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 loss of virulence [abstract]. Flavobacterium 2015. p. 30.

Interpretive Summary:

Technical Abstract: 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. gldN, which encodes a core component of the T9SS, was deleted in F. columnare strain C#2. 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 in zebrafish and yellow perch and complementation restored virulence. Cell-free spent media from cultures of wild type and complemented cells caused rapid mortality, 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 it had decreased virulence similar to the gldN mutant. 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.