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ARS Home » Northeast Area » Leetown, West Virginia » Cool and Cold Water Aquaculture Research » Research » Publications at this Location » Publication #408027
Research Project: Improving Salmonid Health through Breeding, Vaccination and Microbiome Modulation

Location: Cool and Cold Water Aquaculture Research

Title: Gliding motility proteins GldJ and SprB contribute to Flavobacterium columnare virulence

Author
item THUNES, NICOLE - US Department Of Agriculture (USDA)
item Evenhuis, Jason
item Lipscomb, Ryan
item PEREZ-PASCUAL, DAVID - Institut Pasteur - France
item STEVICK, REBECCA - Institut Pasteur - France
item Birkett, Clayton
item GHIGO, JEAN-MARC - Institut Pasteur - France
item MCBRIDE, MARK - University Of Wisconsin

Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/1/2024
Publication Date: 3/22/2024
Citation: Thunes, N.C., Evenhuis, J., Lipscomb, R.S., Perez-Pascual, D., Stevick, R.J., Birkett, C., Ghigo, J., Mcbride, M.J. 2024. Gliding motility proteins GldJ and SprB contribute to Flavobacterium columnare virulence. Applied and Environmental Microbiology. 206(4). https://doi.org/10.1128/jb.00068-24.
DOI: https://doi.org/10.1128/jb.00068-24

Interpretive Summary: Columnaris disease is problematic for multiple fish species in aquaculture and is caused by the bacterium Flavobacterium columnare. F. columnare cells move on fish tissues by gliding motility, but it is unknown if this gliding motility is critical for this bacterium to cause disease (i.e., be virulent). In this study, multiple motility genes (SprB, SprF and GldJ) were mutated to produce strains that were deficient in their gliding motility. These mutant strains were shown to be avirulent, or to have reduced virulence, in zebrafish and rainbow trout. This study demonstrates the importance of gliding motility genes for virulence and informs scientists of potential targets for novel vaccine development to protect farmed rainbow trout against columnaris disease.

Technical Abstract: Flavobacterium columnare causes columnaris disease in freshwater fish and is a major problem for aquaculture systems. Virulence mechanisms of F. columnare are incompletely understood and adequate control measures are lacking. The F. columnare type IX secretion system (T9SS) is required for gliding motility and for virulence. The T9SS and gliding motility machineries share core components, but each also have some components that are unique. Previous studies demonstrated that gldN (required for gliding and for secretion) and porV (required for secretion of many proteins but not required for gliding) are both required for virulence, implicating T9SS-mediated secretion in virulence. In contrast, it is not known if motility is important for virulence. Here, we constructed F. columnare sprB, sprF and gldJ mutants that were defective for motility but that maintained T9SS function, and analyzed these to understand the role of motility in virulence. Wild-type cells formed spreading colonies on agar and moved rapidly on glass surfaces. In contrast, sprB and sprF deletion mutants formed nonspreading colonies on agar, and moved poorly on glass. Both mutants exhibited reduced virulence in rainbow trout fry. A gldJ deletion mutant was nonmotile, secretion deficient, and avirulent in rainbow trout. To separate the roles of GldJ in secretion and in motility, we generated gldJ truncation mutants that produce nearly full-length GldJ. Mutant gldJ563, which produced GldJ truncated at amino acid 563, was defective for gliding but was competent for secretion as measured by extracellular protease activity. The gldJ truncation mutant displayed reduced virulence in rainbow trout fry, suggesting that motility contributes to virulence. Fish that survived exposure to the sprB deletion mutant or to the gldJ563 mutant exhibited partial resistance to later challenge with wild-type cells.