Protein markers and mechanisms of Bacterial Cold Water Disease in Rainbow Trout (Oncorynchus mykiss) revealed using mass spectrometry proteomic analysis
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Titel:
Protein markers and mechanisms of Bacterial Cold Water Disease in Rainbow Trout (Oncorynchus mykiss) revealed using mass spectrometry proteomic analysis
Beschreibung:
Aquaculture is a rapidly expanding agricultural field, especially at the international level. One of the largest issues which arise from raising high densities of fish in a confined area is infection and rapid transmission of disease within the population. There are currently few federally approved pharmaceutical treatments for fish, making rapid and accurate diagnosis essential for maintaining healthy populations. The current study focuses on the infection of rainbow trout (Oncorynchus mykiss) by the gram‐negative bacteria Flavobacterium psychrophilum which manifests as Bacterial Cold Water Disease (BCWD). The approach involves examining the physiological effects of infection in these fish at the protein level. Using LC‐MS techniques, the majority of proteins in the kidney, spleen, plasma, and muscles at site of infection are analyzed for differential abundance between infected and control populations. Artificially infected cohorts are compared against fish taken from an active hatchery to determine whether lab results are reflected in a real‐world context. Sets of proteins which change in abundance as a response to BCWD infection make ideal candidates as bio‐markers which can be used in the development of diagnostic tools. This method also reveals the underlying mechanisms of the infection and response through gene ontology and pathway analysis. Plasma was found to have the greatest regulation in terms of significantly different protein abundance. For this reason and the relative ease of sampling plasma without fish sacrifice, plasma appears to the best tissue for diagnostic purposes. The greatest protein regulation in the plasma was seen in enzymes involved in glycolysis, actin cytoskeletal regulation, immune response, and oxidation‐reduction regulation.Support or Funding InformationSupported by NSF Grant IOB‐1355098