Prospecting genomic regions associated with Columnaris disease in two commercially important rainbow trout breeding populations

Authors: SILVA, RAFAEL - Orise Fellow; Vallejo, Roger; Evenhuis, Jason; Leeds, Timothy - Tim; Gao, Guangtu; PARSONS, JAMES - Troutlodge, Inc; MARTIN, KYLE - Troutlodge, Inc; LOURENCO, DANIELA - University Of Georgia; Palti, Yniv

Submitted to: American Society of Animal Science Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 3/6/2017
Publication Date: 7/1/2017
Citation: Silva, R., Vallejo, R.L., Evenhuis, J., Leeds, T.D., Gao, G., Parsons, J., Martin, K., Lourenco, D., Palti, Y. 2017. Prospecting genomic regions associated with Columnaris disease in two commercially important rainbow trout breeding populations [absctract]. American Society of Animal Science Annual Meeting. 95:103.P209.

Interpretive Summary:

Technical Abstract: Flavbacterium Columnare, the causative agent of Columnaris disease (CD), is distributed around the world in fresh water sources, infecting freshwater finfish species. Recently it has been identified as an emerging problem for the rainbow trout aquaculture industry in the US. Two live-attenuated vaccines have been commercialized, but their efficacy in rainbow trout is still not clear. The purpose of this study was to prospect genomic regions that explain large portion of the additive genetic variance of CD resistance in rainbow trout. Two commercially important aquaculture populations were investigated. The National Center for Cool and Cold Water Aquaculture (NCCCWA) odd-year line, with resistance to bacterial cold water disease (BCWD); and the Troutlodge, Inc., May odd-year (TLUM) nucleus breeding population, which provided 54,325 and 36,265 pedigree records; in which 8,453 and 3,986 fish had CD resistance phenotype records, respectively. Fish that survived to 21 days post immersion challenge were recorded as resistant (phenotype=2) and those that did not were considered susceptible (phenotype=1). Genotypes for 57k SNP (Affymetrix Axiom®) were available for 1,185 and 1,137 fish from NCCCWA and TLUM, respectively. The SNP effects and variances were estimated using the weighted single-step genomic BLUP approach for genome-wide association (WssGBLUP), which uses pedigree, genotypes, and phenotypes from genotyped and ungenotyped animals. The weighting strategy accounted for 1Mb SNP-windows. Genomic regions that explained more than 1% of the additive genetic variance were considered associated with CD resistance. A total of 13 windows (located on chromosome 8, 9, 10, 14, 17 and 21) were found to be associated with CD resistance in the NCCCWA population. Two windows, located at 59-60 Mb and 61-62 Mb on chromosome 17, explained 12% and 11.33% of the genetic variance for CD resistance in that population, respectively. A total of 16 windows located on nine chromosomes were detected in the TLUM population. Only three similar windows (located on two chromosomes) were detected in both populations. The results suggest that CD resistance has an oligogenic architecture, and the SNP windows found to be associated are not informative enough for selection decisions across populations. Some positive genetic correlation has been previously shown between CD and BCWD resistance in the NCCCWA population. One factor which might have contributed to detecting different QTL for CD resistance in the two populations is the previous five generations of selective breeding of the NCCCWA population for BCWD resistance compared to no intentional selection pressure for disease resistance in the TLUM population.