Genetic architecture of resistance to bacterial cold water disease in rainbow trout is altered in response to genetic changes in causative bacterial pathogen
Abstract
Bacterial cold water disease (BCWD) causes considerable mortality and economic losses for the global rainbow trout aquaculture industry. Currently, there is no effective commercially available vaccine for the disease caused by Flavobacterium psychrophilum (Fp). For the past 20 years, the USDA-ARS injection challenge model has successfully used a single strain (CSF259-93) of the pathogenic Fp bacteria for selective breeding of resistant rainbow trout and to characterize the genetic architecture of BCWD resistance in commercial US breeding populations. Previously, we identified similar genetic architecture in two important commercial rainbow trout populations with strong QTLs for survival response on chromosomes Omy8 and Omy25p (OmyA31) and another large-effect QTL that was detected on Omy3 only in one of the two populations. The objectives of this study were to (1) characterize the genetic architecture of resistance to BCWD in a third important commercial US breeding population (TLUN= Troutlodge, Inc. November-spawning breeding population) using our standard Fp1 strain (CSF259-93); (2) evaluate the genetic architecture of resistance to a different Fp2 strain (ARS-037-11) in the TLUN breeding population; and (3) estimate the heritability and genetic correlation of resistance to BCWD inflicted by the two Fp strains. Offspring (N= 2073) from 108 TLUN 2018 year-class full-sib families were challenged with one of the two strains in separate experiments and genotyped. Each fish was whole-genome sequenced (WGS) at low genome coverage (~1x) and genotypes from 4.6M SNP were imputed in the offspring population using high coverage WGS (>10x) of the parents. Heritability for BCWD resistance was moderate with estimates of 0.45-0.53 and 0.37-0.46 for the different Fp2 and standard Fp1 strains, respectively, and genetic correlation between survival to both Fp strains was low to moderate (0.19-0.36). Three moderate-large effect QTLs with additive genetic variance (AGV) of 2-22% were detected on chromosomes Omy3, 5 and OmyA31 for resistance to the different Fp2 strain, and 10 moderate-effect QTLs (AGV= 2-10%) on chromosomes Omy3, 8, 13, 17, 20, 24, 25 (Omy25q) and OmyA31 for the standard Fp1 strain. The most notable difference was a new large-effect QTL (AGV= 22%) for resistance to the different Fp2 strain that was detected on chromosome Omy5. Our findings suggest that (1) resistance to BCWD can be improved through selective breeding in this important commercial breeding population; (2) the genetic architecture of resistance to BCWD caused by either Fp strain is oligogenic which can be exploited through marker-assisted selection; (3) the low-moderate genetic correlation and the unique QTLs detected for resistance to each Fp strain suggest that selective breeding for multiple Fp strains should be considered when breeding for BCWD resistance; and (4) the high density SNP panel used in the GWAS enabled finer profiling of SNP effects within the narrower QTL regions.
Keywords: 2026
How to Cite:
Vallejo, R., Liu, S., Evenhuis, J., Tsuruta, S., Long, R., Wiens, G., Martin, K. & Palti, Y., (2026) “Genetic architecture of resistance to bacterial cold water disease in rainbow trout is altered in response to genetic changes in causative bacterial pathogen”, World Congress on Genetics Applied to Livestock Production Digital Archive 2026(1): 2294207. doi: https://doi.org/10.31274/wcgalp.24317
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