Heritable variation in resistance to pathogens has been reported in many fish species, but little is known about its genetic architecture. To extend understanding, an investigation was made of the association of resistance to proliferative kidney disease (PKD) in 4 second filial generation (F2) families of Atlantic salmon with molecular markers from different genetic linkage groups in the species’ genome, following a natural disease outbreak. PKD causes serious mortality in cultured salmonids. In addition to mortality, associations with growth-related traits were also examined, as immune responses are energetically costly and have been observed to reduce growth. Associations were investigated for 34 microsatellite markers and 5 restriction fragment length polymorphism (RFLP) loci from 3 regions of the growth hormone 1 gene (GH1). The phenotypic and genotypic character of survivors was compared with unexposed fish derived from the same families. Mortality was not size-selective, but growth in the survivors was reduced, and fish had a lower condition factor than unexposed fish, suggesting an energetic cost to resistance. Five markers showed significant allele frequency differences between survivors and unexposed fish, albeit in single families. Prior to correction for multiple tests, 2 of these markers were also linked to variation in growth-related traits among survivors, along with a further 7 markers. Though sample sizes constrained the power of the analysis, the study points to regions of the salmon genome that may contain quantitative trait loci related to PKD resistance, on which further work on the genetic architecture of PKD resistance in this species could focus.
- Proliferative kidney disease
- Atlantic salmon
- Marker-trait associations
- Quantitative trait locus
Cauwelier, E., Gilbey, J., Jones, C. S., Noble, L. R., & Verspoor, E. (2010). Genotypic and phenotypic correlates with proliferative kidney disease-induced mortality in Atlantic salmon. Diseases of Aquatic Organisms, 89(2), 125-135. https://doi.org/10.3354/dao02191