Fine mapping and functional annotation of a QTL for resistance to tilapia lake virus in Nile tilapia (Oreochromis niloticus).

Disease resistance is one of the main targets of animal breeding programs. In recent years, incorporating genomic information to accelerate genetic progress has become one of the priorities of the industry. Here, we combined population-scale whole-genome sequencing with differential gene expression and functional annotation analyses to study resistance to tilapia lake virus (TiLV) in a breeding Nile tilapia (Oreochromis niloticus) GIFT population. Fish with survival data from a natural TiLV outbreak were sampled and genotyped for 6.7 M SNPs using whole-genome resequencing and imputation. Our results confirmed a QTL located in the proximal end of Oni22, identifying 74 out of the top 99 markers associated with binary survival within a 10 Mb window. The marker explaining the highest genetic variance of TiLV resistance is located at 1.7 Mb and presents a substitution effect of 0.15. Additionally, other SNPs in several other chromosomes explained a high percentage of the genetic variance, with an important number located in 2 separate regions of Oni09. These results suggest an oligogenic architecture underlying resistance to TiLV, with several QTLs with moderate effect and many with small effect. Host transcriptomic analyses identified genes differentially expressed between resistant and susceptible genotypes according to the QTL in Oni22, highlighting proteosome subunit beta type-9a, and ha1f as potential causal genes. This is the first study combining whole-genome sequencing at a population scale with genomic approaches to assess the underlying genomic basis for TiLV resistance. Our results confirm and narrow down a QTL underlying this key trait in a major aquaculture species worldwide, and found novel QTLs in other chromosomes. The identified markers and genes have the potential to improve resistance to TiLV in Nile tilapia, significantly improving animal health and welfare.