Genetic Basis for Resistance Against Viral Nervous Necrosis: GWAS and Potential of Genomic Prediction Explored in Farmed European Sea Bass (Dicentrarchus labrax)

Abstract

Viral nervous necrosis (VNN) is an infectious disease caused by the red-spotted grouper nervous necrosis virus (RGNNV) in European sea bass and is considered a serious concern for the aquaculture industry with fry and juveniles being highly susceptible. To understand the genetic basis for resistance against VNN, a survival phenotype through the challenge test against the RGNNV was recorded in populations from multiple year classes (YC2016 and YC2017). A total of 4,851 individuals from 181 families were tested, and a subset (n∼1,535) belonging to 122 families was genotyped using a ∼57K Affymetrix Axiom array. The survival against the RGNNV showed low to moderate heritability with observed scale estimates of 0.18 and 0.25 obtained using pedigree vs. genomic information, respectively. The genome-wide association analysis showed a strong signal of quantitative trait loci (QTL) at LG12 which explained ∼33% of the genetic variance. The QTL region contained multiple genes (ITPK1, PLK4, HSPA4L, REEP1, CHMP2, MRPL35, and SCUBE) with HSPA4L and/or REEP1 genes being highly relevant with a likely effect on host response in managing disease-associated symptoms. The results on the accuracy of predicting breeding values presented 20–43% advantage in accuracy using genomic over pedigree-based information which varied across model types and applied validation schemes.

Whole-genome sequencing identifies interferon induced protein IFI6 as a strong candidate gene for VNN resistance in European sea bass

“…Our results show that heritability estimates for VNN survival using imputed genotypes (0.21-0.22 on the observed scale) are of the same magnitude as values obtained in previous studies on NNV-infected sea bass, 0.08 to 0.23 on the observed scale in [10,23] and 0.15 to 0.43 on the liability scale in [18,39]. The number of breeders used to obtain challenged individuals as well as the number of experimental individuals, the method of infection during viral challenges, the age and size at challenge and the genetic origin and/or the experimental design are parameters that may explain the differences between the estimates of NNV survival in these studies [39].…”

“…None of these genes have been previously reported in the literature in view of association studies for survival to VNN. Interestingly, LG12_QTL_2 and these two genes are located more than 2.5 Mb away from the QTL region identified by Vela-Avitúa et al [23] and where the HSP70 gene is located, which was also reported in a transcriptomic analysis of response to VNN in Asian sea bass [41]. This may be a consequence of the much higher precision of our localisation, as the LG12_QTL_2 region is only 127 kb, while the region identified in [22] is 7 Mb wide.…”

“…Indeed, we have privileged an infection by the VNN via the contamination of the circulating water in the batch, i.e. we find the presence of the virus in the aquatic environment as encountered by the fish in rearing facilities (tanks, sea cage), whereas Vela-Avitúa et al [23] have preferred a contamination by injection. Thus, the defence mechanisms involved in the immune response of fish may be different and therefore the gene regions highlighted by GWAS may also be different.…”

“…For this, genome-wide association studies (GWAS) have become a powerful tool in genetics and commonly applied in animal breeding [21, 22] e.g. in different sea bass species and populations for VNN resistance [10, 18, 19, 23]. They reported the identification of quantitative trait loci (QTL) and even the identification of SNP variants impacting the survival rate of sea bass exposed to NNV.…”

“…For this, genome-wide association studies (GWAS) have become a powerful tool in genetics and commonly applied in animal breeding [21,22] e.g. in different sea bass species and populations for VNN resistance [10,18,19,23].…”