Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo Salar)

Article excerpt

ABSTRACT

Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem in the production of Atlantic salmon (Salmon salar). IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populations show clear genetic variation in resistance. To determine whether this genetic variation includes loci of major effect, a genomewide quantitative trait loci (QTL) scan was performed within 10 full-sib families that had received a natural seawater IPN challenge. To utilize the large difference between Atlantic salmon male and female recombination rates, a two-stage mapping strategy was employed. Initially, a sire-based QTL analysis was used to detect linkage groups with significant effects on IPN resistance, using two to three microsatellite markers per linkage group. A dam-based analysis with additional markers was then used to confirm and position any detected QTL. Two genomewide significant QTL and one suggestive QTL were detected in the genome scan. The most significant QTL was mapped to linkage group 21 and was significant at the genomewide level in both the sire and the dam-based analyses. The identified QTL can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality.

INFECTIOUS pancreatic necrosis (IPN) is a viral disease that currently presents a major problem in the production of Atlantic salmon, and other salmonid species, in many countries. This highly contagious disease has the unusual characteristic of affecting farmed salmon during two specific windows of the life cycle (Roberts and Pearson 2005). In the freshwater phase of the salmon life cycle, IPN outbreaks in fry have been observed for several decades, with up to 70% mortality. In the marine environments, the emergence of problematic IPN outbreaks (up to 40% mortality) is more recent, coinciding with the dramatic expansion of salmon aquaculture (Roberts and Pearson 2005). The causative agent for IPN is a double-stranded, nonmembraned RNA birnavirus, of which several subtypes have been characterized (Roberts and Pearson 2005). Levels of mortality during an IPN outbreak are determined by numerous factors, although it is increasingly clear that a strong genetic component to IPN resistance exists in salmon (Guy et al. 2006).

The elucidation of the molecular genetic basis of economically important traits in all salmonid species is complicated by the structure and properties of their genome. The salmonid genome is thought to have undergone a relatively recent duplication event (25-100 million years ago) and is currently evolving toward a fully diploid state (Allendorf and Thorgaard 1984; Allendorf and Danzmann 1997). Salmonid fish exhibit several remnants of their tetraploid ancestry, including some exchange of chromatid segments between ancestrally homeologous chromosome arms following the formation of multivalent structures at meiosis (Wright et al. 1983). These structures are also thought to constrain recombination, particularly toward centro-meric regions of the chromosome (Allendorf and Danzmann 1997; Sakamoto et al. 2000). Interestingly, these phenomena are unique to male meiosis, and as a result there are striking sex-specific differences in linkage maps within salmonid species, with estimations of female:male map distance ratios of 3.25 in rainbow trout (Oncorhynchus mykiss) (Sakamoto et al. 2000), 3.92 (Gilbey et al. 2004) or 8.26 (Moen et al. 2004a) in Atlantic salmon, and 2.64 for brown trout (Salmo trutta) (Gharbi et al. 2006). The implications of these recombination differences for mapping quantitative trait loci (QTL) include the increased power of QTL detection, combined with the reduced ability to position the QTL in males (Hayes et al. 2006).

Several Atlantic salmon genetic linkage maps currently exist (e.g., Gilbey et al. 2004; Moen et al. …