Confirmation and fine-mapping of a major QTL for resistance to infectious pancreatic necrosis in Atlantic salmon (Salmo salar): population-level associations between markers and trait

Abstract

Background: Infectious pancreatic necrosis (IPN) is one of the most prevalent and economically devastating diseases in Atlantic salmon (Salmo salar) farming worldwide. The disease causes large mortalities at both the fry-and post-smolt stages. Family selection for increased IPN resistance is performed through the use of controlled challenge tests, where survival rates of sib-groups are recorded. However, since challenge-tested animals cannot be used as breeding candidates, withinfamily selection is not performed and only half of the genetic variation for IPN resistance is being exploited. DNA markers linked to quantitative trait loci (QTL) affecting IPN resistance would therefore be a powerful selection tool. The aim of this study was to identify and fine-map QTL for IPN-resistance in Atlantic salmon, for use in marker-assisted selection to increase the rate of genetic improvement for this trait.

The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

“…same region of Atlantic salmon LG 21 explains much of the genetic variation in IPN resistance in fry (48%) and post-smolts (83%), and do not suggest a large role for any of the other LGs (Moen et al, 2009). The confirmation of the LG 21 major QTL by two independent research groups in two distinct populations is a strong evidence that the QTL effect is genuine and robust.…”

“…The largest QTL, on Atlantic salmon linkage group (LG) 21, was estimated to explain between 21 and 32% of the within-family phenotypic variation in IPN resistance during this field outbreak (Houston et al, 2008a, b), and was subsequently confirmed by Moen et al (2009). A further genome-wide significant QTL was detected on LG 28 (LG denoted as given in the ASalBase map http://www.asalbase.org/sal-bin/map/index), with a suggestive QTL on LG 19 (Houston et al, 2008b).…”

Quantitative genetics of disease resistance in vaccinated and unvaccinated Atlantic salmon (Salmo salar L.)

“…A quantitative trait loci explaining a very large proportion of the genetic variation in IPN resistance has been detected in Atlantic salmon (Houston et al, 2009;Moen et al, 2009). In our study, evidence was found of significantly favourable genetic correlations of resistance to furunculosis in unvaccinated fish with resistance to both IPN and ISA (unvaccinated fish).…”

Genomics and Genome Sequencing: Benefits for Finfish Aquaculture

“…A major QTL for IPN resistance in Atlantic salmon has been identified and confirmed Moen et al, 2009a). A four-marker haplotype has been identified that strongly segregates with IPN resistance in Norwegian Atlantic salmon broodstock, providing a solid framework for linkage-based MAS in this population (Moen et al, 2009a).…”

“…It is no surprise therefore, that several QTL have been identified for body weight and condition factor in Atlantic salmon (Baranski et al, 2010;Boulding et al, 2008;Moghadam et al, 2007;Reid et al, 2005) (Moghadam et al, 2007;Kuttner et al, 2011). QTL for several other traits in salmonids have been mapped, including upper temperature tolerance (Jackson et al, 1998;Perry et al, 2001;Somorjai et al, 2003), spawning time (O'Malley et al, 2003), developmental rate (Nichols et al, 2008), and resistance to pathogens Gilbey et al, 2006;Houston et al , 2009Houston et al , 2010Jones et al, 2002;Moen et al 2007Moen et al , 2009a. Given that many of the microsatellite markers derived from one salmonid species amplify the DNA from other salmonid species, it has been relatively straightforward to carry out comparative analyses of the rainbow trout, Arctic charr and Atlantic salmon genomes .…”