Abstract
BackgroundGenetic variation has been shown to play a significant role in determining susceptibility to the salmon louse, Lepeophtheirus salmonis. However, the mechanisms involved in differential response to infection remain poorly understood. Recent findings in Atlantic salmon (Salmo salar) have provided evidence for a potential link between marker variation at the major histocompatibility complex (MHC) and differences in lice abundance among infected siblings, suggesting that MHC genes can modulate susceptibility to the parasite. In this study, we used quantitative trait locus (QTL) analysis to test the effect of genomic regions linked to MHC class I and II on linkage groups (LG) 15 and 6, respectively.ResultsSignificant QTL effects were detected on both LG 6 and LG 15 in sire-based analysis but the QTL regions remained unresolved due to a lack of recombination between markers. In dam-based analysis, a significant QTL was identified on LG 6, which accounted for 12.9% of within-family variance in lice abundance. However, the QTL was located at the opposite end of DAA, with no significant overlap with the MHC class II region. Interestingly, QTL modelling also revealed evidence of sex-linked differences in lice abundance, indicating that males and females may have different susceptibility to infection.ConclusionOverall, QTL analysis provided relatively weak support for a proximal effect of classical MHC regions on lice abundance, which can partly be explained by linkage to other genes controlling susceptibility to L. salmonis on the same chromosome.
Highlights
Genetic variation has been shown to play a significant role in determining susceptibility to the salmon louse, Lepeophtheirus salmonis
quantitative trait locus (QTL) modelling of lice abundance in family 3 To further characterize QTL effects identified on linkage groups (LG) 6 in the dam of family 3 (Figure 4b), we modelled lice abundance as a function of QTL genotypes, body weight, and sex (Table 2)
The QTL detected on LG 6 in the dam of family 3 was significant at the experimentwide threshold but a causal link with major histocompatibility complex (MHC) variation is unlikely due to its predicted location at the opposite end of MHC class II
Summary
Genetic variation has been shown to play a significant role in determining susceptibility to the salmon louse, Lepeophtheirus salmonis. Kolstad et al [8] estimated average heritabilities of 0.14 and 0.26 for susceptibility to infection in multiple year-classes following natural and experimental challenges, respectively. Together, these results confirm earlier evidence of genetic variation for susceptibility to L. salmonis in Atlantic salmon [9] and indicate that host genes play a significant role in determining infection levels
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