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Open Access Research article

Genetic dissection of MHC-associated susceptibility to Lepeophtheirus salmonis in Atlantic salmon

Karim Gharbi1*, Kevin A Glover2, Louise C Stone14, Elizabeth S MacDonald1, Louise Matthews1, Unni Grimholt3 and Michael J Stear1

Author Affiliations

1 Institute of Comparative Medicine, University of Glasgow, Glasgow, G61 1QH, UK

2 Institute of Marine Research, N-5817 Bergen, Norway

3 CEES, Department of Biology, University of Oslo, Oslo, Norway

4 School of Biosciences, University of Birmingham, Birmingham, B15 2TT, UK

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BMC Genetics 2009, 10:20  doi:10.1186/1471-2156-10-20

Published: 27 April 2009

Abstract

Background

Genetic 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.

Results

Significant 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.

Conclusion

Overall, 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.