AQUA 2024

August 26 - 30, 2024

Copenhagen, Denmark

UNRAVELLING THE GENETIC ARCHITECTURE OF AMOEBIC GILL DISEASE AND GILL LESIONS IN ATLANTIC SALMON

Afees Ajasa1,2*, Solomon Boison, Hans Magnus Gjøen and Marie Lillehammer

1Nofima (Norwegian Institute of Food, Fisheries and Aquaculture research), PO Box 210, N-1432 Ås, Norway                                                                                                                                        2Department of Animal and Aquacultural Sciences, Norwegian University of Life Sciences, N-1430 Ås, Norway                                                                                                                   afees.ajasa@nofima.no



Gill diseases pose a significant concern to the salmon industry; in Norway for instance, they are ranked among the leading causes of mortality in salmon farming. Genome-wide association studies (GWAS) can help to unravel the genetic architecture of susceptibility to gill diseases and help to guide mitigation efforts. Amoebic gill disease (AGD) is one of the major gill diseases affecting salmon. Furthermore, during a production cycle, fish gills get exposed to different kinds of pathogens which may cause lesions on the gills. In this study, we conducted a GWAS of AGD and gill lesions on two distantly related cohorts of Atlantic salmon: Norwegian and Canadian.

The Norwegian cohort consists of four (sub) populations that were gill-scored during outbreaks of AGD from 2016 to 2018, while the Canadian cohort consisted of six (sub) populations that were gill-scored at harvest from 2017 and 2018. The total number of fish in the Norwegian and Canadian cohorts is 8506 and 12823, respectively. All cohorts are from the breeding nucleus of Mowi Norway and Canada West and were all genotyped with 55K SNP chip. After quality control, 50456 SNPs remained for the Norwegian cohort, while 50144 SNPs remained for the Canadian cohort. GWAS was conducted with GCTA (--mlma option). In addition to the polygenic effect, the model for AGD had year as a fixed effect, while that for gill lesions had sex and cage nested within year as fixed effects. Genome-wide significance level was defined as 0.05/no of markers.

While only chromosome 12 was implicated in the risk of AGD (Figure 1), both chromosomes 2 and 12 were implicated in the risk of gill lesions (Figure 2), which suggests that chromosome 12 has a pleiotropic effect on AGD resistance and overall gill health. The proportion of genetic variance explained by the lead SNP associated with the risk of AGD was 7%, while the proportion of genetic variance explained by the lead SNP for risk of gill lesions on Chromosomes 2 and 12 is 3 and 10%, respectively.

Our results provide novel insight into the genetic architecture of AGD and overall gill health in Atlantic salmon.