Data from: Genome-wide association and genome partitioning reveal novel genomic regions underlying variation in gastrointestinal nematode burden in a wild bird

Identifying the genetic architecture of complex phenotypes is a notoriously difficult problem that often impedes progress in understanding adaptive eco-evolutionary processes in natural populations. Host-parasite interactions are fundamentally important drivers of evolutionary processes, but a lack of understanding of the broad genetic basis has made it particularly difficult to understand the mechanisms of host life-history trade-offs and adaptive dynamics involved. Here we examine the genetic basis of gastrointestinal nematode burden (Trichostrongylus tenuis) in 695 red grouse (Lagopus lagopus scotica) individuals genotyped at 384 genome-wide SNPs. We use genome-wide association and genome partitioning to identify individual SNPs of large effect and chromosomes that explain more phenotypic variation than expected from their gene content and thus harbour multiple interacting SNPs with individually undetectable effects. Genome-wide association identified five SNPs on five chromosomes that accounted for differences of up to 499 worms per bird but together explain only 4.9 % of the phenotypic variance. These SNPs are linked to genes representing a range of physiological categories including the immune system, xenobiotic protein detoxification and energy metabolism. Genome partitioning suggested that three chromosomes may harbour a multitude of additional genes of minute individual but large combined effect, accounting for 17.8 % of the phenotypic variance. These results highlight novel genes underlying nematode burden in this system and suggest that this phenotype is somewhere between being a purely oligogenic phenotype based on few large-effect genes and a purely polygenic phenotype based on an infinitesimal number of genes with individually minute but large combined effects.