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 underlying 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 genes involved in the
host's response to chronic parasite insult makes it particularly
difficult to understand the mechanisms of host life history trade-offs and
the adaptive dynamics involved. Here, we examine the genetic basis of
gastrointestinal nematode (Trichostrongylus tenuis) burden in 695 red
grouse (Lagopus lagopus scotica) individuals genotyped at 384 genome-wide
SNPs. We first use genome-wide association to identify individual SNPs
associated with nematode burden. We then partition genome-wide
heritability to identify chromosomes with greater heritability than
expected from gene content, due to harbouring a multitude of additive SNPs
with individually undetectable effects. We identified five SNPs on five
chromosomes that accounted for differences of up to 556 worms per bird,
but together explained at best 4.9% of the phenotypic variance. These SNPs
were closely linked to genes representing a range of physiological
processes including the immune system, protein degradation and energy
metabolism. Genome partitioning indicated genome-wide heritability of up
to 29% and three chromosomes with excess heritability of up to 4.3% (total
8.9%). These results implicate SNPs and novel genomic regions underlying
nematode burden in this system and suggest that this phenotype is
somewhere between being based on few large-effect genes (oligogenic) and
based on a large number of genes with small individual but large combined
effects (polygenic).