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One way to capture this information is by constructing a Polygenic Risk Score.
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For this reason, when constructing a polygenic score, RSR is often used in combination with a heuristic procedure, known as linkage disequilibrium pruning, which selects SNPs that are not too strongly correlated.
Correlation between expression of a useful trait and a linked molecular marker could be used to construct a genetic linkage map by placing many monogenic and polygenic traits within specific regions of the plant genome (Mondini et al. 2010).
To this end, we construct a meta-model by taking a linear combination of the two predictors, namely the predicted value from the optimal penalized regression model and the GWAMA-based polygenic score (see Materials and Methods).
Additional polygenic genes in the region surrounding the knockout construct, a locus on chromosome 1 known to be a hotspot for genes implicated in SLE, also contribute to the development of disease.
The traits were generated by summing a polygenic effect and a random effect.
The remaining familial risk is likely to be explained by a polygenic model where breast cancer susceptibility is conferred by a large number of low-penetrance alleles.
Therefore, a disorder dominated by a polygenic model will be one in which several common variants of modest effect contribute to risk for disease in each affected individual.
Body shape was also shown to be under polygenic control and genotypic parallelism appears to be present in three of the five lakes as revealed by a polygenic analytical approach.
We construct the polygenic score for each individual by adding the number of reference alleles he or she carries at the selected SNPs, pre-multiplied by the corresponding SNP effect sizes reported in the GWAMA article.
A polygenic score is constructed by adding up the individual alleles that are reliably related to this trait, where each allele is weighted by effect sizes estimated from a GWAS (Dudbridge 2013).
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