|Title||Using whole-genome sequence data to predict quantitative trait phenotypes in Drosophila melanogaster.|
|Publication Type||Journal Article|
|Year of Publication||2012|
|Authors||Ober, U, Ayroles, JF, Stone, EA, Richards, S, Zhu, D, Gibbs, RA, Stricker, C, Gianola, D, Schlather, M, Mackay, TFC, Simianer, H|
|Keywords||Animals, Bayes Theorem, Chromosome Mapping, Drosophila melanogaster, Genetics, Population, Genome, Insect, Genotype, Linkage Disequilibrium, Models, Genetic, Models, Theoretical, Phenotype, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Selection, Genetic, Sequence Analysis, DNA|
Predicting organismal phenotypes from genotype data is important for plant and animal breeding, medicine, and evolutionary biology. Genomic-based phenotype prediction has been applied for single-nucleotide polymorphism (SNP) genotyping platforms, but not using complete genome sequences. Here, we report genomic prediction for starvation stress resistance and startle response in Drosophila melanogaster, using ∼2.5 million SNPs determined by sequencing the Drosophila Genetic Reference Panel population of inbred lines. We constructed a genomic relationship matrix from the SNP data and used it in a genomic best linear unbiased prediction (GBLUP) model. We assessed predictive ability as the correlation between predicted genetic values and observed phenotypes by cross-validation, and found a predictive ability of 0.239±0.008 (0.230±0.012) for starvation resistance (startle response). The predictive ability of BayesB, a Bayesian method with internal SNP selection, was not greater than GBLUP. Selection of the 5% SNPs with either the highest absolute effect or variance explained did not improve predictive ability. Predictive ability decreased only when fewer than 150,000 SNPs were used to construct the genomic relationship matrix. We hypothesize that predictive power in this population stems from the SNP-based modeling of the subtle relationship structure caused by long-range linkage disequilibrium and not from population structure or SNPs in linkage disequilibrium with causal variants. We discuss the implications of these results for genomic prediction in other organisms.
|Alternate Journal||PLoS Genet.|