Height in humans is often cited as the classical complex trait under possible buy Mitoxantrone selection of unknown. In both horses and dogs, selection has been strong and sustained, and breed populations tend to be small.Interestingly, and in line with our experiment, the major allele at the IGF locus stems from a standing genetic variant, despite many factors that may theoretically favor largeeffect de novo mutations. In chickens, modern breeding practice and selection from large populations yielded a purchase Mitoxantrone highly polygenic genetic architecture for body weight, with some of the best empirical evidence for epistasis. But unlike these previous QTL studies or selection experiments, in which either the genetic architecture of a trait or the selection value were estimated separately, sometimes from only few parental individuals or lines, ER studies sample a much broader pool of alleles and continually compete them against each other.Thus, our approach allowed simultaneous inference of genetic architecture and distribution of effect sizes, is more likely to be representative of the population at large, and is more akin to genomewide association studies, except that here we can also directly connect a trait to its selective value and capture the trajectory of any given allele.Parallel evolution is often seen as a hallmark for detecting selection. This underscores that parallelism depends on both shared selection pressure and the availability of largeeffect loci that confer a substantial selection advantage. With increasing population size, selection would be better able to detect variants with more subtle effects.To our surprise, the same loss of NKX function in human SMMD patients manifests in opposite ways in different bone types as short trunk and long limbs enhancers. For example, it remains unclear how such a major allele could segregate in the general mouse stock. It could be that this allele has the same effect in the general mouse population but is conditionally neutral under nonselective breeding and simply escaped notice.Further work should focus on dissecting the mechanisms behind the dynamics of selective sweeps andor polygenic adaptation by resequencing the entire selection pedigree, testing how the selection response depends on the genetic architecture, and the extent to which linkage places a fundamental limit on our inference of selection.Five outlier individuals with a skeletal dysplasia of unknown etiology were removed from LS and excluded from further analysis.Missing data in LS were filled in with random individuals that best matched the pedigree.Trait data were analyzed to determine response to selection based on the measured traits and their rank orders based on the selection index.Each chromosome was represented by a set of junctions, which recorded the boundaries between genomes originating from different founder genomes; at the end, the SNP genotype was reconstructed by seeding each block of genome with the appropriate ancestral haplotype.This procedure is much more efficient than following each of the very large number of SNP markers.Crossovers were uniformly distributed, at a rate equal to the map length; a component determined by the sum of effects of evenly spaced discrete loci. The two genetic components had variance proportional to the corresponding map length, and the heritability was estimated from the observed trait values.