  For many traits, including susceptibility to common diseases in humans,
causal loci uncovered by genetic mapping studies explain only a minority of the
heritable contribution to trait variation. Multiple explanations for this
"missing heritability" have been proposed. Here we use a large cross between
two yeast strains to accurately estimate different sources of heritable
variation for 46 quantitative traits and to detect underlying loci with high
statistical power. We find that the detected loci explain nearly the entire
additive contribution to heritable variation for the traits studied. We also
show that the contribution to heritability of gene-gene interactions varies
among traits, from near zero to 50%. Detected two-locus interactions explain
only a minority of this contribution. These results substantially advance our
understanding of the missing heritability problem and have important
implications for future studies of complex and quantitative traits.
