Exploring the mechanistic bases of heterosis from the perspective of macromolecular complexes.

Heterosis is defined as greater biomass, fertility or other traits in heterozygotes, polyploids or hybrids compared to their genetically divergent (often homozygous) parents. Heterosis was noticed by various civilizations and scientifically reported by Darwin himself. Despite the importance of heterosis, its molecular bases are still enigmatic. Several genetic models have been proposed but fail to give mechanistic insights. Here we show how dominant negative interactions might give rise to heterotic responses. We also explore a biochemical model of gene dosage effects in macromolecular complexes in a similar context. With the help of heuristic examples and computer simulations we find that heterotic individuals display higher allelic diversity and smaller average multimer concentrations than nonheterotic ones. As intuitively expected, the existence of heterosis involving multimeric complexes arises when the inbred parents have on average smaller genetic values than the maximum possible. Despite its simplicity, the dosage model accounts for the puzzling phenomenon of "progressive heterosis" in which polyploids with increasing genetic diversity exhibit progressively greater heterosis.