The genetical control of heterosis is usually explained in terms of additive/dominance gene action and digenic interaction of segregating loci, and the contribution of epistasis categorized either as duplicate or complementary following the classical relationships observed among the Mendelian genes. In this paper we have explored the alternative relationships between the additive/ dominance/epistatic components for obtaining classical ratios and investigated their role in promoting heterosis. The study has shown that while the classical duplicate and complementary relationships supress heterosis, other relationships not only boost its magnitude but also allow more or less unrestricted expression of genotypic variation in the F, generation. Removal of another important restriction of no interaction between the segregating loci and the background genotype further revealed that heterosis is boosted in the presence of such interactions. However, these interactions do not affect the genetical interpretation of heterosis because their contribution is maximized only when the parental lines display dispersion of alleles at the segregating loci and dominance is unidirectional.
