Gene interaction, environment and hybrid vigour

Abstract

Abstract The manifestation of heterosis has been found mainly in characters which are the end-points of complex processes of growth and differentiation and controlled by many genes, such as weight, height, organ size or shape and rate of maturity. Even a character like the synthesis of a particular anthocyanin, which can be completely blocked by a single major gene, is no real exception, for the amount of synthesis is affected by a large number of interacting genes. Anthocyanin synthesis shows heterosis in Antirrhinum species hybrids (Dayton 1954). Again the bio­chemical models of heterosis in Neurospora are, in one example, the result of complementary effects of two dominant genes controlling amino-acid synthesis (Beadle & Coonradt 1944). The other example shows a heterotic effect of two alleles at one locus, one a sulphonamide-requiring mutant and the other its sup­pressor, but the effect is caused by a restoration of a delicate synthetic balance involving homocysteine, p-aminobenzoic acid and methionine (Emerson 1952). The two types of gene interaction generally postulated to explain heterosis— (1) complementary dominant genes which are non-allelomorphic and (2) over-dominance of alleles at the same locus—have different consequences in breeding behaviour, differences of great importance in a breeding program aimed at utilizing heterosis. But in terms of gene action there is, on the modern view, little if any difference between them. One criterion adopted in genetics which is useful in distinguishing two closely linked genes from alleles is that, when two hypomorphic genes together restore the wild phenotype—in other words show heterosis—then they are not allelomorphic but are closely linked genes in repulsion with complementary effects. On this basis a ‘single locus’ with an heterotic effect would be evidence not for over-dominance but for the compound structure of the locus, This complex locus would then be distinguished from two complementary dominant genes only in the strength of the linkage between its components. Thus even if we accept the evidence for ‘single-locus’ heterosis (cf. Schuler 1954), there is, as yet, nothing to contradict and much to support complementary dominant genes as the main cause.