--Donald S. Robertson
It has been suggested that many quantitative trait loci (QTLs) may be wild type alleles of loci for which qualitative mutants involving quantitative traits have been found--e.g., dwarfs (plant height), defective kernels (seed size), etc. (MNL 58:10, 1984; J. Theor. Biol. 117:1, 1985). This hypothesis suggested that quantitative patterns of inheritance occurred because there were slight differences in the efficiency of gene products as a result of the molecular polymorphism found in wild type alleles. Such slightly different alleles, all of which produce basically the same, but nonetheless slightly different phenotypes, are called isoalleles. The effect of such isoalleles has been shown by Hageman et al. (Adv. Agron. 19:45, 1967) to be primarily additive. An additive model will explain the classical quantitative inheritance pattern (see Figure 1). Such a simple model, however, does not explain heterosis.
Results expected in the F1 and F2 populations:
1. The F1 population would show very narrow variation around a value of 1150.
2. The F2 population would show the typical bell-shaped curve for the distribution of phenotypes in the F2 populations. The extreme values of this curve would approach those of the parents.
Figure 3. The biochemical pathway model of quantitative inheritance and heterosis: an example.
The effect of gene products from isoalleles does not have to be completely additive. The model will still work even if dominance is found for some loci.
Recent results reported in Science (Stewart et al., Science 241:1216, 1988) support The Biochemical Pathway Model. These workers demonstrated that the level of gibberellin production was low in the four inbreds tested and, as expected, the inbreds were shorter than hybrids. In addition, the inbreds showed significant growth response to exogenously applied gibberellin. Most of the hybrids between these inbreds, on the other hand, were taller than either parent (heterosis) and showed very little if any response to exogenously applied gibberellin. B. O. Phinney has shown that some dwarf mutants block steps in the gibberellin biosynthetic pathway (Plant Growth Substances, Springer-Verlag, p. 55, 1985). Thus the wild type alleles at these dwarf loci produce enzymes regulating steps in this pathway. It is obvious that in the inbreds studied by Stewart et al., the gibberellin pathway was not functioning to its full potential. Otherwise, the inbreds would not respond to exogenously applied gibberellin. This low gibberellin production could be the result of wild type isoalleles in the inbreds at one or more steps that produce low efficiency gene products that limit the total amount of gibberellin produced. Most hybrids had complementing isoalleles that would allow full or near full production of gibberellin (as suggested by the model). In such a situation, exogenously applied gibberellin has little effect. One hybrid did not show a heterotic response as measured by gibberellin production in seedlings. This hybrid had a correspondingly greater response to exogenously applied gibberellin than the other hybrids tested. Again, this is a result predicted by the model for inbreds with poor combining ability for plant height. Such inbreds have isoalleles responsible for enzymes with low efficiencies for the same step(s) in the gibberellin biosynthetic pathway.
This model is not proposed as the sole explanation for heterosis. There
is undoubtedly more than one mechanism responsible for this complex phenomenon.
Enhanced biosynthesis due to enzymatic polymorphism, as proposed by Schwartz
and Laughner (Science 166:626, 1969), also could be responsible for a portion
of the heterotic response, along with other, as yet, undiscovered mechanisms.
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