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FISHER'S theory of the evolution of dominance is based on the fact that heterozygotes for rare deleterious alleles, maintained by recurrent mutation from the wild-type allele at the locus, greatly outnumber homozygotes in a random-mating population at equilibrium1. The fitness of a heterozygote carrying a mutant and the wild-type allele can be written as 1 − hs (1 ⩾ h ⩾ 0), compared with fitnesses of 1 and 1 − s for wild-type and mutant homozygotes respectively. Fisher postulated that mutant alleles were originally semidominant, so that h > 0. He explained the fact that most mutations are observed to be recessive or nearly recessive to wild type as the result of selection for modifier genes which increase the fitness of the heterozygotes alone. He pointed out that selection to improve the fitness of the mutant homozygotes is likely to be relatively ineffective because of their rarity compared with the heterozygotes, and also because the presence of the wild-type allele in heterozygotes renders them more amenable to selection towards the wild type. Using this theory, the level of dominance of the mutant alleles, h, is gradually reduced towards zero, while s remains constant. Wright2 criticised this because the heterozygotes for mutant alleles are so rare that the intensity of selection on a gene which modifies h is of the same order as the rate of mutation, u, to deleterious alleles at the locus undergoing dominance modification. He suggested that such a weak selection pressure is unlikely to overcome the effects of random genetic drift, or the selective consequences of pleiotropic effects of the dominance modifier. Later theoretical work3,4 has confirmed Wright's conclusion about the intensity of selection on dominance modifiers, so that many geneticists have come to doubt the validity of Fisher's theory3. The principle of dominance modification when applied to balanced polymorphisms (for example, Batesian mimicry5) is not, of course, subject to this objection and is generally accepted. Fisher1, however, believed that the recessivity of mutant genes demonstrated the ability of even a minute selection pressure to cause significant evolutionary change. The issue cannot be settled by purely theoretical considerations, and it is evident that some empirical evidence capable of providing a critical test is required. (Demonstrations that dominance can be modified by artificial selection6,7, although of great interest, are not relevant to the question of the efficacy of selection pressures as small as those postulated in Fisher's theory.) This paper points out recent experimental evidence on the heterozygous effects of mutations affecting viability in Drosophila8 that seems to be inconsistent with Fisher's theory, and also looks at two alternative theories proposed by Haldane9.

The neo-Darwinian synthesis that resulted from the integration of Mendelian genetics into evolutionary theory has dominated evolutionary biology for the last 30 to 40 years, due largely to its agreement with a huge body of experimental and observational data. The classic works representative of this school of thought come from the fields of genetics (Fisher, 1930; Wright, 1931; Haldane, 1932; Dobzhansky, 1937; Muller, 1940), development (de Beer, 1940), zoology, (Huxley, 1942; Mayr, 1942; Rensch, 1959), botany (Stebbins, 1950), and paleontology (Simpson, 1944, 1953). These authors broadly agree with Darwin's view that most important evolutionary changes at the level of the visible phenotype, as revealed by paleontological and systematic studies, have resulted from natural selection acting on variation within populations. This variation is ultimately due to mutations that arise at random with respect to the direction of selection. A role for evolutionary forces other than selection and mutation, such as random genetic drift, is of course recognized by neo-Darwinists, but selection is regarded as the main guiding force of phenotypic evolution. Within this general framework, there has been plenty of room for vigorous disagreements about the relative importance of different processes, such as the Wright-Fisher debate on the significance of random genetic drift. Recently, however, certain elements of neo-Darwinism have been sharply challenged by advocates of the "punctuated equilibria" theory of evolution (Eldredge and Gould, 1972; Gould, 1977, 1980; Stanley, 1975, 1979; Gould and Eldredge, 1977). Indeed, Gould (1980) states

The genetic structure of populations , The genetic structure of populations , مرکز فناوری اطلاعات و اطلاع رسانی کشاورزی

In a recent paper in Current Biology, Nozaki et al. [1] report evidence that males of the anisogamous Volvocine alga, Plerodina starri, have an active copy of a gene PsPlesMID, which is similar in sequence to the CrMID gene of the green alga Chlamydomonas reinhardtii. In C. reinhardtii, there is no size difference between male and female gametes — it is isogamous — but gametes are divided into two mating types (MT+ and MT−), controlled by a complex genetic locus mt, such that zygotes can only be formed by fusions of gametes with different mating types [2,3].