The Powers of Natural Selection

‘Darwin … believed … that even minor evolutionary changes take place too slowly for’ their observation in detail to be practicable. ‘The science of ecological genetics … has demonstrated that selection for advantageous qualities is far more powerful than Darwin and his immediate successors had thought, and consequently that evolutionary adaptations take place far more rapidly than they had conceived possible. Even in 1930 R.A. Fisher, a great authority on the subject, suggested that a one per cent selective advantage represents an approximate upper limit in natural conditions, and he was criticised for putting it too high. Today we know that 20 or 30 per cent, and often much greater values, are common and usual.’ (Ford, 1973, cf. also Ford, 1959)

These are the words of E.B. Ford, the greatest geneticist since Johann Mendel (named Gregor in religion, Russell, 1976), and the greatest lecturer I have ever heard – as an ex-soldier undergraduate, I was privileged to hear his enthralling lectures in 1945-8. We owe these discoveries about the power and speed of natural selection in large part to Ford himself, his brilliant followers Kettlewell and Sheppard, and his great colleague Sir Ronald Fisher, who ‘occupies, in the biological sciences of the 20th century, a central position rather like that of Einstein in physics’ (Russell, 1976), through his contributions to statistics, scientific method and cybernetics. Reading recent publications, I have realised that these great discoveries, made in the mid-20th century, have been largely lost sight of. I therefore believe a reminder of them would be timely, especially for eugenicists, who should have a deep understanding of the working of natural selection. Hence this series of articles.

The relative neglect of these discoveries is, I think, due to the preoccupation of contemporary biologists with the truly sensational recent developments in the biochemistry of genetics. In 1943, Oswald Avery discovered the function of DNA (deoxyribonucleic acid), and in 1952 Rosalind Franklin discovered its structure (Maddox, 2002). These discoveries have led to the rapid development of biotechnology, genetic engineering, genomics and proteomics. These new developments have thrown interesting light on some fine details of genetics and evolution (Wills, 1991). But they do not in any way invalidate the facts I shall be discussing, and in population genetics, the field of these facts, it is still perfectly appropriate to use the terms and concepts of classical genetics. I can briefly remind readers of these as follows (Russell, 1959, Sheppard, 1975).

The complement of chromosomes in an animal or plant cell ‘is in fact made up of two sets, one originally derived from the organism’s father, the other from its mother’ taking the form of ‘a series of homologous pairs; each pair consists of one chromosome from each parental set. The genes are arranged linearly along the chromosomes, and each position on a chromosome is called a locus … As a result of mutation’ (faulty replication) ‘a given gene may take a number of different forms, called alleles. But only two of these can be represented at a given locus, one on each of the homologous chromosomes. If two alleles at a given locus are identical, the organism is said to be homozygous for the corresponding gene, if two alleles at a given locus are different, it is said to be heterozygous.’ (Russell, 1959) During sexual reproduction, the chromosomes of each pair are distributed independently to the paternal or maternal gamete (sperm or ovum), which only gets one set. Hence new genetical combinations are produced in each generation. Crossing over, in which pieces of a chromosome are interchanged between the members of a pair, permits further recombination of alleles. Chromosomal mutations also occur through imperfect replication of whole chromosomes. The one of these I need notice here is inversion, in which a stretch of chromosome is broken off and replaced the reverse way round: within such an inversion crossing over rarely occurs. Genes on one chromosome, normally transmitted together, are said to be linked. Those within an inversion are especially tightly linked.

The complete set of alleles carried by an individual animal is called its genotype. The complete set of characters constituting the actual animal is called its phenotype. The phenotype is the joint product of the genotype and the developmental environment. The relative contribution of these two factors to a given phenotypic character can be measured, giving a measure called heritability, with values from 0 to 1. The phenotype and the immediate environment combine to produce what Burch and I called the dramatype, ‘the pattern of performance in a single physiological response’ (Russell and Burch, 1959).

A distinction can be made between major genes, which determine characters with discontinuous differences, such as eye colour, and groups of polygenes, usually linked, which additively combine the small effects of each to determine the value of continuous characters, such as height. Sometimes several major genes, whose co-operation is important, are very closely linked to constitute a supergene: Kettlewell found such a supergene, made up of three genes, whose co-operating alleles can produce melanism (darkening), which, as I shall discuss later can be advantageous in industrial districts, in the moth Lasiocampa quercus. (Ford, 1976) The genotype of an individual is sometimes called the gene complex, to emphasise the fact that an adaptive set of alleles interact to produce a balanced and coherent system. All the alleles present in a population, together with their relative frequencies, make up what is called the gene pool. (Sheppard, 1975)