Of course directional selection can achieve much in years. The house sparrow, Passer domesticus, arrived in British Columbia in 1900, and in the American South-West in 1904; by 1964 they had become much darker in the former region and much paler in the latter region, thus forming two distinct geographical races (the minimum time for which had been estimated in 1930 as 5000 years!). (Ford, 1973). In a study of the mice (Mus musculus) on the island of Skokholm, Berry and Jakobson found substantial changes in genetically controlled skeletal characters between 1957 and 1968. (Berry, 1990). In 1977, small groups of lizards were introduced to a Caribbean islet with no indigenous lizards. Ten years later natural selection had adapted their legs to suit the thin twigs of the islet’s vegetation. (Jones, 1999).
A very striking example of rapid directional selection since the Second World War has been selection for resistance to antibiotics, herbicides and pesticides. ‘The Murray Collection is a series of reference strains of harmful bacteria gathered between 1914 and 1950 … Every strain is … susceptible to every one of the dozens of antibiotics used today’. (Jones, 1999). Now ‘more than 50% of some species of clinical bacteria isolated in the Western world are resistant to some common antibiotics’, and in poor countries ‘up to 80% of the bacteria are resistant to drugs like ampicillin, trimethoprim and chloramphenicol’. (Amyes and Young, 1997). Vancomycin was considered the ‘antibiotic of last resort’ for the treatment of multiple drug-resistant Staphylococcus aureus, ‘and now the first case of fully vancomycin-resistant S. aureus has been reported’. (Coates, Hu, Bax and Page, 2002). ‘Multiple drug resistance in fungal pathogens of agricultural and clinical significance is extremely important’, and constitutes the ‘increasing threat posed by fungal pathogens of mammals and plants’. (Adams, 1997). ‘The first herbicide-resistant weed’ was discovered in 1968. ‘To date, at least 57 weed species … have evolved resistance to’ certain herbicides. (Townson, 1997).
‘In the past 50 years more than 500 arthropod species have become resistant to the toxic action of insecticides … The effort put into designing and synthesizing new pesticides cannot match the speed at which resistance develops within insect species.’ (Jowett, Huang and Murray, 1997). The resistance is sometimes controlled by major genes, and sometimes by polygenes. They are clearly selected and spread very rapidly. Between 1956 and 1963 the number of resistant species rose from 20 to 81. (Sheppard, 1975). In fact the evolution of complete resistance seems generally to take seven years. (Spielman and D’Antonio, 2002). However some resistance can be selected in two years. (Ford, 1975). Sheppard (1969) pointed out that first resistance is selected and spreads, then it is enhanced by polygenes which modify the action of the main controlling gene. We shall meet these modifiers in a different context in a later section.
Rats in several European countries and in the United States have become resistant to the anticoagulant rat-poison Warfarin. (Sheppard, 1975). Resistance is controlled by a single major gene. Warfarin was introduced in 1950, and the first resistant British rats (Rattus norwegicus) were reported in 1958. Round Welshpool resistance was found to spread at the rate of 4.6 kilometres per year, ‘similar to the rate at which the species colonizes new territory’. (Berry, 1990). However the number of resistant rats in a population never reaches anywhere near 100%. ‘For, in places where this pesticide is used, the homozygous resistants die of Vitamin K deficiency’ (needing twenty times as much of this Vitamin as the non-resistant rats – Sheppard, 1975) ‘while many of the non-resistant animals die of poisoning’. The fitness ratios of the non-resistants, the heterozygotes and the resistant homozygotes have been calculated as 0.7, 1.0 and 0.0. (Ford, 1975). We shall see more examples of this situation of heterozygote advantage in later sections.