Natural and artificial selection

In 1858, Charles Darwin and Alfred Russel Wallace jointly proposed the mechanism of evolution by natural selection. Darwin developed the idea over twenty years following his voyage on HMS Beagle (1831–36); Wallace independently reached the same conclusion while collecting in the Malay Archipelago. The full publication, On the Origin of Species, followed in 1859.

The mechanism has four observations and one inference:

Observation 1 — Variation exists. Individuals within a population show heritable variation in their phenotypes. Differences arise from mutation (creating new alleles), meiosis (crossing over + independent assortment) and random fertilisation (shuffling alleles into new combinations).

Observation 2 — Overproduction of offspring. Organisms produce more offspring than the environment can support. Resources (food, water, shelter, mates) are limited; not every offspring can survive to reproductive age.

Observation 3 — Competition. Because more offspring are produced than can be supported, individuals compete for resources — both within the species (intraspecific) and between species (interspecific). This is the 'struggle for existence' Darwin emphasised.

Observation 4 — Selection pressure. Environmental factors — predators, disease, climate, food availability — act as selection pressures. Individuals with phenotypes better matched to the environment are more likely to survive to reproductive age and to reproduce successfully.

Inference: differential reproduction and allele frequency change. Survivors reproduce and pass on their advantageous alleles to the next generation. Less well-adapted individuals leave fewer offspring (or none). Over many generations, the proportion of the population carrying the advantageous alleles rises, and the population becomes increasingly adapted to its environment.

If the change is great enough — and the population is reproductively isolated — a new species can eventually arise (see Evolution subtopic 17.3).

Key insight. Natural selection is not Lamarck's inheritance of acquired characteristics. Individuals do not 'adapt' or 'change' during their lifetime in response to the environment. Instead, alleles already present (by random mutation) are selected by the environment. The variation is generated first; selection acts on it afterwards.

Natural selection takes three different forms depending on which phenotypes are favoured.

1. Stabilising selection. Favours the mean (modal) phenotype and selects against both extremes. Reduces variation but the mean stays the same. Common in stable environments where the population is already well adapted — the optimum is already at the mean.

Distribution effect: the bell curve becomes taller and narrower but stays centred on the same mean.

Example: human birth weight. Babies of very low birth weight (< ~2.5 kg) are at higher risk of hypothermia, infection and developmental delays. Babies of very high birth weight (> ~4.5 kg) face complications of delivery and a higher risk of metabolic disorders. Infant mortality is lowest at around 3.0–3.5 kg. Selection therefore acts against both extremes, keeping mean birth weight stable over generations.

2. Directional selection. Favours one extreme of the phenotype at the expense of the mean and the other extreme. The mean shifts towards the favoured extreme. Common when the environment changes or a new selection pressure is introduced (e.g. industrial pollution, antibiotic, pesticide).

Distribution effect: the bell curve shifts to one side; the previous extreme becomes the new mean.

Examples:

• Peppered moth in industrial Britain — see next section.
• Antibiotic resistance in bacteria — see later section.
• Pesticide resistance in insects — DDT-resistant Anopheles mosquitoes.
• Beak size in Darwin's medium ground finch (Geospiza fortis) during the 1977 drought — only the largest-beaked birds could crack remaining hard seeds, so mean beak size rose in the next generation (Grant & Grant studies).

3. Disruptive selection. Favours both extremes at the expense of the mean. Can split a population into two distinct subgroups and, if reinforced by reproductive isolation, contribute to sympatric speciation.

Distribution effect: the bell curve becomes bimodal (two peaks).

Example: African seed-cracker finch (Pyrenestes ostrinus). Small-beaked birds eat soft seeds efficiently; large-beaked birds crack hard seeds. Medium-beaked birds are inefficient at both and starve, so the population splits into small-beaked and large-beaked morphs.

The peppered moth (Biston betularia) is the most famous textbook example of natural selection observed in human history.

The polymorphism. Two forms exist, controlled by alleles at a single gene: the light typica form (mottled grey-white) and the dark melanic carbonaria form. The dark allele arose by random mutation and was rare (<2% of moths) before the Industrial Revolution.

Pre-industrial Britain. Tree trunks were covered in pale lichens. The light typica form was camouflaged against this background; the dark carbonaria form was conspicuous. Birds (mainly tits and robins — the selection pressure) preferentially picked off dark moths. The light allele was therefore at very high frequency.

Industrial Britain (1850–1950). Soot from coal-burning factories killed lichens and blackened tree trunks. The environment changed, and the selection pressure reversed: now the dark moths were camouflaged against soot-blackened trunks, while the light moths were conspicuous and eaten by birds.

Bernard Kettlewell's mark-release-recapture experiments in the 1950s confirmed the predation hypothesis: he released equal numbers of light and dark moths in polluted and unpolluted woods, and recaptured a higher fraction of the matching-camouflaged form in each.

Within ~50 generations (one per year), the frequency of the dark allele rose from ~1–2% to over 90% in industrial regions such as Manchester and Sheffield. This is directional selection — the population mean shifted from light to dark.

Post-Clean Air Acts. The 1956 Clean Air Act, and subsequent legislation, dramatically reduced soot emissions. Lichens returned, tree trunks lightened, and the selection pressure reversed yet again. The frequency of the dark form has fallen back to <10% in most of the UK by 2000. This reversibility is exceptionally powerful evidence: when the environment returns to its earlier state, the population evolves back.

Why this is a textbook case. It demonstrates:

• Variation pre-exists (the dark allele was present before pollution).
• The environment selects, not 'guides' the mutation.
• Selection is measurable within human generations.
• The same population shifts in opposite directions when the environment changes.
• The mechanism is Darwinian — no Lamarckian 'response' is needed.

The peppered moth therefore neatly illustrates directional natural selection on a heritable trait under a quantifiable selection pressure.

Artificial selection (selective breeding) operates by the same principles as natural selection — heritable variation + differential reproduction — but the selecting agent is human, not the environment. Humans choose which individuals breed, based on traits useful to people.

General method.

1. Select individuals with desired phenotypes from the existing population (e.g. cows with the highest milk yield, wheat plants with the largest grain).
2. Cross-breed them to produce the next generation.
3. From the offspring, again select those with the best desired phenotype.
4. Repeat over many generations — gradually the population becomes enriched for the desired alleles.

Example 1 — Dairy cattle (Holstein-Friesian). Selective breeding for high milk yield, often combined with artificial insemination from prize bulls, has more than tripled the milk yield of the average dairy cow: from ~3,000 L per lactation in 1960 to over 10,000 L today. Modern dairy cows have been bred for udder shape, milk-protein content, mastitis resistance and feed conversion efficiency.

Example 2 — Wheat (Triticum aestivum). Wheat varieties are selectively bred for high grain yield, short stems (less prone to lodging in storms — the 'Green Revolution' dwarf varieties of Norman Borlaug, 1960s), disease resistance (rust-resistant alleles introgressed from wild relatives) and environmental tolerance (drought, salinity). Modern wheat yields are 3–5× the pre-1960 levels.

Example 3 — Dogs. Approximately 200+ breeds of domestic dog have been derived from the grey wolf in around 15,000 years — extraordinary genetic divergence for such a short timescale. Border collies were selected for herding behaviour; greyhounds for sprint speed; pugs for facial appearance; retrievers for soft-mouthed carrying. Dogs are a vivid demonstration of how much phenotypic change selective breeding can produce.

Disadvantages of artificial selection.

1. Loss of genetic diversity. Repeated selection narrows the gene pool because only a small subset of breeding individuals contribute to each generation. Once-common alleles can be lost permanently.

2. Inbreeding depression. To 'fix' desired traits, breeders often mate closely related individuals (siblings, parent-offspring). This increases homozygosity — including for harmful recessive alleles that are usually masked in heterozygotes. Symptoms include reduced fertility, lowered disease resistance, increased frequency of genetic disorders, and reduced vigour. Pure-bred dogs are notorious examples: dalmatians and deafness, German shepherds and hip dysplasia, pugs and breathing problems.

3. Vulnerability to disease. Genetically uniform crops can be devastated by a single new pathogen — illustrated by the Irish potato famine (1845–52, Phytophthora infestans on uniform potato variety) and the 1970 southern corn leaf blight in the US (uniform maize cultivars).

4. Loss of ancestral traits. Selectively bred organisms often cannot survive in the wild. Broiler chickens cannot walk well; dairy cows produce more milk than their calves can drink; many dog breeds cannot give birth without veterinary intervention.

Compare with natural selection. Both rely on heritable variation and differential reproduction, but they differ in who selects (humans vs environment), the traits favoured (human-useful vs wild-fit), the speed (often faster vs typically slower) and the effect on diversity (generally reduces vs generally maintains).

Antibiotic resistance in bacteria is the clearest modern demonstration of directional natural selection operating on a human timescale.

The mechanism — step by step.

1. Pre-existing variation by random mutation. Within a large bacterial population, a small number of cells already carry an allele for resistance that arose by spontaneous random mutation (mutation rates ~$10^{-9}$ per base per replication, but with $10^{10}+$ bacteria in an infection, resistant cells are essentially guaranteed). Crucially, the mutation occurs before the antibiotic is applied. The antibiotic does not cause mutation — it selects pre-existing variants.

2. Mechanisms of resistance. Different mutations confer resistance by different means:

• Enzyme inactivation — e.g. β-lactamase hydrolyses the β-lactam ring of penicillin, destroying the antibiotic before it can act.
• Modified target protein — methicillin-resistant Staphylococcus aureus (MRSA) produces an altered penicillin-binding protein (PBP2a) to which methicillin cannot bind effectively.
• Efflux pumps — membrane proteins that actively expel the antibiotic from the cell.
• Reduced uptake — modifications to porins that prevent the antibiotic entering the cell.

3. Antibiotic acts as a strong selection pressure. When the antibiotic is administered, susceptible cells are killed but resistant cells survive.

4. Differential reproduction. Bacteria divide every 20–30 minutes. A single resistant cell can produce billions of descendants within a day, all carrying the resistance allele. Within a generation or two, the population is dominated by resistant cells.

5. Horizontal gene transfer. Bacteria can also acquire resistance from other bacteria — even from different species — via three mechanisms:

• Conjugation: direct cell-to-cell transfer of resistance plasmids (R-plasmids) through a pilus.
• Transduction: transfer by bacteriophages that pick up bacterial DNA and inject it into a new host.
• Transformation: uptake of free DNA released by dead bacteria.

This makes resistance spread far faster than vertical inheritance alone could achieve, and explains how resistance alleles can leap between gut bacteria and pathogens, or between species in different hosts.

6. Human factors that accelerate selection.

• Incomplete antibiotic courses — partially resistant cells survive and acquire further mutations.
• Over-prescription for viral infections (against which antibiotics are useless).
• Prophylactic use in livestock farming (low-dose antibiotics in feed) — vast bacterial populations exposed.
• Hospital settings — high antibiotic use selects for multi-drug-resistant strains; close contact spreads them.

Outcome — public health crisis. Multi-drug-resistant strains now include MRSA, VRE (vancomycin-resistant enterococci), XDR-TB (extensively drug-resistant Mycobacterium tuberculosis) and carbapenem-resistant Enterobacteriaceae. The WHO classifies antibiotic resistance as one of the top global health threats of the 21st century, with an estimated 10 million deaths per year by 2050 if unchecked.

Why this matters for the syllabus. Antibiotic resistance is a textbook example of directional natural selection because:

• Variation pre-exists (mutation).
• A defined selection pressure is applied (the antibiotic).
• Differential survival is dramatic (resistant survive; susceptible die).
• Allele frequency change is rapid and measurable.
• It is happening now, observable in real hospitals.