17.2 Natural and Artificial Selection

Natural selection is a population process: inherited variation exists, environmental selection pressures affect survival and reproductive success unequally, and advantageous heritable alleles can become more frequent over generations.

• A population produces more offspring than can usually survive because resources and other conditions are limited.
• Individuals with different heritable phenotypes experience a selection pressure differently; those with a favourable phenotype are more likely to survive to reproduce.
• Their offspring inherit some of the associated alleles, so the frequency of advantageous alleles increases across generations while other alleles may decrease.

Fitness means reproductive success in a particular environment, not strength or perfection. A change in the environment can alter which phenotype is favoured, and selection does not guarantee that every well-adapted individual survives.

Individuals do not change their alleles because they need to adapt. Selection acts on existing phenotypic variation; the measurable evolutionary change is a shift in allele frequencies in a population over generations. This card does not classify selection types, use antibiotic resistance, or apply Hardy–Weinberg equations.

Selection patterns describe which phenotype values are favoured or selected against in an environment. Stabilising selection favours the intermediate phenotype, directional selection favours one extreme, and disruptive selection favours both extremes over the intermediate.

• Stabilising: both extremes are selected against, so intermediate phenotypes have the greatest survival or reproductive success; the distribution becomes narrower around a similar mean.
• Directional: one extreme is favoured, usually after a change in the environment or selection pressure; the population distribution shifts towards that extreme and the mean changes.
• Disruptive: both extremes are favoured while intermediate phenotypes are selected against; the distribution separates towards two peaks and intermediate values become less common.

To identify the pattern, compare the phenotype distribution before and after selection, locate the values with the greatest reproductive success, and ask which values the environmental pressure removes or favours. The graph shape is evidence for the pattern; it is not a complete explanation of the underlying genetic architecture.

“Favoured” means better suited to that particular environment, not universally better. A selection label describes the outcome for phenotype values; it does not by itself prove that the trait is genetic, calculate a test statistic, or identify a fixed outcome when the environment changes.

Allele frequencies can change across generations through non-random selection or through chance. Natural selection changes frequencies when a heritable phenotype gives some individuals greater survival or reproductive success in a particular environment; genetic drift changes frequencies by random sampling, especially when the population is small.

• Natural selection: an environmental pressure consistently favours some heritable phenotypes over others, so the associated alleles tend to increase or decrease directionally across generations. The direction depends on which phenotype is advantageous in that environment.
• Genetic drift: chance differences in which individuals survive or reproduce change allele frequencies, without the change needing to favour a phenotype. The effect is stronger in small populations, where random sampling is a larger fraction of the population.
• Founder effect: a special small-population event in which a few individuals start a new population. Their allele frequencies may differ from the source population simply by chance, so the new population can show reduced variation or unusual allele frequencies.
• Bottleneck: a sharp reduction in population size leaves a small, chance sample of the original alleles. Frequencies can then differ from the original population, and the remaining variation may be reduced.

To interpret a change, ask three questions: (1) did an environmental pressure consistently favour a heritable phenotype, suggesting natural selection; (2) was there a small-population or sampling event, suggesting drift; and (3) did a few colonising individuals or a population reduction define the event, suggesting founder effect or bottleneck? Compare allele frequencies before and after the event, but do not infer a cause from the direction of change alone.

Natural selection is non-random with respect to the environmental pressure, whereas drift is random with respect to which alleles are sampled. Drift is not the same as an allele being useful, and a founder effect is not a purposeful adaptation. These mechanisms can be discussed without Hardy–Weinberg calculations or a specific antibiotic case.

Antibiotic resistance is a natural-selection outcome in a bacterial population. Bacterial cells may already differ genetically, and some may carry an allele that makes them less affected by an antibiotic.

• Variation first: resistance alleles arise through random mutation; antibiotic use does not create the mutation.
• Selection pressure: when the antibiotic is present, susceptible bacteria are more likely to be inhibited or killed, while resistant bacteria are more likely to survive.
• Differential reproduction: surviving resistant bacteria reproduce and pass the resistance allele to offspring, so its frequency increases over generations.
• Population outcome: repeated or inappropriate antibiotic use can make resistant strains more common, reducing the effectiveness of treatment.
• Spread: resistance alleles can be passed vertically during reproduction and, where supported by the source, can also spread between bacteria through plasmid-mediated horizontal transfer.

Use antibiotics only when appropriate and follow the prescribed course and guidance. This reduces unnecessary selection for resistance, but it does not reverse an established allele-frequency change immediately. Infection control, surveillance and development of new treatments can also matter; feasibility depends on biological, social and economic conditions.

Antibiotics select resistant bacteria; they do not deliberately make individual bacteria resistant. Resistance is a population change across generations, not an adaptation chosen by a bacterium. This card explains the selection mechanism and responsible-use boundary, not Hardy–Weinberg calculations, a full treatment protocol or a universal claim about every infection.

The Hardy–Weinberg model links allele frequencies to genotype frequencies for a gene with two alleles. Let p be the frequency of one allele and q the frequency of the other; frequencies are proportions of the population, so p + q = 1.

• p² is the expected frequency of one homozygous genotype.
• 2pq is the expected frequency of the heterozygous genotype.
• q² is the expected frequency of the other homozygous genotype.
• The three genotype frequencies sum to 1 because they represent all possible genotypes at this two-allele locus.

Use the model in this order:

1. Identify whether the data give an allele frequency or a genotype frequency; write the matching part of the equation.
2. If a homozygous recessive frequency q² is given, find q by taking its square root.
3. Use p = 1 − q (or q = 1 − p).
4. Calculate p², 2pq and q² as required, keeping all frequencies as proportions between 0 and 1.
5. Check that the three genotype frequencies add to 1 before interpreting them.

The prediction assumes a large population, random mating, no natural selection, no mutation and no migration into or out of the population. If these assumptions are not reasonable, an observed departure from the expected frequencies may indicate that one or more assumptions is violated, but the calculation alone does not identify which cause is responsible.

Hardy–Weinberg is a conditional model, not a statement that real populations must have these frequencies. It predicts expected genotype frequencies from allele frequencies under its assumptions; it does not by itself prove evolutionary change, identify a specific selection mechanism or replace experimental evidence.

Artificial selection, or selective breeding, is directional human choice: people select organisms with a desirable phenotype and breed them so that the trait becomes more common or more strongly expressed over many generations. It depends on heritable variation, even when the alleles underlying the phenotype are not fully known.

Use this repeated chain:

1. Identify phenotypic variation in the population.
2. Select individuals showing the desired phenotype.
3. Choose a suitable breeding partner showing the desired phenotype; the SME method cautions against closely related partners.
4. Breed the selected individuals.
5. Let offspring mature, test the target phenotype, and select the strongest performers for further breeding.
6. Repeat the selection and breeding process over generations, while recognising biological limits to how extreme a trait can become.

• Artificial selection: humans set the breeding target and repeatedly choose parents with the desired phenotype.
• Natural selection: environmental pressures affect which phenotypes survive and reproduce; there is no deliberate human breeding target.
• In both cases, a lasting population change requires heritable differences and differential reproductive success, but the selecting agent and direction of selection differ.

Selecting for one desired phenotype can also increase genetically linked traits, some of which may harm health. Avoiding closely related breeding partners is an explicit control in the SME method; this card does not claim a fixed amount of genetic-diversity loss or a guaranteed outcome. Artificial selection is therefore a trade-off between the target trait, biological limits and possible linked effects, not a promise of unlimited improvement.

The selection acts on observed phenotypes, not necessarily on a known genotype. This card covers the general process and its contrast with natural selection; it does not add particular breed examples, Hardy–Weinberg calculations or unsupported genetic detail.

Selective breeding examples show the same causal pattern in different contexts: humans choose a heritable target phenotype, reproduce selected organisms, and obtain a desired result over generations. The target is usually a useful product or function, but the outcome can bring biological trade-offs.

• Wheat and rice disease resistance: breeding for resistance to fungal or bacterial disease can reduce crop damage and increase yield. In wheat, introducing a resistance allele from another wheat species can take many generations and collaboration between breeders and researchers.
• Maize hybridisation: heavy inbreeding can increase homozygosity and the chance that harmful recessive alleles combine, causing inbreeding depression with weaker, less vigorous plants. Outbreeding can increase heterozygosity and hybrid vigour, giving taller, healthier plants and greater yield; farmers may also need uniform height and ripening time.
• Cattle milk yield: selecting high-yield females and breeding with high-yield lines can increase milk yield and economic benefit. However, selecting strongly for a production trait may neglect survival and health; the SME notes greater risk of ailments such as mastitis, milk fever and lameness in selectively bred cattle.

For an example, identify the human target, the selected heritable feature, the intended production or functional result, and the trade-off. Keep the direction of the claim narrow: disease resistance can protect yield, maize outbreeding can improve vigour and uniformity under the stated breeding design, and high milk yield can carry health costs. These are context-specific outcomes, not guarantees for every selectively bred population.

Target → cross-generation result → boundary:

• Crop disease resistance → less disease damage and higher yield → the resistance programme may take many generations.
• Maize hybridisation → heterozygosity, vigour and useful uniformity → breeding design must balance variation, homozygosity and harmful recessive alleles.
• Cattle milk yield → economic production gain → extreme focus on one production trait can neglect health and survival.

Artificial selection is human-directed and product-focused, unlike natural selection, where the environment determines which traits are better suited. This card uses only the stated SME examples; it does not add numerical yield changes, breed-specific claims or a general prediction that selective breeding always improves welfare.