17. Selection and Evolution

Phenotypic variation is the difference in observable characteristics between individuals of the same species. The difference may arise from genetic factors, environmental factors, or an interaction between both.

• Genetic differences can be passed to offspring when they are present in the genetic material of gametes, so they can contribute to inherited differences between individuals.
• Environmental conditions can alter how an organism grows or functions without changing the inherited genetic information; those environmental effects are not passed to offspring as the same phenotype.
• A phenotype can reflect both: genotype sets biological possibilities, while the environment affects how those possibilities are expressed.

A useful cautious framework is: phenotype = genotype expressed in an environment. It is not a literal numerical equation and does not mean that every phenotype can be separated into independent genetic and environmental percentages.

Variation is a population-level comparison, not a label that every individual is “different in every way”. This card defines causes of phenotypic variation; it does not classify discontinuous or continuous distributions, explain detailed genetic mechanisms, or test differences between sample means.

Discontinuous variation places individuals into distinct, recognisable categories. Continuous variation gives a measurable range, with intermediate values between the extremes.

• Discontinuous: the phenotype is qualitative and category-based; a value does not fall between the categories. Example: ABO blood groups.
• Continuous: the phenotype is quantitative and measured on a scale; individuals can take values across a range. Examples: human height or mass.
• In a table or graph, separated categories support a discontinuous interpretation, whereas a spread of values across a range supports a continuous interpretation.

The pattern describes what is observed, not automatically why it occurs. Discontinuous traits are often associated with large effects at one gene locus, while continuous traits commonly reflect many small genetic effects together with environmental influence; the genetic basis must be checked rather than inferred from the appearance alone.

Continuous does not mean “not genetic”, and discontinuous does not by itself prove a single-gene cause. This card classifies the observed variation; it does not develop the detailed genetic architecture or apply a t-test to sample means.

Genetic variation is variation in the DNA base sequence or allele combinations between individuals of a species. It can create different inherited possibilities for phenotype; environmental conditions then affect how those possibilities are expressed.

• Mutation changes a DNA base sequence and can create a new allele. For the change to be inherited, it must occur in genetic material that contributes to gametes.
• Crossing over, independent assortment and random fertilisation create new combinations of existing alleles, rather than automatically creating new alleles.
• A gene is a DNA sequence at a locus; different alleles are alternative versions of that sequence. Their effects can be large at one locus or small and additive across several genes.

Discontinuous phenotypes are commonly associated with a large effect at one gene locus, whereas continuous phenotypes commonly reflect many small genetic effects together with environmental influence. This is a tendency within the syllabus boundary, not a cause that can be diagnosed from the phenotype alone.

Recombination reshuffles existing alleles; mutation can introduce a new allele. Environmental effects can change phenotype without changing the inherited DNA and are not themselves inherited as the same phenotype. Detailed t-test calculations and natural-selection frequency changes are outside this card.

A t-test compares the means of two samples to judge whether their difference is larger than would be expected from variation within the samples. It tests the difference between means, not whether the data are biologically important by themselves.

• Use the test for two sets of continuous data that are approximately normally distributed, with approximately equal standard deviations; calculate a standard deviation for each sample.
• State the null hypothesis: there is no statistically significant difference between the two population means, and any observed difference is due to chance.
• Design the comparison fairly: keep relevant conditions the same, use comparable samples and sample sizes where appropriate, and identify the measured variable before analysing the means.

• Calculate or obtain each sample mean and standard deviation, then use the supplied t-test formula.
• Calculate degrees of freedom: v = (n₁ − 1) + (n₂ − 1).
• Compare the calculated t with the critical value for v at the chosen significance level. If t is greater than the critical value, reject the null hypothesis; otherwise, do not reject it.
• State the conclusion about whether the difference between the two means is statistically significant and relate it to the experimental comparison.

Rejecting the null hypothesis supports a statistically significant difference; it does not prove causation or establish biological importance. Failing to reject it does not prove that the means are identical. Do not say that “the data” are significant: the difference between the means is significant or not.

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.

Evolution is a change in the gene pool of a population across generations. A gene pool is the collection of genes and their alleles in an interbreeding population of one species; a change in allele frequencies changes the genetic composition of that population over time.

• Variation: members of a population can carry different alleles, and their phenotypes reflect genotype together with environmental influence.
• Population process: mutation introduces new genetic differences; natural selection, genetic drift and founder effects can change allele frequencies across generations.
• Outcome: as the gene pool changes, the frequencies of phenotypes in the population may also change.
• Scale: the evolutionary change is measured across a population and generations, not as a purposeful change in one individual.

An individual can acclimatise or alter its phenotype during its lifetime without that being evolution. Evolution requires a heritable change in population allele frequencies across generations; organisms do not change their alleles because they “need” to adapt. “Better adapted” is environment-dependent, not a universal improvement.

Use the gene-pool model to explain population change without moving into DNA-sequence evidence or the detailed allopatric/sympatric speciation pathways. Species definitions depend on investigation, but the central claim here is the population-level change in allele frequencies over time.

DNA sequence comparison provides evidence for evolutionary relationships. DNA from suitable samples can be sequenced and aligned; the more similar the nucleotide sequences of two organisms, the more closely related they are inferred to be.

• Obtain DNA from an organism or fossil sample and determine its base sequence.
• Compare homologous sequence regions between organisms.
• Shared sequence similarities support common ancestry and closer evolutionary relatedness.
• Greater sequence differences are consistent with a longer time since the groups separated, because differences can accumulate over generations.
• Multiple sequence comparisons can be used as evidence for a phylogenetic relationship or tree.

Interpret the evidence comparatively: similarity supports a closer relationship relative to a less similar comparison, while differences support greater evolutionary distance. The inference concerns relative relatedness or relative recency of separation; it does not supply an exact time or, by itself, identify every mutation, pathway or ancestor.

Similar DNA does not mean that two organisms are identical or that sequence comparison alone proves a complete evolutionary history. A sequence comparison is evidence that must be interpreted with the sampling and comparison context. This card owns DNA evidence, not the general definition of evolution or the detailed genetic-isolation pathways of speciation.

Speciation is the formation of a new species from a pre-existing population. Genetic isolation is required: the separated populations no longer exchange genes sufficiently for their gene pools to remain the same.

Allopatric pathway — geographic separation:

1. A geographic barrier divides one population.
2. The groups cannot interbreed across the barrier, so gene flow stops or is greatly reduced.
3. Mutation, natural selection and genetic drift act independently in the two populations.
4. Their allele frequencies and phenotypes diverge over many generations.
5. Reproductive differences accumulate until the groups can no longer successfully interbreed; separate species have formed.

Sympatric pathway — separation in the same area:

1. There is no geographic barrier, but ecological or behavioural differences separate groups within the area.
2. The groups use different environments or behaviours and no longer exchange genes sufficiently.
3. Different selection pressures and genetic changes drive divergence.
4. Reproductive isolation develops, so the groups no longer successfully interbreed and can become separate species.

The starting separation differs, but the required logic is shared: isolation → reduced gene flow → independent gene-pool change → phenotypic divergence → reproductive isolation → speciation. A single visible difference or barrier is not, by itself, proof that two species have already formed; the change takes many generations and must include reproductive isolation.

In sympatric speciation, distinguish the factor that first separates the groups from the later differences that prevent interbreeding. Allopatric means geographic isolation; sympatric means no geographic barrier. This card owns the isolation-to-speciation mechanism, not the general evolution definition or DNA-sequence evidence.