The big idea: Natural selection is not just a story about the distant past — it is happening now, fast enough to measure in living populations.
Whenever a population has variation and the environment favours some variants over others, the helpful allele becomes more common over generations. That is natural selection in action.
The exam tests this through a handful of real case studies: antibiotic resistance in bacteria, herbicide resistance in weeds, the sickle-cell trait (heterozygote advantage), and Endler's guppies. They all follow the same recipe.
Natural selection in action, generalised: a varied population, a selection pressure that removes the unfavoured variant, then the favoured allele becoming common over generations.
Interactive diagram
Explore the labelled diagram, charts and maps for this topic in full study mode.
- Natural selection
- The process by which variants better suited to their environment survive and reproduce more, so their alleles become more common over generations.
- Selection pressure
- A factor in the environment (e.g. a drug, a predator, a disease) that affects which variants survive and reproduce.
- Variation
- Differences between individuals in a population; the raw material natural selection acts on. It often arises from random mutation.
- Allele frequency
- How common a particular form of a gene (an allele) is in a population. Natural selection changes it over generations.
- Resistance
- The ability of an organism (e.g. a bacterium or a weed) to survive a chemical, such as an antibiotic or herbicide, that would normally kill it.
- Heterozygote advantage
- When carrying two different alleles (a heterozygote) gives higher fitness than either homozygote, so both alleles are kept in the population.
The one sentence behind every case: Variation already exists → a selection pressure removes some variants → the survivors reproduce → the favourable allele becomes more common.
Learn that chain once and you can answer every case study by slotting in the right pressure and the right variant.
Each case study is the same mechanism wearing a different costume. Read each one as the chain variation → pressure → survival → allele frequency rises.
A crucial subtlety the IB loves: the resistance does not appear because of the drug. The variation is already there by chance; the drug just selects which variants survive.
1. Antibiotic resistance in bacteria
- A random mutation in a bacterium's DNA makes it resistant — this happens before the antibiotic is used.
- When the antibiotic is given, it kills the susceptible bacteria but the resistant ones survive.
- The survivors reproduce rapidly (and can pass the resistance gene to others, even on plasmids), so the resistant allele becomes common.
- Now the antibiotic no longer works — the population has evolved resistance.
Antibiotic resistance read through the same machine: a mixed population of resistant and susceptible bacteria, the antibiotic (the pressure) kills the susceptible ones, and the resistant survivors reproduce until resistance is common.
Interactive diagram
Explore the labelled diagram, charts and maps for this topic in full study mode.
2. Herbicide resistance in weeds
- A few weeds carry a resistance allele by chance (variation).
- Spraying a herbicide is a selection pressure — it kills the non-resistant weeds.
- The resistant weeds survive and reproduce, passing on the allele.
- As herbicide use rises year after year, the proportion of resistant weeds rises too — exactly the trend a graph would show.
3. Sickle-cell trait — heterozygote advantage
- There are two alleles: normal (HbA) and sickle (HbS). Two copies of the sickle allele cause sickle-cell anaemia, often lethal.
- In malaria regions the disease is a strong selection pressure — but carriers (one of each allele) are more resistant to malaria.
- So in those regions the heterozygote has the highest fitness: better than the malaria-prone normal homozygote AND the anaemic sickle homozygote.
- Because carriers survive and reproduce best, the sickle allele is kept at a moderate frequency — it is not eliminated despite causing a lethal disease.
4. Endler's guppies
- Male guppies vary in colour and spot pattern (variation).
- Where predators are common, bright males are spotted and eaten — so dull, camouflaged males are favoured.
- Where predators are rare, females prefer bright males (sexual selection), so showy males are favoured.
- Over just a few generations the population's colouration shifts to match the predation pressure — natural selection observed in real time.
Heterozygote advantage — say it precisely: The sickle-cell question is hard because you must explain a paradox: a lethal allele that should be removed is instead kept in the population.
The answer is balancing selection — the heterozygote survives best, so selection favours keeping both alleles around. In a region without malaria, the sickle allele loses this advantage and stays rare.
Avoid saying the carrier is 'immune' — say more resistant to / less affected by malaria.
| Step | What happens | In every case study |
|---|---|---|
| 1. Variation | Individuals differ, often because of a random mutation | Resistance alleles, sickle alleles and colour alleles all arise by chance |
| 2. Selection pressure | Something in the environment kills or out-competes some variants | Antibiotic, herbicide, malaria, or predators |
| 3. Differential survival | The favoured variant survives and reproduces more | Resistant microbes / carriers / camouflaged males leave more offspring |
| 4. Allele frequency change | The helpful allele becomes more common over generations | Resistance spreads; the sickle allele persists; colour shifts |
Know your predicted grade
Take timed mock exams and get detailed feedback on every answer. See exactly where you're losing marks.
Try Mock Exams Free7-day free trial • No card required
How this is tested: On Paper 2 a 5-mark Outline asks how changes in bacterial nucleic acids lead to antibiotic resistance — score the chain mutation → resistant variant → antibiotic kills susceptible → resistant survive and reproduce → resistance becomes common.
Also on Paper 2, a 7-mark Explain asks how the sickle-cell trait spread despite the lethal homozygous disease — the key word is heterozygote advantage.
On Paper 1 a 1-mark item may give a trend graph (herbicide use vs % resistant weeds) and ask you to suggest why resistance rose — the herbicide selects the rare resistant variant. Another 1-mark item asks what Endler's guppies demonstrated.
IB-style question — outline how bacteria become antibiotic-resistant
Outline how a change in the nucleic acid of bacteria can lead to a population becoming resistant to an antibiotic. [5]
How to score all five marks
- Where the variation comes from. A random mutation in the bacterial DNA produces a bacterium that is resistant to the antibiotic. (This happens by chance, not because of the antibiotic.)
- Variation in the population. So the population contains both resistant and susceptible bacteria — there is variation.
- The selection pressure acts. When the antibiotic is used it kills the susceptible bacteria but the resistant ones survive.
- Differential reproduction. The surviving resistant bacteria reproduce, passing on the resistance gene to their offspring (and they can spread it horizontally, e.g. on plasmids).
- Allele frequency rises. Over generations the resistance allele becomes more common, so most of the population is now resistant and the antibiotic no longer works. (Award 1 mark per distinct point, max 5.)
Final answer
A random mutation in bacterial DNA produces a resistant variant; the population now varies; the antibiotic kills susceptible bacteria but resistant ones survive; survivors reproduce and pass on the resistance gene (e.g. via plasmids); so the resistance allele becomes common and the antibiotic stops working.
✓ Why this scores full marks: It gives five separate, ordered points — mutation, variation, the antibiotic selecting, survivors reproducing, allele frequency rising.
The make-or-break detail: the mutation comes first, by chance. Writing 'the antibiotic made the bacteria resistant' is the classic error and loses marks — the drug selects, it does not create the resistance.
| Case study | Selection pressure | Favoured variant | What is observed |
|---|---|---|---|
| Antibiotic resistance in bacteria | An antibiotic | Bacteria with a resistance mutation | Susceptible bacteria die; resistant ones survive and multiply, so infections stop responding to the drug |
| Herbicide resistance in weeds | A herbicide (e.g. a weedkiller) | Plants with a resistance allele | As spraying continues, resistant weeds make up more and more of the population |
| Sickle-cell trait (heterozygote advantage) | Malaria | Heterozygous carriers (one normal, one sickle allele) | Carriers survive malaria better than either homozygote, so the sickle allele is kept at moderate frequency where malaria is common |
| Endler's guppies | Predation (and mate choice) | Dull males where predators are common; bright males where they are rare | Male colouration shifts within a few generations, showing evolution in real time |