AQA-GCSE-CST-B6 · Inheritance, variation and evolution

Inheritance, variation and evolution.

Written for AQA 8464 Official specification ↗ Updated 2026.07.10

HookFive billion identical bananas

Britain gets through roughly five billion bananas a year, and almost every single one is the same variety, the Cavendish. More than that, they are very nearly the same plant: Cavendish bananas are grown not from seed but from cuttings, so each new plant is a clone of its parent, genetically identical, produced with no second parent and no shuffling of genes. That uniformity is what makes them cheap and predictable in a supermarket — and it is also a loaded gun. A soil fungus called Panama disease is spreading through banana plantations, and because every Cavendish is genetically the same, a strain that can kill one plant can kill them all. It has happened before: the Cavendish only exists on our shelves because the previous supermarket banana, the Gros Michel, was wiped out by an earlier strain of the same disease in the mid-twentieth century. The banana's greatest strength, being identical, is also its fatal weakness: no variation.

That trade-off — the price of having no variation — is the thread running through the whole of B6. This section runs from how organisms reproduce and how gametes are made, through the structure of DNA and the mathematics of a genetic cross, to the biggest idea in biology: that variation, passed on and filtered over vast stretches of time, is how life evolves. By the end you should be able to fill in a Punnett square, explain natural selection as a chain of cause and effect, and say why a hospital superbug and a fossil in a cliff are telling the same story.

ModelTwo ways to reproduce — and meiosis in the middle

Sexual reproduction involves two parents and the joining of gametes — sex cells — at fertilisation: the egg and sperm in animals, egg cells and pollen in flowering plants. Because each offspring receives a mix of genes from two parents, sexual reproduction produces variation. Asexual reproduction involves only one parent and no gametes; the offspring are genetically identical clones, produced by ordinary cell division (mitosis) — which is exactly how the Cavendish banana is grown.

Gametes are made by a special kind of cell division called meiosis, which happens only in the reproductive organs. Meiosis starts with a normal body cell, copies the chromosomes, then divides twice to make four gametes, each with only half the chromosome number — in humans, 23 instead of 46 — and each genetically different from the others. When two gametes fuse at fertilisation the full number is restored, and the new cell then divides by mitosis to build an embryo. Halving and then doubling is what keeps the chromosome number constant across the generations while shuffling the genes.

Each strategy is a trade-off. Sexual reproduction creates variation, which gives a population a survival advantage if the environment changes — but it needs two parents, and takes time and energy. Asexual reproduction is fast, needs only one parent and is efficient in a stable habitat — but with no variation, a single disease or change can destroy the whole population, the banana's exact predicament. Many organisms hedge by doing both: a strawberry plant sends out runners (asexual) and also flowers (sexual).

ModelDNA and the genome

The genetic material is DNA, a large molecule (a polymer) wound into a double helix of two strands and packaged, inside the nucleus, into structures called chromosomes. A gene is a small section of DNA that codes for a particular sequence of amino acids, which fold up to make a specific protein; it is the order of the coded information along the DNA that determines which protein is built. The entire genetic material of an organism is its genome.

Sequencing the whole human genome — first drafted in 2000, after a decade of international work — has become important for medicine: it lets researchers search for the genes linked to particular diseases, understand and treat inherited disorders, and trace how human populations migrated across the world in prehistory. At GCSE you need the idea of a coded sequence held in a double helix, plus what a gene and a genome are and why sequencing the genome matters — the detailed chemistry of the individual building blocks belongs to the separate-science course, not to this one.

MechanismReading a genetic cross — alleles and Punnett squares

Genes come in different versions called alleles. Because you inherit one chromosome of each pair from each parent, you carry two alleles of every gene. If the two alleles are the same you are homozygous; if they differ you are heterozygous. A dominant allele shows its effect even when only one copy is present, and is written with a capital letter; a recessive allele only shows its effect when both copies are present, and is written in lower case. Your combination of alleles is your genotype; the characteristic it produces is your phenotype.

A Punnett square is a grid that predicts the offspring of a cross. You write the two alleles of one parent along the top and the two of the other down the side, then fill each cell by combining them. The proportions it gives are probabilities for each offspring, not guarantees — a family can easily not match the ratio, because each conception is an independent event. The worked example builds one for a real inherited condition.

Worked example

Cystic fibrosis is caused by a recessive allele; call the healthy dominant allele F and the recessive allele f. Suppose one parent has cystic fibrosis, so must be homozygous recessive, \(ff\), and the other is an unaffected carrier, \(Ff\). The cross is \(Ff \times ff\). The carrier parent can pass on F or f; the affected parent can only pass on f. Filling the four cells of the Punnett square combines these into Ff, Ff, ff and ff — a genotype ratio of \(2\,Ff : 2\,ff\), which is \(1:1\), and a phenotype ratio of one unaffected carrier to one affected child, also \(1:1\). So each child has a \(\tfrac{1}{2}\) (50%) chance of having cystic fibrosis, even though only one parent has the condition. Because each conception is independent, the chance that the couple's first two children are both affected is \(\tfrac{1}{2} \times \tfrac{1}{2} = \tfrac{1}{4}\), not a half — multiplying independent probabilities is the step examiners most often see dropped. Note too that a healthy-looking carrier can still have an affected child: being unaffected is not the same as carrying no faulty allele.

CaseInherited disorders and sex determination

Some disorders are caused by inheriting particular alleles. Polydactyly — having extra fingers or toes — is caused by a dominant allele, so it can be passed on by just one affected parent. Cystic fibrosis — a disorder of cell membranes that clogs the lungs and pancreas with thick mucus, affecting around one in 2,500 UK newborns — is caused by a recessive allele, so a child can only have it by inheriting a copy from both parents, who may themselves be unaffected carriers (roughly one person in 25 carries a copy). Embryos made by IVF can be screened for such alleles before implantation, which raises ethical questions AQA expects you to weigh: it could reduce suffering, but it also raises worries about cost, about rejecting embryos, and about where to draw the line on selecting characteristics.

Sex is determined by one pair of chromosomes, the 23rd. Females have two X chromosomes (XX); males have one X and one Y (XY). Every egg carries an X; a sperm carries either an X or a Y, so it is the sperm that decides the sex. A Punnett cross of \(XX \times XY\) gives XX, XX, XY and XY — a \(1:1\), or 50:50, ratio of females to males, which is why the sex ratio at birth is close to even.

MechanismVariation, natural selection and evolution

Differences between individuals of the same species are called variation, and they arise from the genes an organism inherits (genetic causes), from its environment (environmental causes), or from a combination of the two. All genetic variation originates in mutation — a random change to the DNA. Most mutations have no effect on the phenotype; a few influence it slightly; and very rarely a single mutation determines a phenotype outright. Mutations occur continually, giving natural selection a constant supply of new variation to act on.

Natural selection is the mechanism of evolution, and examiners want it written as an ordered chain of cause and effect. Within a species there is genetic variation. Organisms compete for limited resources, and more offspring are produced than can survive. Individuals with the characteristics best suited to the environment are more likely to survive that struggle and reproduce. They pass the alleles for those advantageous characteristics on to their offspring, so over many generations those alleles become more common and the species gradually changes. That is the definition of evolution: a change in the inherited characteristics of a population over time, through natural selection, which may result in the formation of a new species. The theory holds that all species alive today descended from simple life forms that first appeared more than three billion years ago — the idea Charles Darwin set out in 1859, and which is now supported by a mountain of evidence.

CaseHumans take the wheel — selective breeding and genetic engineering

Selective breeding (artificial selection) is natural selection with a human doing the choosing. Over many generations, breeders pick the individuals with the desired characteristic — disease resistance or high yield in crops, high milk production in dairy cattle, gentleness in dogs, large or unusual blooms in flowers — and breed them together so the characteristic strengthens. Its danger is a shrinking gene pool: repeatedly breeding closely related individuals (inbreeding) can concentrate harmful alleles and leave a whole breed vulnerable to a single disease — the same lack-of-variation problem as the banana, reached by a different route.

Genetic engineering goes further and faster by transferring a gene directly from one organism into another. Bacteria have been engineered to produce human insulin for treating diabetes; crops (GM crops) have been given genes for herbicide tolerance, resistance to insect pests, or added nutrients — 'golden rice' carries genes that let it make a vitamin A precursor. The evaluation examiners want weighed sets higher yields and clear medical benefits against uncertainty about the effects on wild populations and human health, and against ethical objections. In genetic engineering a gene is moved deliberately in a single step; in selective breeding whole organisms are chosen over many generations. Keeping that distinction clear is a reliable mark.

DataThe evidence — fossils, extinction and resistant bacteria

Two main lines of evidence support evolution: the fossil record and, more recently, our understanding of genetics. Fossils are the remains of organisms from thousands or millions of years ago. They form when the hard parts of an organism, such as bone, do not decay and are gradually replaced by minerals; when softer parts are preserved because conditions — very low oxygen, low temperature, or lack of water — stop microbes decaying them; or as impressions and traces such as footprints and burrows. Scientists cannot be certain how life on Earth began, because many early organisms were soft-bodied and left few fossils, and many fossils that did form have since been destroyed by geological activity — which leaves gaps in the record.

The most powerful modern evidence is evolution you can watch: antibiotic-resistant bacteria such as MRSA. A random mutation gives one bacterium resistance to an antibiotic. When the antibiotic is used, the non-resistant bacteria die but that resistant one survives and reproduces rapidly, passing on the resistance allele, until the whole population is resistant — natural selection in days rather than aeons. To slow it, doctors are urged not to over-prescribe antibiotics and to prescribe specific ones, patients must complete the full course, and the use of antibiotics in farming should be restricted; new antibiotics are developed slowly and at great cost, so we cannot rely on simply outrunning resistance. And when a species can no longer survive the conditions it faces — through environmental change, new predators, new diseases, new competitors, a single catastrophic event, or human activity — it becomes extinct, exactly as the Gros Michel banana nearly did.

ModelClassification — from Linnaeus to three domains

Living things have to be organised before they can be studied. In the eighteenth century Carl Linnaeus classified organisms into a nested hierarchy — kingdom, phylum, class, order, family, genus, species — and gave each a two-part Latin name in the binomial system, genus then species, such as Homo sapiens. As microscopes and then the chemistry of cells improved, scientists could see far more detail than Linnaeus ever could, and the scheme was revised.

In the 1970s Carl Woese used comparisons of the molecules inside cells to propose the three-domain system, dividing life at its broadest level into Archaea (primitive bacteria, often living in extreme places), Bacteria (true bacteria) and Eukaryota (everything with complex cells — protists, fungi, plants and animals). Because classification now reflects how closely related organisms actually are, it can be drawn as evolutionary trees that show how species have diverged from common ancestors — the same idea of shared descent that runs through the whole of B6, from the banana on your shelf to the bacteria in a hospital ward.

VocabularyKey terms the mark scheme pays for

Gene
A small section of DNA that codes for a particular sequence of amino acids, and therefore for a specific protein.
Allele
A different version of a gene. You carry two alleles of each gene, one inherited from each parent.
Genome
The entire genetic material of an organism. Sequencing the human genome aids medicine, the study of inherited disorders and the tracing of human migration.
Meiosis
Cell division in the reproductive organs that produces four genetically different gametes, each with half the chromosome number of the parent cell.
Dominant / recessive allele
A dominant allele is expressed with only one copy present (capital letter); a recessive allele is only expressed when two copies are present (lower-case letter).
Homozygous / heterozygous
Homozygous means the two alleles of a gene are the same (FF or ff); heterozygous means they are different (Ff).
Genotype / phenotype
The genotype is the combination of alleles an organism carries; the phenotype is the characteristic those alleles produce.
Mutation
A random change to the DNA. It is the origin of all genetic variation; most have no effect, a few affect the phenotype, and very rarely one determines it.
Natural selection
The process by which individuals best suited to their environment survive, reproduce and pass on their alleles, so those alleles become more common over generations.
Selective breeding
Choosing organisms with a desired characteristic and breeding them over many generations. It can shrink the gene pool and leave a breed vulnerable to disease.

TrapsMisconceptions that cost marks

“Meiosis and mitosis are basically the same, and gametes have the full number of chromosomes.”
Actually: Mitosis makes two genetically identical cells with the full chromosome number, for growth and asexual reproduction. Meiosis makes four genetically different gametes with half the number; fertilisation then restores the full number.
“Animals evolve by changing themselves to suit their environment during their lives.”
Actually: Individuals do not evolve; populations do, over generations. Natural selection acts on variation that already exists from random mutation — not on characteristics an organism develops during its own lifetime.
“A dominant allele must be the most common one in a population.”
Actually: Dominance describes how an allele is expressed, not how common it is. Polydactyly is caused by a dominant allele yet is rare, while many recessive alleles are common. Frequency and dominance are unrelated.
“Bacteria deliberately become resistant when they meet an antibiotic.”
Actually: Resistance comes from a random mutation that was already present by chance. The antibiotic does not create it — it simply kills the non-resistant bacteria, leaving the resistant one to reproduce. Selection is not directed.
“A 1:1 or 3:1 ratio means the offspring will divide up exactly that way.”
Actually: The ratio is a probability for each independent conception, not a quota. A small family can easily not match it, just as four coin tosses need not give exactly two heads.

ExamWhat examiners want

Genetic-cross questions are pure method marks: draw the full Punnett square, label the parental genotypes and the gametes, and quote both the ratio and the probability (as a fraction or a percentage). State that each offspring is an independent event, and multiply the probabilities when a question asks about two or more children — the single most common lost mark on inheritance questions. AQA also hands marks (AO1) for using the vocabulary precisely, so keep gene and allele, genotype and phenotype, and homozygous and heterozygous distinct.

For natural selection, always answer as an ordered chain: variation from mutation → competition and a selection pressure → the best-suited survive and reproduce → they pass on their alleles → the allele becomes more common over many generations. Stress 'populations, over many generations' — never individuals changing themselves. For antibiotic-resistance questions this same chain, applied to the specific bacterium in the question, is the mark scheme (AO2), so adapt it to the context rather than reciting it generically.

For the required recall topics — the uses and importance of the genome, how fossils form, the causes of extinction, and the Linnaean and three-domain classification systems — learn the set points so you can bank them quickly. Watch the command word: 'describe' the pattern in a set of data, 'explain' it using natural selection, and on 'evaluate' questions about IVF screening or GM crops give both sides and then a judgement, because the final mark is for the conclusion.

Retrieve

Test yourself

Question 1 of 8

Vofti has 90 questions on AQA-GCSE-CST-B6 — every one hook-first, every one mapped to this section of the AQA spec.

Last updated · 2026.08.09 AQA GCSE Combined Science: Trilogy · Spec AQA-GCSE-CST-B6