Mutation, Alleles and Genetic Change

Q1 — Sample Band 6 response, peppered moth data (8 marks), annotated

A mutation is a change in the DNA sequence of a gene; it is the routine source of brand-new alleles in a population. The carbonaria allele therefore originated in the peppered-moth lineage as a mutation in the gene controlling wing pigmentation, producing a new variant of that gene. [1 — defines mutation + identifies it as the source of the carbonaria allele]

Mutation is random with respect to need: the environment does not direct the exact DNA change required. Industrial soot, therefore, could not have caused the carbonaria allele to arise. The allele would have been generated by chance copying errors in DNA, regardless of whether trees were clean or sooty. [1 — applies "random with respect to need" to refute "soot caused the mutation"]

The graph shows that in 1848 the carbonaria allele was already present at low frequency (≈1%) and the typica allele dominated the gene pool (≈99%). By 1898 the situation has nearly reversed: carbonaria ≈98%, typica ≈2%. The identities of the two alleles do not change across this 50-year window — the same two variants exist throughout — only their frequencies shift. [1 — uses the data to argue identity vs frequency, with at least two numerical references]

This is the key distinction the lesson asks for. Mutation supplied the carbonaria variant at some earlier point (possibly long before 1848); natural selection acted on the heritable variation already present in the population. Pale moths were more visible to bird predators on soot-darkened bark and were preferentially eaten, so the dark carbonaria allele's frequency rose generation after generation. [1 — distinguishes mutation (creates allele) from selection (changes frequency)] Meiosis and fertilisation in the moth lifecycle reshuffled the two pre-existing alleles each generation but did not create either of them. [1 — explicitly rules out meiosis/fertilisation as the source]

The claim that moths "evolved dark wings because they needed camouflage" is therefore misleading. Moths did not produce a new allele in response to need: that would invert the order of events. What actually happened is that an existing dark allele, originally arising at random, conferred better camouflage once trees became sooty and so was selected for. [1 — evaluates the "because they needed" claim against the lesson framing] A defensible reformulation is: "An existing carbonaria allele, originally produced by random mutation, increased in frequency in industrial regions because the environmental change made it advantageous; selection — not need — is the explanation for the rise." [1 — provides a defensible reformulation in lesson terminology]

The data therefore illustrate the central claim of Module 6 Lesson 1: mutation is the source of new alleles; meiosis and fertilisation reshuffle them; and selection changes their frequency. The peppered-moth case is a frequency change in a pre-existing gene pool, not the manufacture of a new allele on demand. [1 — overall integrated judgement linking the dataset to the lesson framework]

Marking criteria.

• 1 mark — Defines mutation as a change in DNA sequence and identifies it as the source of the carbonaria allele.
• 1 mark — Applies "random with respect to need" to argue that soot did not cause the mutation.
• 1 mark — Uses the graph (at least two specific percentages or years) to show that frequency changes, not allele identity.
• 1 mark — Identifies natural selection as the process that changes carbonaria's frequency, with a correct selective mechanism (bird predation on more visible moths).
• 1 mark — Explicitly distinguishes the role of mutation from the role of meiosis/fertilisation/selection (each does a different job).
• 1 mark — Evaluates the popular "because they needed" claim using lesson framing and rejects it as misleading.
• 1 mark — Provides a defensible reformulation that mentions a pre-existing allele, random mutation, environmental change and selection.
• 1 mark — Integrated final judgement that links the moth data back to the central lesson claim (mutation creates, selection redistributes).

Q2 — Sample Band 6 response, MRSA source critique (7 marks), annotated

The spokesperson's interpretation contains three biological flaws. [1 — overall evaluative judgement]

First, "antibiotics cause S. aureus to mutate into MRSA so they can survive" inverts the order of events. Mutation occurs randomly with respect to need; the methicillin-resistance allele (typically mecA, carried on a mobile element) was already present in some S. aureus isolates before any individual patient's antibiotic course began. The antibiotic kills susceptible cells but spares cells already carrying the resistance allele; those then reproduce. The antibiotic does not "instruct" the bacterium to produce the allele. [1 — identifies the inversion of "mutation occurs first, selection later"]

Second, the AGAR data (32% in 2002 → 39% in 2006 → 18% in 2018) are frequency data, not "mutation creation" data. Each percentage represents the proportion of S. aureus bloodstream isolates that already carry the resistance allele at the time of sampling. A rise from 32% to 39% under high antibiotic use, and a fall to 18% after stewardship limits antibiotic exposure, demonstrate selection acting on existing variation: heavy antibiotic use favours resistant cells; reduced antibiotic use removes that selective advantage, and the cost of carrying the resistance allele then allows the susceptible cells to recover their share of the population. [1 — uses AGAR data to argue frequency change under selection, not allele creation]

Third, "the bacteria will simply un-mutate back to the harmless form" is biologically incorrect. The drop in MRSA frequency is not "un-mutation" — the resistance allele still exists in the population, but it is now at lower frequency because the selective pressure favouring it has been removed and it may carry a small fitness cost in the absence of methicillin. [1 — refutes "un-mutation" and explains the actual mechanism (selection direction reversed, allele still present)]

An experimental test of whether the resistance allele exists before antibiotic exposure is the classic Lederberg replica-plating approach. Grow S. aureus on a master plate with no antibiotic, replica-plate to plates containing methicillin, and check whether resistant colonies recovered on antibiotic plates correspond to specific colonies already on the master. If they do, the resistance allele predated the antibiotic exposure — exactly what is observed in real experiments. [1 — proposes a valid experimental approach (Lederberg replica plating or equivalent fluctuation test)]

A defensible rewrite of the spokesperson's claim would be: "The MRSA resistance allele exists in S. aureus populations independently of antibiotic use. Heavy antibiotic exposure selects for bacteria already carrying it, raising its frequency; stewardship programs reduce that selection pressure, lowering its frequency. The allele itself is not created or destroyed by antibiotics — only its frequency in the population changes." [1 — defensible rewrite using lesson terminology (allele frequency, selection, mutation)]

This integrates the lesson framework — mutation creates new alleles, selection changes their frequency — directly with the AGAR dataset, showing why the spokesperson's "antibiotics cause mutation" framing is both biologically and policy-relevantly wrong (it implies antibiotic use makes new problems, when in fact it amplifies pre-existing ones). [1 — explicit final integrated judgement linking lesson framework to dataset and to public-health implications]

Marking criteria.

• 1 mark — States an overall evaluative judgement that the spokesperson is wrong / partly wrong.
• 1 mark — Correctly identifies the order-of-events flaw (mutation does not occur because of need; it occurs first, selection later).
• 1 mark — Uses the AGAR data (at least two of: 32%, 39%, 18%) to argue that the data show frequency change driven by selection, not allele creation.
• 1 mark — Refutes "un-mutation" specifically — the allele still exists, only its frequency falls.
• 1 mark — Proposes a valid experimental approach (Lederberg replica plating / fluctuation test) that could show the allele pre-exists antibiotic exposure.
• 1 mark — Provides a defensible rewrite that uses lesson terminology (allele frequency, selection, random mutation).
• 1 mark — Integrated final judgement that links the lesson framework to the dataset (and ideally to the policy implication).