Regulation of Transcription and Translation: AQA A Level Biology Exam Questions by Topic

AQARegulation of Transcription and TranslationExam Questions
Written by Tom Whitburn

Regulation of transcription and translation (AQA 3.8.2.2) is A-level only, so it's Year 13 content. You need to know how transcription factors move into the nucleus to stimulate or inhibit transcription, including the role of oestrogen; how epigenetic changes, increased methylation of DNA and decreased acetylation of histones, inhibit transcription and matter in diseases such as cancer; and how RNA interference stops mRNA being translated.

The examiners' reports show this topic catches a lot of students out. Only 5% got both marks for explaining how a mutation outside the lactase gene causes lactase persistence, because few thought of a promoter or a transcription factor gene. On RNA interference, 63% scored zero on the poplar question and almost 57% on antisense SUT1 mRNA, mostly by having the RNA bind to the gene and block transcription. And 'switched on' or 'switched off' never earns the mark on its own: say that transcription is stimulated or inhibited.

Start with the transcription factor questions, then the epigenetics ones, and keep RNAi separate in your head: it acts on mRNA, after transcription. Finish with the data questions, where reading a log scale and spotting what a method can't show are the skills being tested. If you'd like help with this topic, my AQA masterclasses run online on Tuesdays at 5.15pm for Year 12 and on Wednesdays or Thursdays at 6.30pm for Year 13.

Want help with this topic? It comes up in my weekly AQA masterclasses. See the timetable →

What you need from GCSE and Year 12

Each question on this page assumes you're secure on these GCSE and Year 12 ideas. If any of them feels shaky, revise it before you start.

  • GCSE: hormones are chemical messengers carried in the blood to target cells.
  • Year 12 (AQA 3.4.2): RNA polymerase transcribes a gene into mRNA in the nucleus, and ribosomes translate mRNA codons into a polypeptide.
  • Year 12 (AQA 3.1.5.1): complementary bases pair up (A with U in RNA), so one nucleic acid strand can bind to another.
  • Year 12 (AQA 3.4.1): in eukaryotes, nuclear DNA is wound around histone proteins.
  • Year 12 (AQA 3.1.4.1): a protein's tertiary structure gives it a specific shape, so a change in its amino acid sequence can stop it binding.

Key terms

These words come up in the questions and mark schemes. Examiners expect you to use them exactly.

  • Transcription factor: a protein that moves from the cytoplasm into the nucleus and binds to DNA (the promoter) to stimulate or inhibit transcription of a target gene.
  • Promoter: the region of DNA next to a gene where transcription factors and RNA polymerase bind to start transcription.
  • RNA polymerase: the enzyme that joins RNA nucleotides to make mRNA during transcription; a transcription factor can help it bind.
  • Oestrogen: a lipid-soluble steroid hormone that diffuses into a cell and binds to a receptor, forming an active transcription factor that initiates transcription.
  • Epigenetics: heritable changes in gene function, without changes to the base sequence of DNA, caused by changes in the environment.
  • Methylation of DNA: adding methyl groups to DNA (often the promoter); increased methylation inhibits transcription.
  • Acetylation of histones: adding acetyl groups to the histones that DNA is wound around; decreased acetylation inhibits transcription, increased acetylation stimulates it.
  • Oncogene and tumour suppressor gene: increased methylation of a tumour suppressor gene or decreased methylation of an oncogene can lead to cancer.
  • RNA interference (RNAi): small RNA molecules such as siRNA bind to complementary mRNA, which is destroyed or not translated.
  • Antisense RNA or DNA: a single strand with a base sequence complementary to an mRNA, so it binds to that mRNA and ribosomes can't translate it.

What these questions cover (AQA 3.8.2.2)

The questions test these statements from the AQA AS and A-level Biology specification (7401/7402):

  • Transcription factors and oestrogen: In eukaryotes, transcription of target genes can be stimulated or inhibited when specific transcriptional factors move from the cytoplasm into the nucleus. The role of the steroid hormone, oestrogen, in initiating transcription. (no written question asks about oestrogen itself; the testosterone and androgen receptor question works in exactly the same way)
  • Epigenetic control: Epigenetic control of gene expression in eukaryotes.
  • What epigenetics is: Epigenetics involves heritable changes in gene function, without changes to the base sequence of DNA. These changes are caused by changes in the environment that inhibit transcription by:
  • Increased methylation of DNA: increased methylation of the DNA or
  • Decreased acetylation of histones: decreased acetylation of associated histones. (no part tests acetylation on its own, but the Huntington's disease and cancer drug questions both credit decreased acetylation of histones inhibiting transcription)
  • Epigenetics and disease: The relevance of epigenetics on the development and treatment of disease, especially cancer.
  • RNA interference: In eukaryotes and some prokaryotes, translation of the mRNA produced from target genes can be inhibited by RNA interference (RNAi).
  • Gene expression data: interpret data provided from investigations into gene expression
  • Genetic and environmental influences: evaluate appropriate data for the relative influences of genetic and environmental factors on phenotype. (no written question on this page asks you to weigh genetic against environmental factors; the Alzheimer's question, where an environmental factor changes when a mutation is expressed, is the closest practice)

How to use this page

Write your answer on paper before you open the mark scheme. Allow about 1.3 minutes per mark: the 18 questions are worth 44 marks, so about 57 minutes in total. Then mark your answer strictly against the mark scheme and read the examiners' tip underneath it. If you'd rather print the questions, download the PDF pack.

Transcription factors and steroid hormones (3.8.2.2)

Question 1

A level Paper 2 · November 2020 · Q02.3 · 2 marks · Medium

Suggest how testosterone bound to the androgen receptor stimulates gene expression.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Stem: testosterone is a steroid hormone that belongs to a group of male sex hormones called androgens. Question: the binding of testosterone to an androgen receptor (AR) changes its shape, and the AR then enters the nucleus and stimulates gene expression; suggest how, 2 marks.
Show the mark scheme Mark scheme, any two: the AR is a transcription factor; binds to DNA or the promoter; stimulates RNA polymerase. Ignore 'binds to bases' or 'binds to gene'; reject active site, enzyme, substrate or induced fit.

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From the examiners' report: Only 54% scored and about half of those got both. Call the AR a transcription factor, say it binds to the promoter, and link it to RNA polymerase, not DNA polymerase.

Question 2

A level Paper 2 · June 2017 · Q06.3 · 2 marks · Medium

Suggest how transcription factors reprogramme skin cells into iPS cells.

Stem: scientists used four transcription factors to reprogramme skin cells to form induced pluripotent stem cells (iPS cells), then made pancreatic cells from them and transplanted them into diabetic mice. Figure 6: fasting blood glucose over 12 weeks for treated diabetic mice (group A), untreated diabetic mice (B) and non-diabetic mice (C). Question: suggest how transcription factors can reprogramme cells to form iPS cells, 2 marks.
Show the mark scheme Mark scheme: attach to a gene, DNA or the promoter region; stimulate or inhibit transcription or RNA polymerase. Genes being expressed, inhibited or switched on or off is not enough on its own.

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From the examiners' report: Over 50% got at least one mark, usually for binding. Say that the transcription factor binds to the promoter and stimulates or inhibits transcription; 'switching genes on' doesn't score, and don't confuse transcription with translation.

Question 3

A level Paper 2 · June 2018 · Q08.3 · 1 mark · Hard

Use a chromatin immunoprecipitation flow chart to say what 'precipitated DNA' contains.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Figure 8: chromatin immunoprecipitation, used to find where a transcription factor binds to DNA. Chemicals bind the transcription factor to DNA; DNA is broken into fragments and an antibody specific to the transcription factor is added; the 'precipitated DNA' is removed and a chemical removes the antibody with the attached transcription factor; the DNA at the transcription factor's site is amplified. Question: use Figure 8 to explain what 'precipitated DNA' consists of, 1 mark.
Show the mark scheme Mark scheme: DNA, transcription factor and antibody. Accept nucleotides for DNA.

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From the examiners' report: Only 26% got this. Follow the flow chart: the transcription factor is bound to the DNA and the antibody is bound to the transcription factor, so you need all three, not just DNA fragments.

Question 4

A level Paper 2 · June 2018 · Q09.3 · 2 marks · Hard

Explain how a mutation outside the lactase gene could cause lactase persistence.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Stem: lactose in milk is hydrolysed by lactase; most mammals stop producing lactase when they stop feeding on milk, but some humans keep producing it as adults (lactase persistence, LP), controlled by a dominant allele. Question: LP is caused by a mutation in DNA that does not occur in the gene coding for lactase; suggest and explain how this mutation causes LP, 2 marks.
Show the mark scheme Mark scheme: a mutation in the promoter for the gene, or in the promoter for a transcription factor, or in the gene for a transcription factor; so the lactase gene continues to be transcribed.

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From the examiners' report: Only 18% got a mark and 5% got both. If the lactase gene is unchanged, think about what controls its transcription: its promoter or a transcription factor, and then say it keeps being transcribed.

Question 5

A level Paper 3 · June 2018 · Q02.4 · 3 marks · Medium

Explain how a NOTCH1 mutation affecting a transcription factor reduced the B cells destroyed by Rituximab.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Earlier part of the same exam question, giving the information this part uses. Stem: chronic lymphocytic leukaemia (CLL) affects B cells; the drug Rituximab binds to CD20 on B cells and kills them. Figure 2: scatter graph of percentage of B cells destroyed (0 to 100) against the amount of CD20 on the B cells (0 to 16 arbitrary units), rising with CD20. About 11% of people with CLL have a NOTCH1 mutation, which leads to a non-functional transcription factor associated with CD20 production. Table 1: median percentage of B cells destroyed was 4 with the NOTCH1 mutation and 22 without. Question: use all the information to suggest how the mutation led to the difference, 3 marks.
Show the mark scheme Mark scheme, any three: the mutation changes the amino acid sequence or tertiary structure of the transcription factor; it can't bind to the CD20 gene or promoter; less mRNA for CD20 is produced or less CD20 is made; so there is little for Rituximab to bind to and fewer B cells are destroyed.

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From the examiners' report: Only 14% got all three and 20% scored zero. The mutation is in the transcription factor, not CD20: change its shape, stop it binding to the CD20 gene, so less CD20 mRNA and protein are made.

Epigenetics: methylation and acetylation (3.8.2.2)

Question 6

A level Paper 3 · June 2025 · Q05.2 · 1 mark · Easy

Describe one effect methylation could have on the CDH1 gene.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Stem: cleft lip and palate (CLP) can be caused by genetic and environmental factors; CDH1 is a gene involved in lip and mouth development. Scientists proposed a 'two-hit' model: a genetic hit (loss of CDH1 function) and an environmental hit (CDH1 methylation caused by inflammation in the fetus). Figure 4: bar chart of percentage CDH1 methylation for normal cells and cells with loss of CDH1 function, untreated or treated with a drug to cause inflammation; treated cells show more methylation. Question: describe one effect methylation could have on CDH1, 1 mark.
Show the mark scheme Mark scheme, any one: reduces or prevents transcription or expression of CDH1; prevents a transcription factor or RNA polymerase binding to the promoter; reduces production of the CDH1 protein. Reject methylation causing mutation; ignore 'switching off'.

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From the examiners' report: About 70% got this. Say methylation prevents transcription of the gene; vague answers about the gene being 'switched off' didn't score.

Question 7

A level Paper 2 · June 2017 · Q10.5 · 2 marks · Hard

Suggest and explain why the age at which the E280A Alzheimer's mutation is expressed varies.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Passage: Alzheimer's disease (AD) is a non-reversible brain disorder; a gene mutation called E280A on chromosome 14 causes early-onset AD at a mean age of 49, but the age at which it is expressed varies (lines 11 to 12). Question: suggest and explain one reason for this, 2 marks.
Show the mark scheme Mark scheme: epigenetics or an environmental factor such as stress, alcohol, toxins, diet, exercise or smoking; methylation of genes or acetylation of histones. Ignore gender and lifestyle.

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From the examiners' report: Over half scored zero, often by blaming acetylcholine levels or mutagens. Name an environmental factor and then the epigenetic mechanism: only 10% added methylation or acetylation for the second mark.

Question 8

A level Paper 2 · June 2019 · Q10.6 · 2 marks · Hard

Suggest and explain one way epigenetics may affect when Huntington's disease symptoms start.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Passage: Huntington's disease is caused when the protein huntingtin, produced because of a dominant mutant allele, damages the brain; symptoms usually start between 30 and 50, linked to the number of CAG repeats, but epigenetics may also affect the age when symptoms start. Question: suggest and explain one way epigenetics may affect the age when symptoms of Huntington's disease start, 2 marks.
Show the mark scheme Mark scheme, marked in pairs: increased methylation of DNA, the gene or allele inhibits transcription; or decreased methylation stimulates transcription; or decreased acetylation of histones inhibits transcription; or increased acetylation stimulates transcription. Reject acetylation of DNA; ignore methylation of histones.

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From the examiners' report: About 42% got a mark and 16% both. Say what is changed (methylation of DNA, or acetylation of histones), whether it increases or decreases, and its effect on transcription.

Question 9

A level Paper 2 · June 2022 · Q10.5 · 3 marks · Hard

Suggest and explain how drugs might reverse the epigenetic changes that cause cancers.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Passage: BRCA1 and BRCA2 code for tumour suppressor proteins; ER-positive breast cancers have receptors for oestrogen; several cancers result from epigenetic abnormalities, and treatment with drugs might be able to reverse the epigenetic changes that cause cancers (lines 16 to 17). Question: suggest and explain how, 3 marks.
Show the mark scheme Mark scheme, any three: drugs could increase methylation of oncogenes; decrease methylation of tumour suppressor genes; increased methylation of DNA inhibits transcription, or decreased methylation stimulates it; decreased acetylation of histones inhibits transcription, or increased acetylation stimulates it. Ignore methylation of histones, acetylation of DNA and proto-oncogenes.

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From the examiners' report: Only 5% got all three and 37% scored. Treat the two gene types separately: increase methylation of oncogenes, decrease methylation of tumour suppressor genes, and explain each in terms of transcription.

RNA interference and blocking translation (3.8.2.2)

Question 10

A level Paper 2 · June 2018 · Q08.4 · 1 mark · Hard

Suggest how single-stranded cDNA could stop the P34 allergy gene being expressed in soybeans.

Question text: soybeans contain a protein called P34 that causes an allergic response; scientists made transgenic soybeans that produce single-stranded cDNA, which prevents transcription of the P34 gene. Question: suggest how single-stranded cDNA could prevent transcription of the P34 gene, 1 mark.
Show the mark scheme Mark scheme: binds to the P34 gene, DNA or mRNA; or binds to the gene for a transcription factor; or binds to the promoter. Reject 'binds to transcription factor'.

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From the examiners' report: Only 30% got this. Use base pairing: the single strand is complementary, so it binds to the P34 gene or its promoter (or to its mRNA). Saying it stops RNA polymerase binding without saying how didn't score.

Question 11

A level Paper 2 · June 2019 · Q10.3 · 3 marks · Medium

Explain how a drug of single-stranded DNA reduces the concentration of huntingtin.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Passage: in the first successful drug trial to reduce huntingtin in the brain, 46 patients received a drug for 4 months; the drug contains single-stranded DNA molecules that inhibit the mRNA needed to produce huntingtin (lines 13 to 14). Question: suggest and explain how this drug could reduce the concentration of huntingtin, 3 marks.
Show the mark scheme Mark scheme: the DNA is complementary to the mRNA; binds to the mRNA for huntingtin; prevents translation. Ignore transcription.

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From the examiners' report: About 21% got all three. Many said the mRNA was 'inhibited' without saying how, or had the drug bind to the gene. Say it's complementary, binds to the mRNA, and so stops translation.

Question 12

A level Paper 3 · November 2021 · Q06.2 · 4 marks · Hard

Suggest how antisense SUT1 mRNA reduces expression of the SUT1 gene in tobacco plants.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Stem: SUT1 is a sucrose co-transporter protein in tobacco leaves. Question text: scientists genetically modified plants with an extra gene so they also made 'antisense' SUT1 mRNA as well as the normal 'sense' SUT1 mRNA; type A plants were modified and type B were not. Question: suggest how the production of antisense SUT1 mRNA in type A plants would reduce the expression of the SUT1 gene, 4 marks.
Show the mark scheme Mark scheme: antisense mRNA is complementary to sense mRNA; binds or base pairs to the sense mRNA, forming double-stranded RNA; ribosomes would not be able to bind; preventing translation or production of SUT1 protein.

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From the examiners' report: Only 2.05% got all four and 56.87% scored zero. The antisense mRNA pairs with the sense mRNA, not the gene, so ribosomes can't bind and SUT1 isn't made. Genes are transcribed; only mRNA is translated.

Question 13

A level Paper 3 · June 2017 · Q06.5 · 3 marks · Hard

Conclude how foreign DNA making single-stranded RNA cut PIP1 to 15% in transgenic poplars.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Context: aquaporins are channel proteins for water; one, PIP1, also transports carbon dioxide. Figure 6 shows a water molecule and a carbon dioxide molecule. Question text: transgenic poplars had foreign DNA leading to single-stranded RNA that specifically inhibited expression of the PIP1 gene; the amount of PIP1 in their leaves was about 15% of that in wild type. Question: what can you conclude about the effect of the foreign DNA? 3 marks.
Show the mark scheme Mark scheme, any three: the single-stranded RNA is complementary to PIP1 mRNA; binds to the mRNA or leads to its destruction; prevents or reduces translation of PIP1; reduces photosynthesis or another process that uses water. 'Less made' is not enough.

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From the examiners' report: 63% scored zero, often by not linking the single-stranded RNA to the mRNA. Say it's complementary to PIP1 mRNA, binds to it, and stops translation; then link less PIP1 to less water or carbon dioxide for photosynthesis.

Question 14

A level Paper 3 · June 2017 · Q06.6 · 1 mark · Hard

Suggest why the transgenic poplars still made some PIP1.

Context as before: transgenic poplars produce single-stranded RNA that inhibits expression of the PIP1 gene, and have about 15% of the wild-type amount of PIP1. Question: the transgenic poplars still produced some PIP1; suggest why, 1 mark.
Show the mark scheme Mark scheme: not all the mRNA is bound by the single-stranded RNA, or there is more mRNA than interfering RNA, or not all the mRNA is destroyed. Accept mutations in the transgene or not all cells having the transgene.

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From the examiners' report: Only 28% got this. Think about numbers: if there's more PIP1 mRNA than interfering RNA, some mRNA is still translated. Not every cell being transformed was also credited.

Question 15

A level Paper 3 · June 2018 · Q05.3 · 3 marks · Hard

Use electrophoresis bands to explain how siRNA reduced CENP-W and tubulin.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Question text: CENP-W is involved in forming spindle fibres, which are made of tubulin; cells were treated with siRNA that causes RNA interference of the CENP-W gene, and samples at 0, 48 and 72 hours were separated by gel electrophoresis. Figure 5: CENP-W and tubulin bands both get smaller from 0 to 48 to 72 hours. Question: suggest how the siRNA produced these results, 3 marks.
Show the mark scheme Mark scheme: siRNA binds to or destroys mRNA for CENP-W; prevents translation of CENP-W; as CENP-W falls, so does tubulin production. Reject siRNA binding to the gene or DNA; siRNA acts on CENP-W mRNA, not tubulin.

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From the examiners' report: About 17% got all three and 37% scored zero. siRNA binds to the CENP-W mRNA and stops its translation; then link less CENP-W to less tubulin. Saying siRNA stops transcription loses the first mark.

Interpreting gene expression data (3.8.2.2)

Question 16

A level Paper 2 · November 2021 · Q07.3 · 5 marks · Medium

Evaluate the use of shRNA and lhRNA to treat hepatitis B, using a bar chart with error bars.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Earlier part of the same exam question, giving the information this part uses. Context: Figure 7 shows the structure of hepatitis B virus (HBV) with HBsAg attachment proteins. Scientists infected mouse liver cells with HBV and added either short hairpin RNA (shRNA) or long hairpin RNA (lhRNA); HBsAg concentration measures HBV replication. Figure 8: mean HBsAg as a percentage of the control, about 7.5% for shRNA and 50% for lhRNA, with error bars of ±2 standard deviations that don't overlap. Question: evaluate the use of the two types of RNAi in treating hepatitis B in humans, without saying how RNAi works, 5 marks.
Show the mark scheme Mark scheme, any five (4 max from points 4 to 10): both are more effective than the control; the difference is significant or not due to chance; as the SDs don't overlap; HBsAg is reduced but not to zero; done in mice, not humans; shRNA 7.5% compared with 50% for lhRNA; no sample size; long-term or side effects not known; no statistical test; done in vitro, not in vivo.

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From the examiners' report: About 14% got all five. Being in mice, not humans, was the most common mark; link the non-overlapping SDs to a significant difference, quote the figures, and add side effects, sample size or in vitro.

Question 17

A level Paper 3 · June 2018 · Q06.4 · 2 marks · Medium

Use a log-scale bar chart to decide which bacterium's amoA mRNA changed more with soil pH.

Question text: each species of nitrifying bacteria has its own amoA gene coding for ammonia monooxygenase; species S (from acid soil) and T (from neutral soil) were grown in soils of different pH and the copies of amoA mRNA measured. Figure 7: bar chart of copies of mRNA per gram of soil on a log scale (10 to 10⁶) against pH 4.9 to 7.5; S falls from 10⁶ to 10⁴ and T rises from 10² to 10⁴. Question: in which species was the number of copies of mRNA more affected by pH from 4.9 to 7.5? Use a calculation, 2 marks.
Show the mark scheme Mark scheme: species S changes by 990 000 and species T by 9 900 per gram of soil; or species S has a 99% change and species T a 9900% change. One mark for '100 times greater' alone.

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From the examiners' report: 42% got both. Convert the powers of ten to numbers before subtracting: students who treated 10⁶ and 10⁴ as 6 and 4 said both changed by 2 and scored nothing.

Question 18

A level Paper 3 · June 2018 · Q06.5 · 4 marks · Hard

Explain why amoA mRNA copies show gene expression but not population growth.

Context: Figure 7 as before, copies of amoA mRNA per gram of soil for species S and T at different pH. Question: this method allowed the scientists to estimate expression of the amoA gene in each culture but not the growth of the bacterial population; explain why, 4 marks.
Show the mark scheme Mark scheme: they didn't count the bacteria or cells; copies of mRNA relate to the amount of enzyme produced; don't know how much mRNA each cell produces; don't know if amoA is linked to cell division or population growth.

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From the examiners' report: The worst-answered part of the paper; 11% didn't attempt it and few scored more than one. Point out that no cells were counted, and that mRNA per cell can vary, so mRNA copies measure expression, not numbers.

Where students lose marks (from AQA examiners' reports and mark schemes)

Each point below is followed by wording that gained marks.

  • Name where the transcription factor binds: Only 54% scored on how the androgen receptor stimulates gene expression; DNA polymerase, methylation and histones were common wrong turns. On iPS cells, many stopped at genes being 'switched on' or 'expressed', which isn't enough.

    ✔ Gains credit: "(AR is) a transcription factor; binds to DNA/promoter; (stimulates) RNA polymerase."

  • Look beyond the gene itself for lactase persistence: Only 18% got a mark and 5% got both. Students mutated the lactase protein, invented new genes or blamed methylation, instead of a promoter or a transcription factor gene.

    ✔ Gains credit: "Mutation in promoter (region/DNA) for the gene OR mutation in gene for transcription factor; lactase gene continues to be transcribed."

  • Say what is methylated and the effect on transcription: On Huntington's disease only 16% got both marks. Many left out DNA or the gene when describing methylation, left out 'increased' or 'decreased', or methylated histones and acetylated DNA, which are both ignored or rejected.

    ✔ Gains credit: "(Increased) methylation of DNA/gene/allele; inhibits/prevents transcription" or "Increased acetylation of histone(s); stimulates/allows transcription."

  • Oncogenes and tumour suppressors need opposite changes: Only 5% got all three marks for how drugs might reverse epigenetic cancers. Oncogenes were rarely mentioned and were often confused with proto-oncogenes, and some said epigenetic changes cause mutations.

    ✔ Gains credit: "(Drugs could) increase methylation of oncogene(s); (drugs could) decrease methylation of tumour suppressor gene(s)."

  • siRNA acts on the mRNA, not the DNA: 37% scored zero on how siRNA reduced CENP-W. Many thought siRNA binds to the gene and prevents transcription; the mark scheme rejects that and wants CENP-W named.

    ✔ Gains credit: "siRNA binds to/destroys mRNA for CENP-W; prevents translation of CENP-W; (as) CENP-W reduces so does tubulin production."

  • Genes are transcribed; mRNA is translated: 56.87% scored zero on antisense SUT1 mRNA and only 2.05% got all four. The ER calls 'translation of the SUT1 gene is prevented' a fundamental mistake, and many had the antisense mRNA binding to the gene.

    ✔ Gains credit: "Antisense mRNA is complementary to 'sense' mRNA; would bind to (sense) mRNA; ribosomes would not be able to bind; preventing translation."

  • Treat a log axis as powers of ten: On the amoA bar chart 42% got both marks. Students who read only the powers said both species fell by 2 and scored nothing.

    ✔ Gains credit: "Species S change of 990,000 (per gram of soil); species T change of 9,900" (or 99% compared with 9900%).

  • mRNA copies don't count the cells: This was the worst-answered part of the paper and 11% didn't attempt it. Few saw that the bacteria were never counted, so the method only shows how much amoA is being made.

    ✔ Gains credit: "They didn't count bacteria/cells; don't know how much mRNA/amoA produced by each cell; don't know if amoA is linked to cell division/growth."

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Download the PDF pack (18 questions, mark schemes at the end)

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Questions, mark schemes and examiners' report extracts © AQA.

Tom Whitburn
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