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Home › Unit 8 — Gene Expression › Regulation Transcription & Translation

Regulation Transcription & Translation

January 11, 2026
This page covers AQA spec point 3.8.2.2 Regulation of transcription and translation, which is within 3.8.2 Gene expression is controlled by a number of features

The diagram below outlines the ways in which gene expression (transcription and translation) can be controlled

  • Regulation of transcription
    • Transcription factors (Steroid hormones)
    • Epigenetic changes
    • Unregulated transcription (Cancer & gene expression)
  • Regulation of translation
    • RNA interference

Transcription Factors

Spec Point

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.

  • Transcription of genes controlled by transcription factors

  • Transcription factors move to nucleus to bind to specific DNA sites of target genes (genes they want to control the expression of)

  • Activators: Increase rate of transcription

    • Bind to specific DNA sites promoter region (or enhancer region)
    • Increase transcription by stimulating the binding of RNA polymerase to the promoter
    • RNA polymerase binds to the promoter region of a gene to initiate transcription

  • Repressors: Decrease rate of transcription

    • Bind to specific DNA sequences called silencer regions
    • Reduce transcription by preventing RNA polymerase binding to promoter
    • As a result, RNA polymerase can’t bind to the promoter, so transcription is reduced or prevented

Oestrogen Receptor (TF)

The image below shows an example of how the steroid hormone oestrogen initiates transcription.

Mechanism for ER

  1. Oestrogen is lipid soluble so diffuses through phospholipid membrane
  2. It binds to the complementary site of the transcription factor (Oestrogen Receptor, ER) inside the cytoplasm
  3. This binding of oestrogen causes the ER to change shape, along with its DNA binding site
  4. ER can now move into the nucleus and bind to specific DNA sites near start of target gene (promoter region).
  5. This stimulates RNA polymerase and allows it to bind to the promoter region
  6. This initiates transcription

Epigenetics

Spec Point

Epigenetic control of gene expression in eukaryotes. 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 the DNA or decreased acetylation of associated histones.

Epigenetics is the heritable changes in gene expression, without changes to the base sequence of DNA. These changes are caused by environmental factors and affect the regulation of transcription.

Epigenome

The epigenome is a collection of chemical marks on your DNA and histone proteins that act like switches, telling your genes when, where, and how strongly to turn on or off, without changing the DNA sequence itself.

The epigenome is flexible and can respond to environmental changes, e.g. stress, diet, and can affect how the genes are expressed.

- Directors cut analogy

A good way to think of it, is the genome is the script, and the epigenome is the director’s cut. Once the script has been agreed (fixed) the director can make edits to how they want the actors to play out the scene (I’m not a movie director so take this with a pinch of salt).

What are these chemical marks/modifications? There are two main mechanisms of epigenetic control highlighted in image below

  1. Acetylation of histones
  2. Methylation of DNA

Acetylation of histones

Before discussing acetylation and deacetylation, it is important to understand that:

  • Histone proteins have a positive charge (+)
    • This is due to the presence of lysine residues on histone tails, which are positively charged.
  • DNA has a negative charge (–)
    • This is due to the phosphate groups in the DNA backbone, which are negatively charged.
  • Adding or removing acetyl groups changes the charge on histones, affecting the attraction between histones and DNA.

Acetylation

  • Involves the addition of an acetyl group to histone tails, using acetyl-CoA
  • Acetylation neutralises (reduces) the positive charge on the histones
  • This reduces the attraction between the positively charged histones and negatively charged DNA
  • As a result, chromatin becomes less condensed (forming euchromatin)
  • DNA becomes more accessible to transcription factors and RNA polymerase, allowing gene transcription to occur

Deacetylation

  • Histone deacetylation involves the removal of acetyl groups from histones
  • Removal of acetyl groups restores the positive charge on histones
  • This increases the attraction between positively charged histones and negatively charged DNA
  • Chromatin becomes more tightly packed (forming heterochromatin)
  • DNA becomes less accessible to transcription factors and RNA polymerase
  • As a result, transcription is reduced or inhibited, and gene expression is decreased

Methylation of DNA

  • Involves the addition of a methyl group (–CH3) to DNA sequence (cytosine bases)
  • This prevents transcription factors and RNA polymerase from binding to promoter
  • This inhibits transcription and expression of the specific gene is reduced or silenced

Spec Point

The relevance of epigenetics on the development and treatment of disease, especially cancer.

Epigenetics plays a role in normal development but can also contribute to disease, such as cancer. For example, cancer cells may show increased DNA methylation of certain genes, causing these genes to be silenced. Potential epigenetic treatments include drugs that inhibit DNA methylation or histone deacetylation, which can lead to the reactivation of genes that have been silenced.

Further detail on cancer and epigenetics is covered in Gene Expression & Cancer

Epigenetics and inheritance

  • Epigenetic markers (e.g histone modification, methylation) can be passed from parent cell to daughter cells within the same individual. For example, when liver cells divide by mitosis, epigenetic markers are maintained in the daughter cells. This helps to preserve cell identity, so liver cells remain liver cells.

  • Some evidence exists to say that epigenetic changes may also persist across generations and be passed to offspring, influencing the gene expression of the offspring. However, the evidence is limited and context dependent.

    • Example of agouti mouse model demonstrates epigenetic inheritance where genetically identical mice have different coat colours due to varying expression of the Agouti gene
    • 2002 study link for interest

RNA Interference

Spec Point

In eukaryotes and some prokaryotes, translation of the mRNA produced from target genes can be inhibited by RNA interference (RNAi).

How does RNA interference work?

  • A small RNA molecule, small interfering RNA (siRNA) can inhibit the translation of mRNA into polypeptide, silencing gene expression for specific proteins.

Mechanism for RNA interference

  1. Dicer enzyme breaks up double stranded RNA (dsRNA) into siRNA
  2. One strand of siRNA binds to a protein complex, RNA-induced silencing complex (RISC)
  3. The RISC-siRNA complex can bind to the target mRNA.
  4. The siRNA strand pairs with complementary bases on mRNA
  5. The enzyme within the protein complex cuts mRNA
  6. The mRNA is degraded and cannot be translated into a polypeptide, so the protein is not produced and the gene is not expressed

I thought RNA was single stranded?

RNA is usually single stranded, such as mRNA. However, double stranded (dsRNA) can occur in some instances, e.g viruses.

Additional For Interest

RNA interference has potential therapeutic applications because it can be used to silence the expression of specific genes whose protein products cause or contribute to disease. https://www.alnylam.com/our-science/the-science-of-rnai

Exam Question Practice

Question 1

Recent research has indicated that several cancers result from epigenetic abnormalities.

Treatment with drugs might be able to reverse the epigenetic changes that cause cancers. Suggest and explain how.

(4 marks)
Hint

Think about how methylation and acetylation affect oncogenes vs tumour suppressor genes differently.

Answer

Mark Scheme

  1. (Drugs could) increase methylation of oncogene(s) (1 mark)
  2. (Drugs could) decrease methylation of tumour suppressor gene(s) (1 mark)
  3. (Increased) methylation of DNA/gene(s) inhibits transcription/expression (of genes) OR Decreased methylation of DNA/gene(s) stimulates transcription/expression (of genes) (1 mark)
  4. Decreased acetylation of histones inhibits transcription/expression (of genes) OR (Increased) acetylation of histones stimulates transcription/expression (of genes) (1 mark)
Comments from mark scheme
  • Ignore methylation of histones and acetylation of DNA/genes
  • Ignore protooncogenes
  • Accept promoter (region) for DNA/gene
  • Ignore ‘switching on’ and ‘switching off’ genes once but accept as alternative(s) for 1 mark if used correctly in context of transcription/expression for both points 3 and 4
Question 2

Effective treatment of ER-positive breast cancers often involves the use of drugs which have a similar structure to oestrogen.

Suggest and explain how these drugs are an effective treatment of ER-positive breast cancers.

(3 marks)
Hint

Think about competitive inhibition - what happens if a similar-shaped molecule binds to the receptor instead?

Answer

Mark Scheme

  1. (Drug) binds to (oestrogen/ER) receptor (1 mark)
  2. Prevents binding of oestrogen/hormone (1 mark)
  3. No/fewer transcription factor(s) bind to promoter OR RNA polymerase not stimulated/activated (1 mark)
Comments from mark scheme
  • Accept (inactive) transcription factor for receptor
  • Reject active site/enzyme-substrate complex once only
Question 3

Describe how alterations to tumour suppressor genes can lead to the development of tumours.

(3 marks)
Hint

Think about what can alter a gene (mutation or epigenetic change) and what tumour suppressor genes normally do.

Answer

Mark Scheme

  1. (Increased) methylation (of tumour suppressor genes) OR Mutation (in tumour suppressor genes) (1 mark)
  2. Tumour suppressor genes are not transcribed/expressed OR Amino acid sequence/primary structure altered (1 mark)
  3. (Results in) rapid/uncontrollable cell division (1 mark)
Question 4

CENP-W is involved in the formation of spindle fibres in mitosis. Spindle fibres are made of molecules of a protein called tubulin.

The scientists treated cells in a culture with small interfering RNA (siRNA). This siRNA causes RNA interference of expression of the CENP-W gene. The scientists took samples of cells at 0, 48 and 72 hours after adding the siRNA. They then used gel electrophoresis to separate CENP-W and tubulin from these samples.

Figure 5 shows the results of the electrophoresis. The size of each band is proportional to the amount of CENP-W or tubulin present.

Suggest how the siRNA produced these results.

(3 marks)
Hint

Think about what siRNA binds to and prevents, and how CENP-W relates to tubulin production.

Answer

Mark Scheme

  1. siRNA binds to / destroys mRNA for CENP-W (1 mark)
  2. Prevents translation of CENP-W (1 mark)
  3. (After / as) CENP-W reduces so does tubulin production (1 mark)
Comments from mark scheme
  • Reject if siRNA binds to gene/DNA
  • Context is important - siRNA acts on mRNA for CENP-W, not tubulin
  • Ref. to CENP-W required once for MP1 and MP2
  • Accept reduces translation of CENP-W

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