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MRCP Part 1 Cell Biology: DNA Repair Mechanisms — The Ultimate List

TL;DR:

 This guide covers MRCP Part 1 DNA repair mechanisms with an exam-focused breakdown of the five most tested pathways, classic disease associations, and common traps. It includes a high-yield table, a short MRCP-style MCQ, and a practical revision checklist to maximise marks. Use it alongside the MRCP hub and question practice for consolidation.


Why this matters for MRCP Part 1

Cell biology questions in MRCP Part 1 are designed to test integration, not memorisation alone. DNA repair mechanisms sit at the intersection of molecular biology, oncology, and inherited disease—making them ideal exam material. Candidates who can quickly identify the type of DNA damage, map it to the correct repair pathway, and recognise the clinical association score consistently higher.

This article supports the core MRCP Part 1 syllabus and should be read alongside genetics and oncology revision.

Key hub for revision:

Scope: what the examiners actually test

In MRCP Part 1, DNA repair questions typically focus on:

  • The type of DNA lesion

  • The primary repair mechanism

  • Key enzymes or genes

  • Associated inherited syndromes

  • Cancer predisposition patterns

Five pathways account for the vast majority of questions. Others appear mainly as distractors.


The 5 most tested DNA repair mechanisms (high-yield)

1. Nucleotide excision repair (NER)

  • Repairs: Bulky, helix-distorting lesions

  • Typical damage: UV-induced thymine dimers

  • Mechanism: Segment of damaged DNA is excised and resynthesised

  • Classic association: Xeroderma pigmentosum

Exam clue: Severe photosensitivity, early-onset skin cancers.

2. Base excision repair (BER)

  • Repairs: Small, non-bulky base damage

  • Examples: Oxidation, deamination, depurination

  • Key enzyme: DNA glycosylase

Exam clue: Single-base lesions with no helix distortion.

3. Mismatch repair (MMR)

  • Repairs: Replication errors (base mismatches, insertion–deletion loops)

  • Key genes: MLH1, MSH2, MSH6, PMS2

  • Classic association: Lynch syndrome (HNPCC)

Exam clue: Microsatellite instability, right-sided colorectal cancer.

4. Homologous recombination (HR)

  • Repairs: Double-strand DNA breaks (DSBs)

  • Template: Sister chromatid

  • Cell cycle: S and G2 phases

  • Key genes: BRCA1, BRCA2

Exam clue: Breast and ovarian cancer predisposition.

5. Non-homologous end joining (NHEJ)

  • Repairs: Double-strand breaks without a template

  • Cell cycle: Any phase

  • Key feature: Error-prone

  • Clinical relevance: V(D)J recombination

Exam clue: Immunodeficiency due to impaired lymphocyte development.


Medical student revising cell biology concepts for MRCP Part 1 examination

One-table summary (exam essential)

DNA damage type

Repair mechanism

Key genes/enzymes

Classic association

UV thymine dimers

Nucleotide excision repair

XP proteins

Xeroderma pigmentosum

Oxidised bases

Base excision repair

DNA glycosylase

—

Replication mismatch

Mismatch repair

MLH1, MSH2

Lynch syndrome

DSB (accurate)

Homologous recombination

BRCA1/2

Breast/ovarian cancer

DSB (error-prone)

Non-homologous end joining

Ku proteins

SCID variants

Lower-yield mechanisms (know, but don’t overlearn)

  • Direct repair: O⁶-methylguanine-DNA methyltransferase

  • Translesion synthesis: Error-prone polymerases bypass lesions

  • Cell-cycle checkpoints: ATM and ATR coordinate repair rather than repairing DNA directly

These usually appear as incorrect options.


Mini-case: MRCP-style question

Question A 21-year-old man develops severe sunburn after brief sun exposure. He has multiple lentigines and has already undergone excision of two basal cell carcinomas. Which DNA repair mechanism is most likely defective?

Answer: Nucleotide excision repair.

Explanation: UV light causes bulky thymine dimers that distort the DNA helix. These lesions are normally removed by nucleotide excision repair. Failure results in xeroderma pigmentosum with marked photosensitivity and early skin malignancy.

For further practice, use the MRCP Qbank:https://crackmedicine.com/qbank/


The 5 most common exam traps

  • Confusing BER with NER

  • Assuming BRCA genes are involved in mismatch repair

  • Forgetting that homologous recombination is cell-cycle specific

  • Choosing “ATM mutation” when a repair pathway is asked

  • Forgetting that NHEJ is inherently error-prone


How examiners phrase DNA repair questions

Look for:

  • Exposure clues: UV light, smoking, chemotherapy

  • Cancer patterns: Early onset, multiple primaries

  • Immune clues: Recurrent infections suggesting NHEJ defects

Always map: clue → damage → repair mechanism → disease.


Practical study-tip checklist

  • Memorise the single summary table above.

  • Pair each pathway with one classic disease only.

  • Practise mixed cell-biology questions weekly.

  • Revisit DNA repair the day before a full mock.

  • Avoid excessive time on rare mechanisms.

Timed practice:


FAQs

Which DNA repair mechanism is most commonly tested in MRCP Part 1?Nucleotide excision repair and mismatch repair appear most frequently, usually with classic clinical syndromes.

How can I quickly differentiate BER from NER in the exam?

BER fixes small, single-base damage; NER removes bulky, helix-distorting lesions such as UV dimers.

Are BRCA genes part of mismatch repair?

No. BRCA1 and BRCA2 function in homologous recombination for double-strand break repair.

Is non-homologous end joining accurate?

No. NHEJ is error-prone but essential when no sister chromatid is available.


Ready to start?

Revise this topic alongside the MRCP Part 1 overview, then test retention using targeted questions in the Qbank and timed sessions in mock tests. For deeper reading, see our sibling post on high-yield MRCP genetics.


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