Biology • Year 12 • Module 5 • Lesson 7
Mitosis — Maintaining Genetic Stability in Somatic Cells
Build HSC Band 5–6 extended-response technique on mitosis, chromosome-number maintenance and the role of genetic stability in growth, repair and asexual reproduction.
1. Extended response — chromosome number through one cell cycle (Band 5–6)
8 marks Band 5–6
Stimulus. Researchers using flow cytometry can measure how much DNA each cell in a human cell-culture sample contains (in "C" units, where 2C is the DNA content of an unreplicated diploid somatic cell). The figure below shows the proportion of cells at each DNA content for a population of human fibroblasts grown in standard conditions. A vertical dashed line marks 2C (unreplicated diploid) and another marks 4C (post-replication, before division). Throughout, the cells are diploid somatic cells with 2n = 46 chromosomes.
Figure 1.1. DNA-content distribution in a population of human fibroblast somatic cells (illustrative, after typical flow-cytometry profiles).
Q1. Analyse and evaluate, using the figure and lesson content, how mitosis maintains genetic stability in this population of somatic cells. In your response you must:
- Identify what the 2C and 4C peaks represent in terms of DNA replication and the events of the cell cycle.
- Use the figure to estimate the proportion of cells in the population that have already replicated their DNA (i.e. are at ~4C) and the proportion that have not.
- Explain, with reference to anaphase and cytokinesis, why a cell at 4C will return to 2C without the chromosome number changing (still 2n = 46).
- Use a named example from the lesson (skin, gut lining, blood cell production or wound repair) to show why maintaining the 2C-to-2C cycle matters for the tissue.
- Reach an evidence-based judgement about whether the figure is consistent with the lesson's claim that mitosis is about stability, not reduction.
2. Extended response — comparing regenerative capacity across two tissues (Band 5–6)
7 marks Band 5–6
Stimulus. A clinical study tracked recovery in two groups of patients over 12 months after equivalent tissue injuries. Group A suffered a 4 cm² full-thickness skin wound. Group B suffered comparable damage to cardiac muscle after a myocardial infarction. Tissue restored (% of original lost area replaced by the original cell type) and residual scar/fibrous tissue (% of injury site) were measured.
| Tissue group | Original cell type replaced (12-month %) | Scar / fibrous tissue (12-month %) | Function recovered (clinical assessment) |
|---|---|---|---|
| A — skin wound | ~94% | ~6% | Near-complete (sensation + barrier restored) |
| B — cardiac infarct | ~3% | ~97% | Permanent reduction in pumping ability |
Illustrative figures consistent with widely reported regeneration outcomes in adult human skin vs cardiac muscle.
Q2. Analyse the difference in regenerative outcome between the two tissues and justify why this difference traces back to the role of mitosis. In your response you must:
- Define mitosis and link it explicitly to growth and repair in somatic cells.
- Identify, from the data, the size of the difference in original-cell-type replacement between the two tissues.
- Explain why skin (high mitotic capacity) can regenerate the original cell type, while cardiac muscle (very low mitotic capacity) is largely replaced by scar tissue.
- Use lesson content to explain the functional consequence of relying on scar tissue rather than on mitosis-driven repair.
- Reach an explicit evaluative judgement linking the data back to the lesson's claim that mitosis is essential for tissue continuity, and stating one limitation of using only this dataset to make that claim.
Q1 — Sample Band 6 response (8 marks), annotated
The 2C peak represents fibroblast cells whose DNA has not yet been replicated for the next mitotic division — each chromosome consists of a single chromatid. The 4C peak represents cells that have completed DNA replication, so each chromosome now exists as two identical sister chromatids; these cells are ready to enter mitosis. [1 — identifies 2C and 4C in terms of replication]
From the figure, approximately 22% of cells are at 4C (already replicated), and approximately 42% are at 2C (unreplicated). The intermediate plateau (~10% each across the 2C–4C span, totalling ~40%) represents cells currently replicating their DNA (S phase). So the figure splits roughly into "already replicated and ready to divide" (~22%) and "not yet replicated or still replicating" (~78%). [1 — quantitative reading from figure]
A cell at 4C carries 46 replicated chromosomes (each as two sister chromatids), so the total DNA is doubled but the chromosome count is still 46. In anaphase, the sister chromatids of each replicated chromosome are pulled to opposite poles, so each future daughter nucleus receives one chromatid (now counted as a chromosome) for every chromosome the parent had. After cytokinesis, the cytoplasm is divided into two cells, each containing 46 chromosomes' worth of DNA — i.e. back to 2C. The DNA content has halved (4C → 2C in each daughter), but the chromosome number has been maintained at 2n = 46. [1 — anaphase/cytokinesis mechanism; 1 — distinguishes DNA content from chromosome number]
This matters for tissues that depend on continual replacement of somatic cells. For example, in the gut lining, surface cells are shed into the lumen every few days and must be replaced by new cells produced by mitosis in the crypt — those replacement cells must be genetically identical (same chromosome number, same hereditary information) so they perform the same absorption and barrier functions. The figure shows that at any moment a large fraction of the population is preparing for or undergoing this 2C → 4C → 2C cycle, exactly as required for tissue maintenance. [1 — named lesson example linked to maintenance]
Crucially, no cell in the figure falls below 2C — there is no peak at 1C, which would indicate chromosome-number reduction (the signature of meiosis). The data are therefore consistent with the lesson's claim that mitosis is about stability, not reduction: DNA content oscillates between 2C and 4C, but chromosome number stays at 2n. [1 — evidence-based judgement]
One limitation: the figure shows DNA content, not chromosome number directly, so this conclusion relies on the assumption that no aneuploidy or chromosomal rearrangement is occurring. Within that assumption, however, the data fully support the lesson's framing. [1 — acknowledges assumption; 1 — overall integration in precise lesson terminology]
Q2 — Sample Band 6 response (7 marks), annotated
Mitosis is cell division that produces two daughter somatic cells with the same chromosome number and hereditary information as the parent cell. Its role in growth and repair is to replace lost or damaged cells with genetically identical new cells of the same type, so the tissue continues to function normally. [1 — definition + growth/repair link]
The data show a striking 31-fold gap in original-cell-type replacement at 12 months: skin restores roughly 94% of the lost tissue as new skin, while cardiac muscle restores only ~3% as new cardiac muscle. Correspondingly, scar tissue replaces only ~6% of the skin injury but ~97% of the cardiac injury. [1 — quantitative comparison from data]
The skin epidermis has a high mitotic index — the basal layer continually divides and is upregulated by injury, so a wound is rapidly closed with new, genetically identical somatic skin cells (Card 4 / Misconceptions box). Cardiac muscle, in contrast, has a mitotic index near zero in adults; the lesson explicitly notes that cardiac muscle has very limited mitotic capacity and cannot easily be replaced after damage. With little mitosis, the dead area is filled instead by proliferating fibroblasts producing collagen — i.e. scar tissue. [1 — links the data to lesson statement about high vs low mitotic capacity]
The functional consequence is significant: scar tissue restores structural integrity (the heart wall is not left as a hole) but does not contract like cardiac muscle. Pumping ability is therefore permanently reduced, as the clinical assessment column shows. Skin can recover near-complete function precisely because mitosis is able to replace like with like rather than substituting a fibrous patch. [1 — functional consequence + contrast with skin]
Connecting back: the lesson's claim that mitosis is essential for tissue continuity is strongly supported. Tissues with active mitosis maintain themselves (skin, gut lining, blood); tissues without active mitosis cannot, and depend instead on scar formation, which trades function for closure. [1 — evaluative judgement linking data to lesson claim]
However, one limitation of this dataset alone is that it compares only two tissues, with no information on factors that vary between them (vascularity, inflammatory response, age of patients). To attribute the difference fully to mitotic capacity, additional evidence — for example histological counts of dividing cells at the wound edge in each tissue, or comparison with tissues of intermediate mitotic capacity such as liver — would be needed. [1 — explicit limitation]
Within those limits, the data are consistent with the lesson's framing: mitosis is the engine of genetic stability and tissue continuity in somatic cells, and tissues that cannot run it pay a long-term functional price. [1 — overall integration in precise lesson terminology]