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Spec mapping: AQA 7402 Section 3.2.1.1 — cell structure of prokaryotic and eukaryotic cells (refer to the official AQA specification document for exact wording).
All living organisms are composed of cells, the fundamental unit of biology. The recognition that life is cellular — and that cells arise only from pre-existing cells — was one of the most consequential intellectual transitions in the history of biology, taking nearly two centuries from the first observations of cellular structure to its consolidation as a unifying theory. At A-Level you are expected to understand not only the morphology of prokaryotic and eukaryotic cells but also why the differences matter: how they constrain metabolism, reproduction, evolutionary trajectory, and clinical vulnerability to drugs. This lesson lays the foundation for everything that follows in the unit, from organelle ultrastructure through to antigen presentation and the immune response.
Key Definition: A prokaryotic cell is a cell that lacks a true membrane-bound nucleus and lacks membrane-bound organelles. Prokaryotes comprise the domains Bacteria and Archaea. A eukaryotic cell possesses a true membrane-bound nucleus enclosing linear chromosomes, and a range of membrane-bound organelles that compartmentalise the cell's metabolism.
The cell theory did not arrive fully formed. Its development illustrates how A-Level biology depends on a chain of observation, microscopy improvement and conceptual synthesis.
The modern cell theory therefore states: (1) all living organisms are composed of one or more cells; (2) the cell is the basic unit of structure and function in living organisms; (3) all cells arise from pre-existing cells by division. Viruses sit outside this theory because they are acellular and cannot reproduce independently.
Eukaryotic cells are found in animals, plants, fungi and protoctists. They share the following features that you must be able to describe in structural and functional terms.
Exam Tip: When asked to compare animal and plant cells, list the features they share (nucleus, mitochondria, ribosomes, ER, Golgi, cell surface membrane) before listing features unique to plant cells (cell wall, chloroplasts, large permanent vacuole, plasmodesmata). Do not write that animal cells have no vacuoles — small temporary vacuoles do occur.
Prokaryotic cells are typically 1–5 µm in diameter, an order of magnitude smaller than most eukaryotic cells (10–100 µm). The small size is consequential: surface area to volume ratio is high, supporting rapid metabolism, and the small cytoplasmic volume can be efficiently regulated without internal compartmentation.
| Feature | Prokaryotic Cell | Eukaryotic Cell |
|---|---|---|
| Typical size | 1–5 µm | 10–100 µm |
| Nucleus | No true nucleus; nucleoid region | True membrane-bound nucleus |
| DNA | Circular, 'naked' (no histones) | Linear, associated with histones |
| Plasmids | Often present | Generally absent (rare in yeast) |
| Ribosomes | 70S (50S + 30S) | 80S (60S + 40S) cytoplasmic; 70S in mitochondria/chloroplasts |
| Membrane-bound organelles | Absent | Present |
| Cell wall | Peptidoglycan (murein) | Cellulose (plants), chitin (fungi), absent (animals) |
| Reproduction | Binary fission | Mitosis (and meiosis) |
| Flagella | Simple flagellin propeller | Complex 9 + 2 microtubule arrangement |
| Cytoskeleton | Rudimentary | Well-developed (microtubules, microfilaments, intermediate filaments) |
Prokaryotes reproduce asexually by binary fission, a process distinct from eukaryotic mitosis: there is no spindle apparatus, no chromosome condensation, no nuclear envelope breakdown (because there is no nucleus to dismantle), and no defined phases.
Binary fission can be very rapid — Escherichia coli can divide every 20 minutes under optimal conditions, meaning a single cell could in principle generate >10⁹ descendants overnight. In practice, exponential growth saturates due to nutrient limitation. Rapid reproduction matters clinically: a beneficial mutation, or a plasmid carrying antibiotic resistance acquired by conjugation, can sweep through a bacterial population within hours, explaining how clinical drug resistance emerges so quickly.
Exam Tip: When comparing binary fission with mitosis, emphasise that binary fission has no spindle, no chromosome condensation and no nuclear envelope breakdown. Both processes produce genetically identical daughter cells barring mutation, but mitosis is part of the eukaryotic cell cycle and has discrete phases (prophase, metaphase, anaphase, telophase).
The endosymbiont theory, championed in its modern form by Lynn Margulis in the 1960s, proposes that mitochondria and chloroplasts originated as free-living prokaryotes engulfed by an ancestral eukaryotic cell.
Evidence supporting endosymbiosis:
The theory not only explains a strange set of organelle features but also reframes the major eukaryotic transition as a collaboration between two cell types rather than the gradual evolution of internal complexity from a single ancestor.
The Danish bacteriologist Hans Christian Gram developed a stain in the 1880s that distinguishes two major classes of bacteria by cell wall architecture. This is not the focus of the AQA spec but provides important clinical context.
Cell size is not a free parameter. The diffusion limit and metabolic considerations constrain how large a cell can grow.
For a spherical cell of radius r:
As cells get larger, their SA:V ratio falls. Material exchange across the cell surface becomes inadequate relative to metabolic demand within the cell volume. This explains why prokaryotic cells, at 1–5 µm, exchange materials efficiently by simple diffusion, while eukaryotic cells in the 10–100 µm range require infoldings (microvilli), specialised transport (organelle systems) and active transport pumps to maintain adequate exchange.
Several adaptations partially circumvent the SA:V constraint:
These adaptations represent recurring evolutionary solutions to the same physical constraint, and AQA examines them as transferable principles applied to gas exchange, kidney function, root water uptake and muscle physiology in later units.
A typical AQA AO2 calculation will give you a micrograph, a scale bar, and ask for the actual size of a cell or organelle. Practise the workflow:
This procedure is consistent with the magnification triangle introduced in lesson 2. AQA expects unit-consistent calculations and clear unit reporting in the answer.
| Feature | Eukaryotic cell | Prokaryotic cell |
|---|---|---|
| Genetic material | Nucleus with nucleolus, linear chromosomes | Nucleoid (no membrane), single circular chromosome |
| Ribosomes | 80S in cytoplasm (mitochondria 70S) | 70S |
| Membrane-bound organelles | Mitochondria, RER, Golgi, lysosomes | None |
| Cytoskeleton | Microtubules + actin + intermediate filaments | Bacterial cytoskeletal homologues (FtsZ, MreB) |
| Cell wall | Cellulose (plants), chitin (fungi); absent in animals | Peptidoglycan |
| Extras | — | Plasmids, capsule, pili, flagella |
| Typical diameter | 10–100 µm | 1–5 µm |
Specimen question modelled on the AQA paper format
Compare and contrast the structure of a prokaryotic cell with that of a eukaryotic animal cell, and explain how two structural differences affect cellular function. [6 marks]
AO breakdown: AO1 (knowledge of structures) 3 marks; AO2 (application to function) 3 marks.
Prokaryotic cells have no nucleus and no membrane-bound organelles, while eukaryotic animal cells have a true nucleus and organelles like mitochondria. Prokaryotic DNA is circular and naked, whereas eukaryotic DNA is linear and wrapped around histones. Prokaryotic cells have a peptidoglycan cell wall that animal cells lack. Prokaryotic ribosomes are 70S; eukaryotic ribosomes in the cytoplasm are 80S. Because prokaryotes are smaller, they have a higher surface area to volume ratio so they can exchange materials more quickly. The peptidoglycan wall is the target of antibiotics like penicillin, which is why penicillin does not damage animal cells.
Examiner commentary: M1 nucleus comparison, M1 DNA comparison, M1 ribosome comparison, M1 cell wall, M1 SA:V link to function, M1 penicillin/peptidoglycan link. This is a complete C-grade answer because every mark-scheme point is named, but the language is plain and the structure–function links are short. To reach A*, the answer needs to deepen the mechanistic explanation.
Prokaryotic and eukaryotic cells share the basic features that define life — a phospholipid cell surface membrane, ribosomes carrying out translation, a genome of DNA, and a cytoplasm of metabolic enzymes — but they differ profoundly in compartmentation and scale. Prokaryotic cells lack a true nucleus: their single circular chromosome lies in the nucleoid region, not separated from translation machinery, which permits coupled transcription–translation and very rapid protein production. Eukaryotic cells confine transcription within the nuclear envelope, allowing mRNA processing (splicing, capping, polyadenylation) before translation. The 70S prokaryotic ribosome (50S + 30S) versus the 80S eukaryotic ribosome (60S + 40S) is exploited clinically — tetracyclines and macrolides bind selectively to 70S ribosomes, so they inhibit bacterial protein synthesis without poisoning the host's 80S ribosomes (though mitochondrial 70S ribosomes can be affected, contributing to side-effects). The peptidoglycan cell wall of bacteria — absent from animal cells — is the target of β-lactam antibiotics like penicillin, which inhibit the transpeptidase cross-linking step. Selective toxicity is therefore a direct consequence of evolved structural differences.
Examiner commentary: M1 nucleus + coupled transcription-translation, M1 DNA + mRNA processing, M1 ribosome difference + selective drug targeting, M1 peptidoglycan + penicillin, M1 SA:V or chromosomal organisation, M1 evaluative selective-toxicity synthesis. The A* response embeds named drug classes and explicit mechanistic links (transpeptidase, coupled transcription–translation) that move beyond surface description.
Many candidates lose marks on this topic by:
Viruses do not fit cleanly into the prokaryote–eukaryote dichotomy because they are not cells. A virus is a particle, typically 20–400 nm in diameter, consisting of:
Viruses cannot reproduce independently. They lack ribosomes, lack metabolism, and cannot synthesise ATP. Replication requires hijacking a host cell's transcription, translation and replication machinery. Whether viruses are "alive" depends on definition: they fail the cell theory criterion (they are not cells), but they evolve by natural selection and store genetic information. The contemporary view is that viruses sit at the boundary of life, and that the question "are viruses alive?" is partly definitional.
Viruses are highly relevant to A-Level Biology immunity (lessons 7–9): viral infection triggers MHC class I antigen presentation, leading to cytotoxic T-cell killing of infected host cells. Different vaccine types (lesson 9) — live attenuated, inactivated, subunit, mRNA, viral vector — exploit different aspects of viral biology to induce immunity without disease.
The structural and biochemical differences between prokaryotes and eukaryotes are not merely taxonomic curiosities — they underpin clinical medicine.
This clinical framing motivates the depth of detail in the AQA spec: students who understand bacterial cell architecture understand why antibiotics work and why resistance arises.
Specimen question modelled on the AQA paper format
Explain how the endosymbiont theory accounts for the structural features of mitochondria and chloroplasts. Evaluate the strength of the evidence for this theory. [9 marks]
AO breakdown: AO1 (knowledge of theory) 3 marks; AO2 (application to organelles) 3 marks; AO3 (evaluation of evidence) 3 marks.
The endosymbiont theory says that mitochondria and chloroplasts came from prokaryotes that were taken in by a larger cell long ago. Mitochondria have a double membrane, which fits because the outer membrane was the host's engulfing membrane and the inner was the original prokaryote. They have circular DNA and 70S ribosomes like bacteria. They can replicate themselves inside the cell. The evidence is strong because of the DNA, ribosomes and double membrane.
Examiner commentary: M1 outline of theory, M1 double membrane explained, M1 circular DNA + 70S ribosomes, M1 self-replication, M1 evidence summary. Covers the key points but the evaluation is thin — A* requires comparison of strengths and limits.
The endosymbiont theory (proposed in modern form by Lynn Margulis in the 1960s) holds that mitochondria and chloroplasts originated as free-living prokaryotes engulfed by an ancestral host cell. Several structural features of these organelles support the theory. Both have a double membrane: the inner membrane is interpreted as the original prokaryote's plasma membrane, the outer as derived from the host's engulfing vesicle. Both contain their own circular DNA, similar in organisation to bacterial chromosomes and unlike the linear, histone-associated DNA of the eukaryotic nucleus. Both possess 70S ribosomes — the same size as prokaryotic ribosomes — explaining why antibiotics targeting prokaryotic ribosomes (chloramphenicol, tetracyclines) can affect mitochondrial protein synthesis as a side-effect. Both replicate by a fission-like process independent of host cell division. Molecular phylogenetics is the most decisive evidence: mitochondrial DNA sequences place mitochondria as relatives of α-proteobacteria (specifically Rickettsia-like), while chloroplast DNA places them as relatives of cyanobacteria. Evaluation of strength. The evidence is overwhelming and convergent — structural, biochemical and molecular data all point the same way. Limitations: the original endosymbiotic event is unobservable (it happened ~1.5 billion years ago), so direct experimental proof is impossible; the mechanism by which the host engulfed an aerobic bacterium remains conjectural; the extensive transfer of organelle genes to the nucleus (most mitochondrial proteins are now encoded by nuclear genes) complicates interpretations. Recent observations of more recent endosymbioses (Paulinella chromatophores, Hatena algae) provide modern analogues that strengthen the theory. The endosymbiont theory exemplifies how multiple independent lines of evidence converging on the same explanation provide robust scientific conclusion even in the absence of direct experimental replay.
Examiner commentary: M1 historical credit, M1 double membrane interpretation, M1 circular DNA evidence, M1 70S ribosomes + antibiotic implication, M1 independent replication, M1 molecular phylogenetics, M1 evaluative point on convergent evidence, M1 limitations identified, M1 modern analogue support. A* answers earn through balanced evaluation rather than evidence listing.
Key Exam Command Words: Compare — give similarities AND differences. Describe — give an account of features. Explain — give reasons for, linking structure to function.
Specification alignment: AQA 7402 Section 3.2.1.1 cell structure (refer to the official AQA specification document for exact wording). Synoptic links: 3.1.5, 3.2.4, 3.4.