AQA A-Level Biology 3.2 Cells: a deep dive on cell structure, division, transport and immunity

What section 3.2 actually demands

Cells is the structural and functional foundation of AQA A-Level Biology. The specification (3.2) runs from the ultrastructure of cells through how we study them, how they divide, how substances cross their membranes, and how the body recognises and defends against foreign cells. The examiners test two linked skills: precise recall of structures, processes and named examples, and the application of those facts to unfamiliar data, calculations and experimental contexts.

This guide walks through all six clusters of the topic in the order most students find easiest to build on, then sets out the exam patterns AQA repeats. Each cluster has a matching dot-point page with practice questions; this overview ties them together.

Eukaryotic cell structure

A eukaryotic cell is defined by a true membrane-bound nucleus and membrane-bound organelles. Membranes compartmentalise the cell so that incompatible reactions can run side by side, each in its own optimised environment.

You must be able to identify and give the function of the cell-surface membrane, the nucleus (with nuclear envelope, pores, chromatin and nucleolus), mitochondria (cristae and matrix, site of respiration), chloroplasts (thylakoids, grana and stroma, site of photosynthesis), ribosomes (80S, the site of translation), rough and smooth endoplasmic reticulum, the Golgi apparatus and its vesicles, lysosomes, the cell wall and the permanent vacuole. You also need the cytoskeleton, the network of protein filaments that supports the cell, moves organelles, and drives chromosome movement and the beating of cilia and flagella.

The most examined idea is the protein production and secretion pathway. A gene is transcribed in the nucleus; ribosomes on the rough endoplasmic reticulum translate the mRNA and the protein folds; a vesicle carries it to the Golgi apparatus, which modifies and packages it into a secretory vesicle; the vesicle fuses with the cell-surface membrane and releases the protein by exocytosis. Mitochondrial ATP powers transport and exocytosis throughout. Learn this sequence as a single story.

Remember the plant-cell extras: a cellulose cell wall, chloroplasts and a large permanent vacuole. Fungal cells have a chitin wall; animal cells have none of these but may contain centrioles.

Prokaryotic cells and viruses

Prokaryotic (bacterial) cells are smaller and simpler. They have no nucleus and no membrane-bound organelles. Their DNA is a single circular loop free in the cytoplasm, not wound around histones, and they may carry plasmids (small rings of DNA often bearing antibiotic-resistance genes), a protective capsule, flagella for movement, and 70S ribosomes. The cell wall is made of murein (peptidoglycan), not cellulose.

When you compare prokaryotes and eukaryotes, structure your answer around clear pairs: nucleus versus free circular DNA, present versus absent membrane-bound organelles, 80S versus 70S ribosomes, and the different wall materials.

Viruses are acellular and non-living. A virus is simply genetic material (DNA or RNA), a protein capsid, and attachment proteins that bind specifically to receptors on a host cell. Some, such as HIV, also have a lipid envelope and carry enzymes such as reverse transcriptase. A virus has no membrane, cytoplasm or organelles of its own and cannot reproduce or metabolise independently, so it must hijack a host cell's machinery to replicate. That dependence is why it is classed as non-living.

Methods of studying cells

The first essential distinction is magnification versus resolution. Magnification is how many times larger the image is than the object; resolution is the smallest distance between two points that can still be seen as separate. Resolution is limited by the wavelength of the radiation used, which is why electron microscopes, using electrons of far shorter wavelength than light, resolve far more than light microscopes.

Know the three microscopes. The optical (light) microscope can view living, coloured specimens but resolves only to about 200 nanometres. The transmission electron microscope (TEM) passes electrons through a thin specimen to reveal internal ultrastructure at about 0.1 nanometre resolution, but the specimen must be dead and in a vacuum, and preparation can create artefacts. The scanning electron microscope (SEM) scans the surface to give a 3D image at lower resolution than the TEM.

For measurement, calibrate an eyepiece graticule (a scale with no fixed real size) against a stage micrometer (a slide engraved with an accurate scale). Find the real size of one graticule division, then measure your specimen and convert. Recalibrate whenever you change the objective lens. The magnification equation is:

Cell fractionation separates organelles for study. Tissue is homogenised in a solution that is cold (to slow enzymes), isotonic (so organelles do not burst or shrink by osmosis) and buffered (to keep pH constant). The filtered homogenate is then spun in an ultracentrifuge at increasing speeds; the densest organelles sediment first. The order is nuclei, then mitochondria (and chloroplasts), then lysosomes, endoplasmic reticulum and finally ribosomes.

The cell cycle and mitosis

The cell cycle is a long interphase followed by mitosis and cytokinesis. Interphase has three parts: G1 (growth), S (DNA replication, producing two sister chromatids per chromosome) and G2 (growth and error checking). Crucially, DNA replicates during interphase, not during mitosis.

Mitosis produces two genetically identical diploid daughter cells through four stages: prophase (chromosomes condense, nuclear envelope breaks down, spindle forms), metaphase (chromosomes line up on the equator), anaphase (centromeres divide and sister chromatids are pulled to opposite poles, requiring ATP), and telophase (nuclear envelopes reform). Cytokinesis then divides the cytoplasm.

The mitotic index is the proportion of cells in mitosis:

A high index indicates rapidly dividing tissue, such as a root tip or a tumour.

Mitosis drives growth, repair and asexual reproduction, and is tightly controlled by genes. Cancer arises when control is lost: a mutation can turn a proto-oncogene into an oncogene that drives continuous division, or switch off a tumour suppressor gene that normally slows division or triggers apoptosis. Either causes uncontrolled mitosis and a tumour. A benign tumour stays in place; a malignant tumour (cancer) invades and can metastasise.

Transport across cell membranes

The fluid-mosaic model describes the membrane as a fluid phospholipid bilayer with proteins scattered through it like a mosaic. Hydrophilic phosphate heads face the water and hydrophobic tails face inward, making the bilayer a barrier to large and charged molecules. Cholesterol controls fluidity; intrinsic proteins (channel and carrier proteins) span the bilayer; glycoproteins and glycolipids handle recognition.

Five processes move substances across:

• Simple diffusion: small non-polar molecules (oxygen, carbon dioxide) cross the bilayer down their gradient, passively.
• Facilitated diffusion: larger or charged molecules cross down their gradient through channel or carrier proteins, passively.
• Osmosis: water moves from higher to lower water potential across a partially permeable membrane, through the bilayer and aquaporins. Water potential is measured in kPa; pure water is 0 and adding solute makes it negative.
• Active transport: carrier proteins use ATP to move substances against their gradient.
• Co-transport: two substances cross together on one carrier, one driving the other. The classic example is sodium-glucose co-transport in the ileum, where a sodium-potassium pump sets up the gradient that drags glucose in against its own gradient.

Rate of transport depends on the gradient (steeper is faster for diffusion and osmosis), temperature, membrane surface area, diffusion distance, and the number of carrier or channel proteins, which sets a plateau for the protein-dependent processes.

Cell recognition and the immune system

Every cell type carries its own surface antigens, and the immune system uses them to tell self from non-self, responding to pathogens, toxins, abnormal (cancer) cells and cells from other individuals.

The response begins with non-specific phagocytosis: a phagocyte binds, engulfs the pathogen into a phagosome, fuses it with a lysosome whose hydrolytic enzymes digest it, then displays the antigens to become an antigen-presenting cell. This activates the specific response.

In the cellular response, a helper T cell with a complementary receptor binds the presented antigen, then releases cytokines that stimulate phagocytes, activate cytotoxic T cells (which kill infected cells), and stimulate B cells. In the humoral response, the B cell whose antibody is complementary to the antigen is selected (clonal selection) and divides by mitosis (clonal expansion) into plasma cells, which secrete antibodies, and memory cells, which persist.

An antibody is a Y-shaped protein with four polypeptide chains, two variable regions forming antigen-binding sites complementary to one antigen, and a constant region. Antibodies agglutinate pathogens for phagocytosis and neutralise toxins.

The primary response (first exposure) is slow; the secondary response (re-exposure) is faster and stronger because memory cells act quickly. Vaccination exploits this by introducing antigens to create memory cells without disease, and herd immunity protects a population once enough people are immune. Antigenic variation, as in influenza, defeats existing memory cells and forces a fresh primary response, which is why flu vaccines change yearly.

Distinguish the immunity types: active (you make your own antibodies, long-lasting) from passive (you receive antibodies, immediate but short-lived), and natural from artificial.

Finally, monoclonal antibodies are identical antibodies from one B-cell clone, all specific to one antigen. They are used to target cancer cells with drugs, in pregnancy tests, and in the ELISA test, which detects an antigen by binding it with an enzyme-linked antibody and developing a coloured product whose intensity shows how much antigen is present.

How section 3.2 is examined

A typical AQA profile for the Cells topic:

• Multiple choice and short answer. Identifying organelles from an electron micrograph, ordering the stages of mitosis, classifying a transport process as active or passive, and distinguishing cellular from humoral immunity.
• Maths. A magnification or actual-size calculation (watch the unit conversion), a mitotic index, or a graticule-calibration question.
• Applied and data questions. Interpreting ELISA results, evaluating a cell-fractionation method, or explaining how a vaccine produces long-term immunity using the primary and secondary responses.
• Extended answers. The secretory pathway, sodium-glucose co-transport, and how mutations in proto-oncogenes or tumour suppressor genes cause cancer are all predictable.

Check your knowledge

A mix of recall and application questions covering the whole of section 3.2. Attempt them under timed conditions, then check against the solutions.

1. Describe the role of the rough endoplasmic reticulum, the Golgi apparatus and vesicles in producing and secreting a protein. (4 marks)
2. Give three differences between a prokaryotic cell and a eukaryotic cell. (3 marks)
3. Explain why a transmission electron microscope has a higher resolution than a light microscope but cannot be used to view living cells. (3 marks)
4. A cell image is 60 mm long at a magnification of times 30 000. Calculate the actual length in micrometres. (2 marks)
5. In a sample of 250 cells, 30 are in mitosis. Calculate the mitotic index, and explain what a high value indicates. (2 marks)
6. Explain how glucose is absorbed into the epithelial cells of the ileum by co-transport. (4 marks)
7. Explain why the secondary immune response is faster and stronger than the primary response. (3 marks)
8. Describe how the ELISA test detects a specific antigen. (4 marks)