Per disputationem veritatem quaerimusCell structure
Animal cell structure 3.2.1.1
- The nucleus is bounded by a double nuclear envelope whose pores regulate large molecules (e.g. mRNA) passing between nucleus and cytoplasm; inside, the nucleolus makes ribosomal RNA and assembles ribosomes, and chromatin is DNA in its uncondensed, transcribable form.
- Rough endoplasmic reticulum is studded with ribosomes and folds and processes the proteins they make; smooth endoplasmic reticulum lacks ribosomes and instead synthesises lipids and steroids.
- The Golgi apparatus receives material from the ER, modifies it (e.g. adding a carbohydrate chain to build a glycoprotein), and packages the finished product into Golgi vesicles addressed to its destination — inside the cell, at the cell-surface membrane, or for secretion.
- Mitochondria have a double membrane, the inner one folded into cristae to increase surface area; the matrix holds the enzymes of the Krebs cycle. They carry their own small circular DNA and 70S ribosomes (like a bacterium's, not the cell's own 80S) and can make some of their own proteins — strong evidence for the endosymbiotic theory that mitochondria evolved from free-living prokaryotes engulfed by an ancestral eukaryotic cell.
- Lysosomes contain hydrolytic enzymes that digest worn-out organelles, ingested pathogens, or (in programmed cell death) the cell's own contents.
- 80S ribosomes (larger than a prokaryote's 70S) are the site of protein synthesis, found free in the cytoplasm or bound to rough ER.
Photosynthetic plant cell structure 3.2.1.1
- A plant cell shares the same core eukaryotic organelles as an animal cell (nucleus, rough/smooth ER, Golgi, mitochondria, 80S ribosomes, cell-surface membrane) but adds three structures an animal cell lacks: a cellulose cell wall, a permanent central vacuole, and (in photosynthetic cells) chloroplasts.
- The cellulose cell wall lies outside the cell-surface membrane, freely permeable, and gives the cell a fixed shape and mechanical support — the source of the outward pressure (turgor) that supports non-woody plant tissue when the cell is full of water.
- The tonoplast is the membrane surrounding the large, permanent cell-sap vacuole, controlling exactly which solutes move between the vacuole's cell sap and the surrounding cytoplasm — the vacuole itself stores water, ions, sugars, and pigments, and its water content is what generates turgor pressure against the cell wall.
- Chloroplasts (like mitochondria) have a double membrane and their own DNA and 70S ribosomes, again supporting an endosymbiotic evolutionary origin — they are the site of photosynthesis, covered in full under Energy transfers.
- Not every plant cell contains chloroplasts (e.g. root cells do not, since they receive no light), so 'photosynthetic plant cell' here specifically describes a cell such as a leaf mesophyll cell.
Bacterial cell structure 3.2.1.2
- Prokaryotic cell: a cell with no nucleus and no membrane-bound organelles — structurally far simpler than, and typically much smaller than, a eukaryotic cell.
- Prokaryotic cells lack a nucleus altogether — their circular chromosomal DNA lies free in the cytoplasm, in a region called the nucleoid, not enclosed by any envelope.
- A murein (peptidoglycan) cell wall, chemically distinct from a plant cell's cellulose wall, gives the bacterium its shape and support.
- Ribosomes are 70S, smaller than a eukaryotic cell's 80S — the same size as the ribosomes found inside mitochondria and chloroplasts, part of the evidence linking those organelles to a bacterial evolutionary origin.
- Plasmids are small circular loops of DNA separate from the main bacterial chromosome, often carrying genes such as antibiotic resistance — they can be present in variable numbers or absent altogether, and are of particular interest in genetic engineering as vectors (see Gene technologies).
- A capsule (an outer slime layer, present in some bacteria) and a flagellum (for motility, also present in only some species) are both variable features, not present in every bacterial cell — shown here but not universal.
- Viruses are smaller again than bacteria (roughly 20–300 nm, against a bacterium's 1–5 μm and a eukaryotic cell's 10–100 μm) and are not cells at all: no ribosomes, no independent metabolism, only genetic material enclosed in a protein coat (capsid), unable to reproduce without taking over a host cell's own machinery.
Microscopy 3.2.1.3
- Magnification: how much larger an image is than the real object — image size divided by actual size.
- Resolution: the minimum distance apart two points can be while still being seen as separate — fixed by the wavelength of the radiation used, not something magnification alone can improve.
- Light microscope: ≈200 nm resolution, up to about ×1500 magnification, can image living/unstained specimens.
- Transmission electron microscope (TEM): ≈0.2 nm resolution, reveals internal ultrastructure, but the specimen must be dead, fixed, stained and viewed in a vacuum.
- Scanning electron microscope (SEM): lower resolution than TEM but far better than a light microscope, produces a 3D-looking image of a specimen's surface.
- Cell fractionation and ultracentrifugation separate a cell's organelles from one another, so each can be studied in isolation. First, cell fractionation: tissue is homogenised (broken open, e.g. in a blender) in a cold, buffered, isotonic solution — cold to reduce enzyme activity that would otherwise damage organelles, buffered to prevent pH changes damaging organelles or enzymes, and isotonic to prevent organelles gaining or losing water by osmosis and bursting or shrinking. The resulting homogenate is filtered to remove debris and whole, unbroken cells.
- Second, ultracentrifugation: the filtrate is spun in a centrifuge at low speed first, producing a pellet of the densest, heaviest structures (nuclei) with everything else remaining in the supernatant (the fluid above the pellet). That supernatant is drawn off and spun again at progressively higher speeds, pelleting the next-densest organelles each time (typically: nuclei, then mitochondria/chloroplasts, then lysosomes, then the endoplasmic reticulum and finally ribosomes) — each pellet can then be resuspended and studied separately.
- Magnifying an image beyond what its resolution actually captured only produces a larger blur — sometimes called empty magnification — since resolution, not magnification, is the real limit on how much genuine detail an image can show.
- Preparing a specimen for microscopy (fixing, staining, sectioning) can introduce artefacts: structures that appear in the resulting image but were never present in the living cell.
- A feature seen under the microscope is more likely to be genuine, rather than an artefact, if it is reproducible across independent sections and, ideally, across independent preparation techniques.
- A calibrated eyepiece graticule used alongside a stage micrometer lets a light microscope make real measurements of a specimen's size, rather than only relative comparisons; a printed scale bar on a micrograph serves the same purpose.
- Organelles separate by ultracentrifugation in order of decreasing DENSITY (not simply size) — denser structures need less centrifugal force to sediment, which is why nuclei (the densest) pellet first at the lowest speed, and progressively less dense organelles require progressively higher speeds and longer spins to pellet in turn.
- It took a considerable period of time for the scientific community to distinguish genuine cell organelles from artefacts introduced during fixation, staining or fractionation — a structure seen only in prepared samples, and never confirmed by an independent technique or in living cells, was historically a real source of doubt, directly paralleling the same fixation/artefact caution that applies to light and electron microscopy above.
Worked examples
Worked example 3.2.1 · 4 marks
A printed micrograph shows a scale bar measuring 30 mm, representing an actual length of 15 μm.
A mitochondrion in the same image measures 6 mm across.
Calculate the magnification of the image and the actual width of the mitochondrion, in μm and in nm.
Show worked solution
First convert the scale bar's real length to the same unit as the image:
Magnification:
so the image is at a magnification of .
The actual width of the mitochondrion is found by rearranging the same relationship: actual size:
This is a sensible result: mitochondria are typically a few micrometres across, so the value is a useful check that the calculation has been done the right way round.
Mark scheme · 4 marks
- Converts the scale bar's real length to 0.015 mm 1 mark
- Calculates magnification = ×2000 1 mark
- Calculates the mitochondrion's actual size as 0.003 mm 1 mark
- Converts correctly to 3 μm and 3000 nm 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.1 · 6 marks
A researcher wants to isolate and study mitochondria in a pure, functional state, separately from the rest of a liver cell's contents.
Describe the sequence of steps required, explaining the purpose of each condition used during homogenisation, and explain why mitochondria are collected before ribosomes but after the nucleus during the ultracentrifugation stage.
Show worked solution
Liver tissue is first homogenised in a solution that is cold (to reduce the activity of hydrolytic enzymes that would otherwise damage or digest the organelles once cells are broken open), buffered (to maintain a constant pH, preventing enzyme denaturation or organelle damage from pH fluctuation), and isotonic (to prevent osmotic movement of water into or out of the organelles, which could otherwise cause them to burst or shrink and be damaged).
The homogenate is filtered to remove any remaining whole cells and large debris.
The filtrate then undergoes ultracentrifugation: spun first at low speed, sedimenting the densest structures into a pellet (the nucleus), with everything else remaining in the supernatant; that supernatant is then spun again at a higher speed, at which point mitochondria sediment into the next pellet.
Ribosomes, being very small and comparatively low in density, do not sediment until much higher speeds and longer spin times are used — organelles separate strictly in order of decreasing density.
Mark scheme · 6 marks
- States the solution must be cold, to reduce hydrolytic enzyme activity 1 mark
- States the solution must be buffered, to maintain constant pH 1 mark
- States the solution must be isotonic, to prevent osmotic damage to organelles 1 mark
- States the homogenate is filtered before centrifugation 1 mark
- States centrifugation proceeds at progressively increasing speed, pelleting denser structures first 1 mark
- Explains organelles separate strictly in order of decreasing density (nucleus, then mitochondria, then ribosomes) 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
All cells arise from other cells
The cell cycle and DNA replication 3.2.2
- Cell cycle: the ordered sequence of growth and division a cell goes through, divided into interphase (G₁, S, G₂) followed by M phase (mitosis and cytokinesis).
- Interphase: G₁ (growth and organelle synthesis) → S (DNA replication) → G₂ (further growth and preparation for division).
- M phase: mitosis (nuclear division) followed by cytokinesis (division of the cytoplasm).
- Interphase is by far the longest part of the cell cycle — a cell spends most of its time growing and preparing, not actively dividing.
- DNA replication happens during S phase: each chromosome, originally one DNA molecule, is copied to become two identical sister chromatids joined at a centromere — still counted as one chromosome (chromosome number is unchanged), but now containing two DNA molecules instead of one.
- The distinction between 'chromosome number' and 'DNA molecule number' is a common point of confusion: replication in S phase doubles the amount of DNA without changing how many chromosomes are present, precisely because the two new DNA molecules (sister chromatids) stay joined together as one chromosome until they are separated later, in anaphase of mitosis.
Mitosis 3.2.2
- Mitosis: nuclear division producing two genetically identical daughter nuclei, each with the same chromosome number as the parent nucleus.
- Prophase: chromosomes condense (become visible as distinct structures) and the nuclear envelope breaks down.
- Metaphase: chromosomes align individually at the equator of the cell, with spindle fibres attached at their centromeres.
- Anaphase: sister chromatids separate and are pulled to opposite poles of the cell — the step that actually separates the two identical copies of each chromosome.
- Telophase: nuclear envelopes reform around each set of chromosomes, which decondense.
- Anaphase is the stage that actually performs the separation guaranteeing genetic identity between the two resulting nuclei — prophase, metaphase and telophase all prepare for or complete this separation but do not carry it out themselves.
- Because DNA was already replicated back in S phase (before mitosis begins), each of the 4 chromosomes shown here already comprises 2 sister chromatids (8 DNA molecules total) throughout prophase and metaphase — anaphase is what finally reduces this back to 4 separate daughter chromosomes moving to each pole.
- Spindle fibres, organised from centrioles, attach specifically at each chromosome's centromere — not at any other point along its length — which is what allows the two sister chromatids of one chromosome to be pulled apart cleanly and reliably in anaphase.
Cytokinesis 3.2.2
- Cytokinesis divides the cytoplasm to produce two separate daughter cells, and overlaps with the final stages of mitosis rather than strictly following it.
- In an animal cell, a cleavage furrow pinches the cell-surface membrane inward until it separates the two daughter cells.
- In a plant cell, the rigid cell wall makes pinching impossible, so instead a new cell plate forms across the middle of the dividing cell, which then develops into a new dividing cell wall.
- The result of mitosis and cytokinesis together is two diploid daughter cells, genetically identical to the parent cell and to each other — the basis of growth, tissue repair, and asexual reproduction.
Cell cycle checkpoints, mitotic index and cancer 3.2.2
- Mitotic index: the proportion of cells in a sample observed to be in mitosis at one moment — a snapshot proportion, not a directly timed rate.
- Uncontrolled division can follow mutations in the genes that normally regulate the cell cycle: a proto-oncogene (which normally promotes controlled division) can become an oncogene that promotes division inappropriately, or a tumour-suppressor gene can lose its normal function of halting division when something is wrong.
- Whether a resulting tumour is benign (localised, non-invasive) or malignant (invading surrounding tissue, capable of metastasis to distant sites) generally depends on further changes beyond the initial loss of cell-cycle control alone.
- Mitotic index is used as a practical measure of how actively a tissue is dividing, calculated as (number of cells in mitosis) / (total number of cells observed) — but being a snapshot proportion rather than a directly timed rate, two tissues with the same mitotic index can still differ in their absolute rate of division if their overall cell cycle lengths differ.
Worked examples
Worked example 3.2.2 · 3 marks
In a sample of 400 cells taken from a region of actively dividing tissue, 44 cells are found to be in one of the four stages of mitosis.
Calculate the mitotic index of this tissue as a percentage, and explain one reason this value alone cannot be used to state how many hours each cell spends in mitosis.
Show worked solution
Mitotic index:
This value is a proportion of cells caught in mitosis at a single instant, not a measure of time directly.
To convert it into a duration, the total length of the cell cycle for that tissue would also need to be known — without that additional figure, an 11% mitotic index is consistent with many different actual durations of mitosis.
Mark scheme · 3 marks
- Calculates mitotic index = 11% 1 mark
- States the value is a proportion caught at one instant, not a direct measure of time 1 mark
- Explains the total cell cycle length is also needed to convert the proportion into a duration 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.2 · 4 marks
A tumour sample is found to have a mitotic index of 18%, compared with 2% in the equivalent healthy tissue.
Explain what this difference indicates about the cell cycle in the tumour cells, and explain, in terms of the cell cycle, how a chemotherapy drug that specifically damages DNA during S phase could preferentially affect tumour cells over most healthy cells.
Show worked solution
A far higher mitotic index in the tumour indicates that, at any given moment, a much larger proportion of the tumour's cells are actively undergoing mitosis than in healthy tissue — consistent with cell cycle checkpoints having failed or being bypassed, allowing tumour cells to divide far more frequently.
A drug that damages DNA specifically during S phase will affect a cell only if that cell happens to be in S phase at the time of exposure.
Because a much larger proportion of tumour cells are cycling through S phase within any given time window, a much larger proportion of tumour cells will be caught and damaged than the proportion of healthy cells caught at the same moment.
Mark scheme · 4 marks
- States the higher mitotic index indicates a much larger proportion of tumour cells are dividing at any moment 1 mark
- Links this to failed or bypassed cell cycle checkpoints 1 mark
- Explains the S-phase drug only affects a cell if it is in S phase at that moment 1 mark
- Explains more tumour cells are in S phase at any given time, so proportionally more are damaged than healthy cells 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Transport across cell membranes
The fluid mosaic model 3.2.3
- Fluid mosaic model: describes the cell-surface membrane as a phospholipid bilayer (hydrophilic heads facing outward on both surfaces, hydrophobic tails facing inward) with proteins embedded in or attached to it.
- It is called 'fluid' because individual phospholipids and proteins can move sideways within their own layer, and 'mosaic' because the embedded proteins are scattered irregularly through the bilayer rather than arranged in any fixed pattern.
- Cholesterol molecules sit within the bilayer and regulate its fluidity, generally making the membrane less fluid (more rigid) and reducing its permeability to small polar molecules and ions.
- Glycoproteins and glycolipids — proteins and lipids with a carbohydrate chain attached — project from the membrane's outer surface and function in cell recognition, letting a cell identify other cells (e.g. as self or non-self, or as a particular cell type).
Simple and facilitated diffusion 3.2.3
- Diffusion: the net passive movement of particles from a region of higher concentration to a region of lower concentration, down a concentration gradient, requiring no input of metabolic energy.
- Simple diffusion: small, non-polar molecules (e.g. O₂, CO₂) move directly through the phospholipid bilayer itself, down their concentration gradient.
- Facilitated diffusion: larger, polar or charged substances move down their concentration gradient via a channel protein (often a gated pore, typically for ions) or a carrier protein (binds a specific molecule and changes shape to move it across).
- Both routes are passive: neither requires ATP, since particles are simply moving down the gradient they are already on — the difference between them is purely which molecules can cross unaided (simple diffusion) versus which need a specific membrane protein to help them across (facilitated diffusion).
- Simple diffusion's rate increases with a steeper concentration gradient, a larger surface area for exchange, and a shorter diffusion distance — the same three factors that govern exchange surfaces generally.
- Facilitated diffusion is still entirely passive despite needing a protein's help — the protein does not add energy, it simply provides a route across the bilayer that the molecule could not otherwise take.
Osmosis and active transport 3.2.3
- Osmosis: the net passive movement of water from a region of higher water potential to a region of lower water potential, through a partially permeable membrane — pure water has a water potential of zero, and any dissolved solute makes the water potential more negative.
- Active transport: the movement of a substance against its concentration gradient, via a carrier protein acting as a pump, requiring ATP.
- Osmosis is a special case of diffusion — water itself moving down ITS OWN gradient (from higher to lower water potential) — passing through aquaporins (water-channel proteins) as well as directly through the bilayer, while any dissolved solute that cannot itself cross the membrane stays behind.
- Active transport moves a substance the 'wrong way' — against its own concentration gradient — which is precisely why it needs an external energy source: ATP is hydrolysed to ADP and inorganic phosphate, and the energy released drives a conformational (shape) change in the carrier protein that moves the substance across.
- Because active transport can move a substance against its gradient, it lets a cell accumulate a substance to a concentration higher than its surroundings, something no passive process (simple diffusion, facilitated diffusion, or osmosis) can ever achieve.
Cotransport in the ileum 3.2.3
- Co-transport: a mechanism in which a single carrier protein couples the movement of two substances — one substance moves down its own concentration gradient, and the energy released by that movement drives a second substance across against its own gradient.
- The sodium–glucose cotransporter in the ileum epithelium is the standard example: a separate sodium–potassium pump on the basolateral membrane actively expels Na⁺ from the epithelial cell using ATP directly, keeping intracellular Na⁺ concentration low.
- Na⁺ then diffuses back into the cell down its electrochemical gradient through the cotransporter on the apical membrane, and this movement is coupled to glucose being carried into the cell at the same time, against glucose's own concentration gradient.
- The cotransporter protein itself does not hydrolyse ATP — it depends entirely on the Na⁺ gradient a separate, directly ATP-driven pump has already set up, so co-transport is sometimes described as 'indirectly active' rather than active transport in its own right.
- Glucose then leaves the epithelial cell into the tissue fluid (and so toward the blood capillary) by facilitated diffusion, down its own concentration gradient — the whole absorption pathway uses all three transport mechanisms (active transport, facilitated diffusion, and the cotransport step itself) working together.
Water potential and cells 3.2.3
- Finding the water potential of plant tissue: cut equal-sized cylinders (or discs) of the plant tissue and blot dry, then weigh and place each into a different concentration from a dilution series of a solute (e.g. sucrose solution, from 0 mol dm⁻³ up to a high concentration) → leave for a fixed time (long enough for water movement to reach equilibrium) → remove, blot dry again and re-weigh → calculate each cylinder's percentage change in mass, → plot percentage change in mass (y-axis) against solute concentration (x-axis) as a calibration curve.
- The concentration at which this calibration curve crosses zero percentage change in mass is the solute concentration whose water potential exactly equals the tissue's own water potential (net water movement is zero at this point) — reading the water potential of that same concentration of solute from a data table or standard curve then gives the tissue's own water potential.
- A cell placed in a solution of lower water potential than its own contents loses water by osmosis: an animal cell shrinks (crenation, since it has no wall to resist this); a plant cell's protoplast (cell-surface membrane and cytoplasm) pulls away from its cell wall (plasmolysis).
- A cell placed in a solution of higher water potential than its own contents gains water by osmosis: an animal cell may burst (lyse), since it has no wall to resist the resulting pressure; a plant cell instead becomes turgid, since its rigid cellulose wall resists further expansion and generates the internal (turgor) pressure that supports non-woody plant tissue.
- This asymmetry — a plant cell is protected from lysis by its wall, an animal cell is not — is why plant and animal cells respond so differently to the same change in surrounding water potential, despite osmosis itself working identically in both.
- Membrane permeability increases with rising temperature (increased phospholipid movement) and can also be disrupted by solvents such as ethanol — the basis of a standard beetroot pigment-leakage investigation, where the extent of membrane damage under different conditions is measured by colorimetry of the pigment released into solution.
Worked examples
Worked example 3.2.3 · 5 marks
| Sucrose concentration (mol dm⁻³) | 0.0 | 0.2 | 0.4 | 0.6 | 0.8 |
|---|---|---|---|---|---|
| Percentage change in mass | +8% | +3% | −2% | −7% | −11% |
Cylinders of potato tissue, all cut to the same initial mass, were placed into sucrose solutions of increasing concentration and left to reach equilibrium.
Percentage change in mass was recorded, shown in the table below.
Estimate the sucrose concentration at which there would be no net change in mass, and explain what this concentration represents in terms of the potato tissue's water potential.
Show worked solution
Plotting percentage change in mass against sucrose concentration gives a downward-sloping line crossing zero percentage change somewhere between 0.2 mol dm⁻³ (+3%) and 0.4 mol dm⁻³ (−2%).
Using linear interpolation: the change of 5 percentage points occurs over a concentration change of 0.2 mol dm⁻³, so zero change is reached at approximately:
At this concentration, the sucrose solution's own water potential exactly equals the water potential of the potato tissue itself — with no net movement of water by osmosis in either direction, there is no net change in the cylinder's mass.
Mark scheme · 5 marks
- Identifies the zero-change point lies between 0.2 and 0.4 mol dm⁻³ 1 mark
- Correctly interpolates to approximately 0.32 mol dm⁻³ 1 mark
- States the solution's water potential equals the tissue's water potential at this concentration 1 mark
- Explains no net osmotic water movement occurs when the two water potentials are equal 1 mark
- Links this to the standard method for determining a tissue's water potential experimentally 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.3 · 4 marks
A red blood cell is placed in a solution and observed to shrink (crenate).
A separate onion epidermal cell is placed in the same solution and observed to plasmolyse.
Explain both observations in terms of the water potential of the solution relative to the two cells, and explain why the two cells show visibly different responses to what is, in both cases, a net loss of water.
Show worked solution
Both observations indicate that the surrounding solution has a lower (more negative) water potential than the water potential inside each cell — water therefore moves by osmosis out of each cell, down its water potential gradient.
The two cells look different because of one key structural difference: the red blood cell has no cell wall, so the entire cell simply shrinks and crenates.
The onion epidermal cell has a rigid cellulose cell wall — as its protoplast loses water and shrinks, the wall itself does not shrink with it, so the protoplast pulls away from the wall (plasmolysis).
Mark scheme · 4 marks
- States the solution has a lower water potential than both cells 1 mark
- States water moves out of each cell by osmosis, down the water potential gradient 1 mark
- Explains the red blood cell has no wall, so the whole cell shrinks (crenation) 1 mark
- Explains the onion cell's wall does not shrink, so the protoplast pulls away from it (plasmolysis) 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.3 · 4 marks
Epithelial cells lining the ileum absorb glucose against its own concentration gradient (from a low luminal concentration into a cell where glucose concentration is already higher) using a sodium-glucose cotransporter.
Explain how this is possible without the cotransporter itself using ATP directly, and name the process that ultimately provides the energy making it possible.
Show worked solution
The sodium-glucose cotransporter itself does not hydrolyse ATP — it moves Na⁺ down its own electrochemical gradient, and couples this favourable movement of Na⁺ to the simultaneous movement of glucose into the cell against glucose's own concentration gradient.
The Na⁺ gradient that makes this possible is itself maintained by the sodium-potassium pump, which actively pumps Na⁺ back out of the cell using ATP hydrolysis directly.
So while the cotransporter itself uses no ATP, the process is still ultimately powered by active transport.
Mark scheme · 4 marks
- States the cotransporter itself does not hydrolyse ATP 1 mark
- Explains Na⁺ moving down its gradient is coupled to glucose moving against its gradient 1 mark
- Names the sodium-potassium pump as maintaining the Na⁺ gradient 1 mark
- States the pump uses ATP hydrolysis directly, ultimately powering the whole process 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Cell recognition and the immune system
Phagocytosis: an innate response 3.2.4
- Antigen: usually a protein, often on a cell surface, that the immune system uses to identify pathogens, cells from other organisms of the same species, abnormal body cells, or toxins as non-self or altered-self.
- Every cell type carries specific surface molecules (many of them proteins) that identify it — this is what lets the immune system distinguish the body's own normal cells from pathogens, cells from other organisms of the same species (e.g. in a transplant or transfusion), abnormal body cells (e.g. cancerous or virus-infected), and toxins, all via the same underlying antigen-recognition principle.
- Phagocytosis is the first, non-specific line of cellular defence: a phagocyte binds a pathogen, engulfs it into a phagosome, and the phagosome fuses with a lysosome to form a phagolysosome, whose hydrolytic enzymes (lysozymes) destroy the ingested pathogen.
- This step requires no specificity for a particular pathogen, but bridges into the specific response — a phagocyte displaying digested antigen fragments on its own surface becomes an antigen-presenting cell (APC), the link between the innate and the specific immune response.
- Antigenic variability — a pathogen's surface antigens changing over time (as in influenza) — can undermine long-term immunity by making existing memory cells no longer complementary to a newly encountered variant, which is why some diseases can be caught repeatedly despite a prior infection, and why some vaccines need regular updating.
T cells coordinate and carry out the cellular response 3.2.4
- Helper T cells (T_H, CD4): bind antigen presented by an antigen-presenting cell, then release cytokines that activate cytotoxic T cells, B cells and phagocytes.
- Cytotoxic T cells (T_C, CD8): directly kill body cells presenting the recognised (foreign or abnormal) antigen on their surface — e.g. virus-infected cells.
- T lymphocytes mature in the thymus (hence 'T' cell) — distinct from B lymphocytes, which mature in the bone marrow.
- The cellular response is named for its mechanism (T cells acting directly on other cells), not because it is somehow separate from antibodies — helper T cell activation is itself required to trigger the humoral (antibody-producing) response covered next, so the two branches are interdependent rather than alternative pathways.
- Only helper and cytotoxic T cells are required by this specification — other T cell types exist but their specific roles are not needed here.
B cells: selection, expansion and differentiation 3.2.4
- Clonal selection: the rare B cell whose antibody shape is complementary to a given antigen is selected by binding it, then multiplies by mitosis (clonal expansion) and differentiates into plasma cells (secrete antibody) and memory cells (persist long-term).
- Primary response: slow to develop and reaches only a low antibody concentration, since very few naive B cells initially match the new antigen and must first undergo clonal selection and expansion.
- Secondary response: much faster and reaches a far higher antibody concentration, since memory cells specific to that antigen are already present in large numbers and can differentiate into plasma cells immediately.
- This is the humoral response — named for its mechanism (soluble antibodies circulating in the blood and lymph), in contrast with the cellular response's direct cell-to-cell action.
- Only a very small proportion of the body's B cells have an antibody shape complementary to any one given antigen at any one time — clonal selection is precisely the process of finding and then massively amplifying that rare match.
- Memory cells are the entire basis of long-term, faster immunity to a previously encountered antigen: they persist for years (sometimes a lifetime) after the original infection has cleared, ready to differentiate rapidly into plasma cells on re-exposure.
Antibodies: specific binding enables pathogen clearance 3.2.4
- Antibody: a protein, secreted by plasma cells, with a binding site complementary in shape to one specific antigen.
- An antibody is a quaternary protein: two identical heavy chains and two identical light chains held together by disulfide bonds, with variable regions at the tips of the chains forming two identical binding sites, each complementary to one specific antigen.
- Formation of an antigen-antibody complex leads to destruction of the antigen by two specific routes: agglutination (antibodies, having two binding sites each, cross-link multiple pathogen cells together into a clump, since each antibody can bind an antigen on two separate cells) and phagocytosis of the resulting clumped bacterial cells (agglutinated cells are far more easily located and engulfed by phagocytes than free-floating, dispersed ones).
- Agglutination itself does not destroy the pathogen — it immobilises and clumps pathogens together, making the subsequent phagocytosis step dramatically more efficient, since a phagocyte can engulf many clumped pathogen cells at once rather than searching for and engulfing them individually.
- The two binding sites per antibody (from its quaternary structure — two heavy and two light chains, each variable region forming one site) are exactly what makes agglutination possible: a single antibody bridging antigens on two different pathogen cells is what starts the clumping.
- This is the same general antigen-antibody binding specificity (variable region shape complementary to one antigen) that underlies every other application of antibodies covered in this topic, including monoclonal antibody therapies and the ELISA test.
Immune memory and vaccination 3.2.4
- Vaccine: a preparation (an attenuated pathogen, an inactivated pathogen, or an isolated antigen) that deliberately triggers a primary immune response and memory cell formation without causing the disease itself, so a future genuine infection is met with a fast secondary response.
- Active immunity: the individual's own immune system produces its own antibodies and memory cells, following either natural infection or vaccination — slower to develop initially, but long-lasting because memory cells persist.
- Passive immunity: ready-made antibodies are supplied from an external source (e.g. maternal antibodies crossing the placenta or in breast milk, or injected antibodies) — immediate protection, but no memory cells are formed, so it is short-lived, lasting only as long as the supplied antibodies themselves persist.
- Herd immunity: when a sufficiently high proportion of a population is immune (through vaccination or prior infection), transmission of the pathogen is substantially reduced, indirectly protecting individuals who cannot themselves be vaccinated (e.g. for medical reasons) or who did not develop immunity.
- The active/passive distinction is fundamentally about WHO produced the antibodies (the individual's own immune system, or an external source), and this single distinction is what explains every other difference between them — active immunity's slower onset (an immune response takes time to develop) and long duration (memory cells persist), against passive immunity's immediate effect (antibodies are already present) and short duration (no memory cells, so protection fades as the supplied antibodies are broken down).
- Herd immunity works because reduced transmission lowers the chance that a susceptible, unvaccinated individual ever encounters the pathogen at all — it is a population-level, indirect protection, distinct from an individual's own direct immunity gained through active or passive routes.
- Vaccination programmes and their required coverage thresholds for effective herd immunity, and the ethical issues around mandating or prioritising vaccination, are genuinely different questions from the biology of how a vaccine works — a well-reasoned evaluation of a vaccination policy question needs both, not just one.
HIV: infection of helper T cells can impair immunity 3.2.4
- AIDS (acquired immunodeficiency syndrome): the condition resulting from HIV's progressive destruction of helper T cells, leaving the immune system unable to mount an effective cellular or humoral response to opportunistic infections.
- HIV structure: an RNA genome (two copies) with associated reverse transcriptase enzyme, enclosed in a protein capsid, itself surrounded by a lipid envelope carrying attachment proteins that bind specifically to the CD4 receptor on helper T cells.
- HIV replication in a helper T cell: attachment proteins bind the CD4 receptor → the viral RNA and reverse transcriptase enter the cell → reverse transcriptase converts the viral RNA into DNA → this DNA is inserted into the host cell's own DNA → the host cell's own machinery is used to transcribe and translate new viral proteins and RNA, assembling new HIV particles that bud off to infect further helper T cells.
- HIV specifically targets helper T cells via their CD4 receptor, and the progressive loss of helper T cells is what disables BOTH the cellular and the humoral branches of the specific immune response, since both depend on helper T cell activation (cytokine release) to proceed — this single mechanism is why HIV infection so broadly compromises immunity rather than affecting just one branch.
- AIDS itself is not usually what directly causes death — it is the loss of effective immunity that leaves the body vulnerable to opportunistic infections and cancers that a functioning immune system would normally control.
- Antibiotics are ineffective against HIV (or any virus) because antibiotics work by disrupting bacteria-specific structures or processes (e.g. cell wall synthesis, bacterial ribosomes) that viruses simply do not have — a virus has no cell wall, no ribosomes of its own, and relies entirely on hijacking the host cell's machinery, so there is no bacterial target for an antibiotic to act on.
Monoclonal antibodies: targeted treatment and diagnosis 3.2.4
- Monoclonal antibodies: a large number of identical antibodies, all produced from a single clone of B cells and so all with an identical binding site, specific to one chosen antigen.
- Targeting medication to specific cell types: a therapeutic drug is attached to a monoclonal antibody specific to an antigen found only on the target cell type (e.g. a cancer cell surface marker) — the antibody delivers the drug specifically to those cells, reducing side effects on healthy tissue compared with a drug that circulates and acts throughout the whole body.
- Medical diagnosis: a monoclonal antibody specific to a chosen antigen (e.g. a hormone, a pathogen antigen, or a disease marker) is used to detect that antigen's presence in a sample, directly (e.g. a pregnancy test detecting hCG) or via a technique such as ELISA.
- ELISA (enzyme-linked immunosorbent assay) test for a specific antigen: a sample is bound to a surface → a monoclonal antibody specific to the target antigen is added, which binds if the antigen is present, and unbound antibody is washed away → a second antibody, complementary to the first antibody and linked to an enzyme, is added and binds, and unbound second antibody is washed away → a substrate solution for that enzyme is added → the enzyme, if present (meaning the target antigen was present), catalyses a reaction producing a colour change → a positive (coloured) result indicates the antigen is present, and the intensity of the colour can indicate roughly how much antigen is present.
- Every monoclonal antibody application in medicine — targeted drug delivery, diagnosis, and ELISA — rests on the exact same underlying property: an antibody's binding site is complementary to one specific antigen, and using antibodies produced from a single clone guarantees every antibody molecule used has that identical specificity, rather than the varied mixture of antibodies a real immune response would produce.
- The commercial or scientific production process for monoclonal antibodies is not required by this specification — only their properties and applications.
- Ethical issues associated with vaccines and monoclonal antibodies include: the use of animals in producing and testing them, informed consent (particularly in trials), equitable access and cost (globally and within a healthcare system), and — specifically for vaccination policy — questions of individual choice against population-level herd-immunity benefit; a well-reasoned evaluation names more than one of these rather than treating the issue as having a single obvious answer.
Worked examples
Worked example 3.2.4 · 4 marks
A patient with a bacterial throat infection is prescribed antibiotics and recovers within days.
A second patient with a viral throat infection is also prescribed antibiotics, but shows no improvement.
Explain, with reference to the specific mode of action of antibiotics, why antibiotics were effective for the first patient but not the second.
Show worked solution
Antibiotics work by disrupting structures or processes specific to bacterial cells — for example, interfering with bacterial cell wall synthesis or targeting bacterial ribosomes.
Because the first patient's infection is bacterial, the antibiotic has a genuine bacteria-specific target to act on.
Viruses, however, are not cells at all: they have no cell wall, no ribosomes and no independent metabolism of their own.
There is consequently no bacteria-specific target within a virus for an antibiotic to disrupt.
Mark scheme · 4 marks
- States antibiotics disrupt bacteria-specific structures/processes (e.g. cell wall synthesis, ribosomes) 1 mark
- States the bacterial infection has a genuine target for the antibiotic 1 mark
- States viruses have no cell wall, ribosomes or independent metabolism of their own 1 mark
- Explains this means there is no bacteria-specific target for the antibiotic to act on in a viral infection 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.4 · 5 marks
A graph shows antibody concentration in the blood following two separate exposures to the same antigen, several weeks apart.
After the first exposure, antibody concentration rises slowly, reaching a low peak before falling away.
After the second exposure, antibody concentration rises far more quickly, reaching a much higher peak.
Explain both differences between the two responses, in terms of the cellular events taking place.
Show worked solution
The first exposure triggers a primary response: very few naive B cells initially have an antibody shape complementary to this new antigen, so clonal selection must first identify the rare matching B cell, before clonal expansion and differentiation into plasma cells can occur — this takes time and produces a low peak.
The second exposure instead triggers a secondary response: memory cells specific to this antigen, produced during the first exposure, are already present in far larger numbers.
These memory cells can differentiate into plasma cells rapidly, so antibody concentration rises much faster and reaches a substantially higher peak.
Mark scheme · 5 marks
- Identifies the first response as a primary response 1 mark
- Explains clonal selection of a rare matching B cell, then expansion and differentiation, causing slow onset and a low peak 1 mark
- Identifies the second response as a secondary response 1 mark
- States memory cells specific to the antigen are already present in far larger numbers 1 mark
- Explains memory cells differentiate into plasma cells rapidly, giving a fast, high peak 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.
Worked example 3.2.4 · 5 marks
A diagnostic laboratory uses an ELISA test to check a blood sample for the presence of a specific viral antigen.
The test is carried out correctly, and produces a strong colour change.
A colleague suggests that this alone proves the patient is definitely currently infected with the virus.
Evaluate this claim, describing what a positive ELISA result of this kind actually demonstrates.
Show worked solution
A positive ELISA result demonstrates that the specific antigen the test was designed to detect is present in the sample, at a level sufficient to bind the monoclonal antibody used and trigger the linked enzyme's colour-producing reaction.
However, the claim that this alone 'definitely proves current infection' overstates what a single test result can establish: reliability depends on the test's own sensitivity and specificity, sample handling, and whether washing steps were followed correctly to remove unbound antibody — an error there could produce a false positive.
Mark scheme · 5 marks
- States a positive result shows the target antigen is present, bound by the monoclonal antibody 1 mark
- States colour intensity can roughly indicate how much antigen is present 1 mark
- States the claim overstates what one result can establish 1 mark
- Identifies test sensitivity/specificity as a factor limiting reliability 1 mark
- Identifies an error at the washing step as a possible source of false positive 1 mark
Do not count matching words alone — ask whether your answer actually makes the same claim.