Denature it.
Run an enzyme past its optimum, poison it two different ways, drop a cell into sucrose and watch a predator-prey cycle swing — three AQA A-Level Biology models.
One enzyme, two poisons and a temperature it cannot survive
FIG. 01 · ENZYMES · 3.1.4.2Raise it and rate climbs, then flattens: every active site is occupied and enzyme concentration becomes the limiting factor.
More kinetic energy means more successful collisions — until hydrogen and ionic bonds in the tertiary structure break.
The dashed curve is always the uninhibited enzyme at the same temperature, for comparison.
In the exam: the distinction that earns marks is where the inhibitor binds. A competitive inhibitor is a similar shape to the substrate, binds the active site, and can be out-competed — so Vmax is unchanged but more substrate is needed to reach it (KM rises). A non-competitive inhibitor binds elsewhere, changing the tertiary structure and so the shape of the active site — Vmax falls and no amount of substrate recovers it. Above the optimum, bonds holding the tertiary structure break, the active site is no longer complementary, and the substrate can no longer form enzyme–substrate complexes. Real denaturation is permanent: this model lets you slide the temperature back, an enzyme would not.
Water potential decides everything
FIG. 02 · TRANSPORT ACROSS MEMBRANES · 3.2.3ψ = −iCRT for the bathing solution: more solute, more negative water potential. Pure water is 0 kPa, the highest value there is.
The cell is drawn at the volume it settles to once osmosis has finished — the wall is the only thing stopping a plant cell bursting.
In the exam: water moves by osmosis from a higher (less negative) water potential to a lower (more negative) one, through a partially permeable membrane, down a water potential gradient — never "sucked", never "attracted". For a plant cell ψ = ψs + ψp: as water enters, the protoplast presses on the wall, ψp rises and the cell becomes turgid. Push the external solution past the cell's own ψs and ψp reaches zero — incipient plasmolysis — after which the membrane pulls away from the wall. An animal cell has no wall, so in dilute solutions it swells and lyses, and in concentrated ones it crenates.
Predators always peak late
FIG. 03 · POPULATIONS IN ECOSYSTEMS · 3.7.4Prey reproduce faster than predators can eat them — until they do not.
How often a meeting between predator and prey ends badly for the prey.
Predator death rate 0.40 and conversion efficiency 0.50 are held fixed.
In the exam: describe the cycle in the right order and the marks follow. Prey numbers rise because food is plentiful; more prey means more food for predators, so predator numbers rise after a delay; heavy predation then cuts the prey population; predators starve and their numbers fall; with fewer predators the prey recover. The predator curve always peaks after the prey curve — that lag is the answer to "explain why the two curves are out of step". This is density-dependent regulation, and in the wild disease, competition and abiotic factors damp the cycle far more than this model does.