Cell cycle control and what goes wrong in cancer

Unit 4 of AP Biology ends with a question the exam likes to ask in many forms: what keeps the cell cycle under control, and what happens when that control breaks? Answers draw on two ideas from the course — the cell cycle is driven by cyclins and cyclin-dependent kinases and guarded by checkpoints, and signaling pathways can be switched permanently on or off by a mutation or a drug. This material trains you to reason from those ideas through invented experiments and scenarios rather than memorized lists.

The first questions work with data. The amount of a CDK stays constant while its activity rises and falls, so you explain the pattern through cyclin binding. A cell population piles up in G2 with very few cells in mitosis, so you identify a checkpoint holding them back. A drug that stops a cyclin from binding its CDK halts progress at the point that complex controls. You also place G0 correctly: a nondividing state from which many cells can re-enter the cycle.

The cancer questions ask what happens when the brakes or the accelerator fail. A receptor that signals without its ligand keeps sending a divide signal; an overactive proto-oncogene speeds the cycle; a tumor-suppressor gene that loses its function lets cells slip past a checkpoint and divide despite damaged DNA. The opposite outcome is apoptosis, programmed cell death: you predict the effect of a chemical that permanently activates a relay protein in a death pathway, and you use a mutant embryo born with webbed feet to show that apoptosis normally sculpts developing tissue.

The signaling questions extend the same logic beyond the cell cycle. Blocking a relay protein in a pathway that promotes division arrests the cycle. Marine bacteria that glow only at high density, and a transfer of cell-free medium that makes a sparse culture glow, reveal quorum sensing, in which a secreted signal reports population density. A pair of items separates long-distance hormonal signaling from local signaling between nearby cells.

The material offers a quiz and a flashcard deck. The quiz explains why each outcome follows from the model and why the tempting alternatives do not. The flashcards review cyclins and CDKs, the G1, G2 and M checkpoints, G0, apoptosis, proto-oncogenes and tumor-suppressor genes, quorum sensing, and local and long-distance signaling. The course does not require the names of specific cyclin-CDK pairs or growth factors, and neither does this material.

  • Explain how cyclin binding controls CDK activity and interpret cell-cycle data
  • Describe the role of the G1, G2 and M checkpoints and of G0
  • Predict the effects of overactive proto-oncogenes, lost tumor-suppressor function and constitutively active receptors
  • Explain apoptosis and its role in development
  • Interpret signaling experiments, including pathway inhibition and quorum sensing

Practice material written by Zestly, based on the College Board AP Biology course framework (topics 4.1 cell communication, 4.3 signal transduction pathways, 4.5 cell cycle and 4.6 regulation of cell cycle).

Sample question

In an invented study of dividing cells, the amount of a CDK protein stays constant through the whole cell cycle, while the concentration of a cyclin rises steadily during interphase, peaks just before mitosis and falls sharply during mitosis. The kinase activity of the CDK peaks just before mitosis. Which explanation fits these data?

See the answer

The CDK is active only when bound to the cyclin, so its activity follows the cyclin concentration rather than the amount of CDK.

Because the amount of CDK is constant, the change in its activity must come from something else. Its activity rises and falls with the cyclin, which fits the model that a CDK is active only when bound to cyclin. The data rule out a rise in CDK amount, and an inhibitor would lower activity when it is most abundant, not raise it.

← Biology

↑ AP