CDK is always there; cyclin comes and goes. Cyclin up → CDK on. Cyclin destroyed → mitosis ends.
The cell cycle doesn't run on a timer. It runs on go/no-go checkpoints. The engine is an enzyme, CDK; the switch is cyclin, a partner protein the cell builds up and then destroys. Lose the checks, and damaged cells keep dividing.
Key terms
- Checkpoint — a control point where the cycle halts unless conditions check out. The big three: G1 (the main one), G2→M, and M.
- Cyclin — a regulatory protein with no enzyme activity. Its level climbs through interphase and falls sharply late in mitosis.
- CDK (cyclin-dependent kinase) — an enzyme that phosphorylates target proteins. Its amount stays steady; it works only when bound to cyclin.
- G0 — a nondividing state entered from G1. Most neurons stay there for life; liver cells can be called back.
- Growth factor — a signal from another cell, such as PDGF, that binds a receptor and pushes the cell past the G1 checkpoint.
How it works
- G1 checkpoint: is the cell big enough, well fed, signaled to divide, and free of DNA damage? Pass → it commits to dividing. Fail → it waits or enters G0.
- DNA damage activates p53. It turns on a gene for a CDK inhibitor, so the cell pauses for repair. Too much damage → p53 triggers apoptosis (programmed cell death).
- Through interphase, cyclin builds up and binds CDK. The CDK was there all along; cyclin is what switches it on.
- G2→M checkpoint: is the DNA fully copied and undamaged? Yes → cyclin-CDK (called MPF) phosphorylates its targets. Chromosomes condense and the nuclear envelope breaks down.
- M checkpoint: anaphase waits until every chromosome is attached to spindle fibers from both poles.
- At anaphase, cyclin is tagged and destroyed. CDK switches off, the phosphates it added are removed, and the cell leaves mitosis.
Why it matters
Cancer is the cell cycle with its checks broken. An oncogene is a division-promoting gene stuck on; a mutated tumor suppressor, like p53, is a failed brake. Either way, damaged cells keep dividing. On the exam, expect a cyclin/CDK graph, a mutant missing a checkpoint, or a cell-fusion experiment. Fuse a mitotic cell with a G1 cell, and the G1 chromosomes condense uncopied. The go signal is in the cytosol.
Exam traps
| Trap | Actually |
|---|
| CDK levels rise and fall with the cycle. | CDK stays steady all cycle. Cyclin rises and falls, and cyclin decides when CDK is on. |
| Cyclin breakdown is what starts mitosis. | Cyclin buildup starts it; destroying cyclin ends it. A cyclin that can't be destroyed traps the cell in mitosis. |
| DNA damage stops the cycle on its own. | A checkpoint stops it after sensing the damage. Break the checkpoint, and the cell divides anyway, passing the damage to its daughters. |
| A neuron is paused partway through the cycle. | It left the cycle from G1 and sits in G0, DNA uncopied. Nothing is half-finished, so it can stay for decades. |
Worked example
A lab measures the DNA content of cultured cells. Untreated: 60% hold 1 unit of DNA, 15% hold between 1 and 2 units, and 25% hold 2 units. After a day with drug X: 90% hold 1 unit, 3% hold between 1 and 2, and 7% hold 2 units. Where in the cycle does drug X most likely act?
- Turn DNA content into phases. 1 unit = G1 (not yet copied). Between 1 and 2 = S (copying). 2 units = G2 or mitosis (copied, not yet divided).
- With drug X, cells pile up at 1 unit while the S and G2/M groups drain. Cells still finish dividing, but they don't start copying again.
- So the block sits at the G1-to-S transition, the G1 checkpoint. Blocking the cyclin-CDK activity that launches replication would produce exactly this pattern.
Drug X blocks entry into S phase. Cells finish the cycle they are in, then stop in G1.
Cells already past the block keep going, divide, and land in G1, so G1 fills while the other groups empty. The near miss is 'drug X blocks mitosis.' A mitosis block would pile cells up at 2 units, not 1.