Switch one on and watch where the cycle stops.
You began as a single fertilised egg. Every one of your roughly 30 trillion cells came from it by the same repeated routine: grow, copy the DNA, divide. That routine is the cell cycle. A typical human cell growing in a dish takes about $24$ hours per cycle, and surprisingly little of that is the dramatic division you see in textbook pictures.
Most of the cycle is interphase: G1 (the cell grows and works), S (every chromosome is copied) and G2 (more growth and final checks). Then comes M phase: mitosis separates the copied chromosomes into two nuclei, and cytokinesis splits the cell. DNA content goes $2C \to 4C$ in S phase and back to $2C$ in each daughter, while the chromosome number stays the same ($2n$). This model uses $2n = 4$ so you can follow every chromosome; human cells have $2n = 46$.
The cycle is driven by cyclin-dependent kinases (CDKs), enzymes that only work when bound to a cyclin. Cyclin levels rise and fall in waves (see the chart under the 3D view), switching on the right jobs at the right time. At checkpoints the cell stops and asks: are there growth signals? Is the DNA intact and fully copied? Is every chromosome attached to the spindle? If not, the cycle waits. When these brakes break, cells divide out of control, and that is the heart of cancer.
Turn on Real timing and notice how briefly the cell spends in mitosis. Reset, switch on DNA damage and watch the cell stop at G1/S; turn it off to "repair" the DNA. Remove the growth factor early in G1 and the cell drops into G0. Detach a kinetochore and the cell waits in metaphase. Finally, add damage or an unattached kinetochore, then disable checkpoints: the cell divides anyway and its daughters inherit the mistakes.
| Phase | What happens | DNA | Chromosomes (model) | Typical time* |
|---|---|---|---|---|
| G1 | Cell grows, makes proteins; restriction point late in G1 | 2C | 4, one chromatid each | ~11 h |
| S | DNA replication; centrosome duplicates | 2C → 4C | 4, becoming 2 chromatids each | ~8 h |
| G2 | More growth; checks the DNA copy | 4C | 4 (8 chromatids) | ~4 h |
| Prophase | Chromatin condenses; spindle starts to form | 4C | 4 (8 chromatids) | ~1 h in total |
| Prometaphase | Nuclear envelope breaks down; kinetochores captured | 4C | 4 (8 chromatids) | |
| Metaphase | Chromosomes line up at the plate; spindle checkpoint | 4C | 4 (8 chromatids) | |
| Anaphase | Sisters separate and move to opposite poles | 4C | 8 (4 per pole) | |
| Telophase | Two nuclei re-form; chromosomes unwind | 4C | 4 + 4 | |
| Cytokinesis | Contractile ring splits the cytoplasm | 2C each | 4 per daughter |
*Typical values for a human cell dividing in culture; real cycles vary from minutes (early embryos) to never (cells in G0).
S phase makes two exact copies of every chromosome, and the spindle gives one copy to each pole. Because each sister chromatid is attached to the opposite pole before anaphase, each daughter receives exactly one copy of every chromosome, the same genetic information as the parent cell. The daughter cells are also smaller: halving the volume of a sphere shrinks its radius by only a factor of $\sqrt[3]{2} \approx 1.26$, which is why the daughter in the sim starts G1 a little smaller and then grows.
Without growth signals, a cell does not pass the restriction point and moves into G0, a stable non-dividing state. Most cells in an adult body are in G0. Some (like liver cells) can re-enter the cycle to repair tissue; others (most neurons) essentially never divide again.
| Checkpoint | The question it asks | Key molecules | If the answer is "no" |
|---|---|---|---|
| Restriction point (late G1) | Are there growth signals? | Growth factors → cyclin D–CDK4/6 → Rb switched off → E2F free | Cell enters G0 |
| G1/S | Is the DNA undamaged? Is the cell big enough? | ATM/ATR → p53 → p21 blocks cyclin E–CDK2 | Stops before S phase; repair or apoptosis |
| G2/M | Is all the DNA copied, with no damage? | Chk1/Chk2 keep cyclin B–CDK1 off | Stops before mitosis |
| Spindle (metaphase) | Is every kinetochore attached to the spindle? | Unattached kinetochores make a Mad2 "wait" signal that blocks APC/C–Cdc20 | Stays in metaphase |
CDK levels stay fairly constant; what changes is the cyclin partner. Cyclin D–CDK4/6 responds to growth factors in G1, cyclin E–CDK2 triggers the start of S phase, cyclin A–CDK2 keeps replication going, and cyclin B–CDK1 (also called MPF, maturation-promoting factor) drives the cell into mitosis. At the metaphase-to-anaphase transition the APC/C tags cyclin B and securin for destruction. With securin gone, separase cuts the cohesin that holds the sisters together, and with cyclin B gone, CDK1 switches off so the cell can leave mitosis. Destroying proteins, rather than just making them, is what keeps the cycle moving in one direction.
Cancer cells typically carry mutations in both the "accelerators" and the "brakes" of the cycle. Too much cyclin D or an always-on Ras protein pushes cells past the restriction point without a real growth signal. Loss of p53, the "guardian of the genome" and mutated in about half of all human cancers, means damaged DNA is copied instead of repaired. A weak spindle checkpoint lets chromosomes go to the wrong cell, causing aneuploidy, a hallmark of many tumours. Several cancer drugs, such as taxol and the vinca alkaloids, work by disrupting the spindle so that dividing cells cannot finish mitosis.
See also: Mitosis, step by step · Meiosis · DNA replication
The cell cycle has two main parts. Interphase is the long preparation stage, made of G1 (growth), S (DNA synthesis, when every chromosome is copied) and G2 (more growth and final checks). M phase is division itself: mitosis (prophase, prometaphase, metaphase, anaphase and telophase) separates the copied chromosomes into two nuclei, and cytokinesis splits the cytoplasm into two daughter cells.
Key takeaway: interphase (G1, S, G2) prepares the cell; M phase (mitosis plus cytokinesis) divides it.It depends on the cell. A typical human cell growing in culture takes about 24 hours: roughly 11 hours in G1, 8 in S, 4 in G2 and only about 1 hour in mitosis. The first divisions of a frog embryo take about 30 minutes because they skip the growth phases, while many adult cells, such as neurons, stop dividing and stay in G0 for years. Turn on "Real timing" in the simulation to see how short mitosis is.
Key takeaway: about 24 hours for a typical human cell in culture, and most of that time is interphase.In S phase the cell copies every DNA molecule, so the amount of DNA doubles from 2C to 4C. Each chromosome now consists of two identical sister chromatids joined at the centromere and held together by cohesin proteins. The number of chromosomes does not change, because chromosomes are counted by centromeres: a human cell has 46 chromosomes before and after S phase, but 92 chromatids after it.
Key takeaway: S phase doubles the DNA (2C to 4C) but not the chromosome number.Checkpoints are control points where the cell checks that it is safe to continue. At the G1/S checkpoint (and the restriction point just before it) the cell checks growth signals, its size and DNA damage. At the G2/M checkpoint it checks that DNA replication is complete and the DNA is undamaged. At the spindle assembly checkpoint, in metaphase, it checks that every chromosome is attached to both spindle poles. If a check fails, the cycle pauses, and if the damage cannot be fixed, the cell may self-destruct (apoptosis).
Key takeaway: checkpoints pause the cycle until growth signals, DNA quality and chromosome attachment are all OK.Cyclin-dependent kinases (CDKs) are enzymes that drive the cell cycle by adding phosphate groups to other proteins. A CDK is only active when it binds a cyclin, and different cyclins rise and fall at different stages: cyclin D in G1, cyclin E at the G1/S transition, cyclin A in S and G2, and cyclin B in G2 and mitosis. Cyclin B with CDK1 (called MPF) starts mitosis. At the start of anaphase the APC/C marks cyclin B for destruction, which switches CDK1 off so the cell can finish dividing.
Key takeaway: cyclins switch CDKs on at the right time, and destroying cyclins switches them off.G0 is a resting state outside the cycle. A cell that does not receive growth signals before the restriction point in G1 leaves the cycle and enters G0. It is still alive and fully working, but it is not preparing to divide. Some cells, like liver cells, can return to the cycle when needed; others, like most neurons and heart muscle cells, stay in G0 almost permanently.
Key takeaway: G0 is a non-dividing resting state; most cells in an adult body are in G0.Cancer is a disease of uncontrolled cell division. Mutations can turn on growth-promoting genes (oncogenes such as cyclin D or Ras) or turn off genes that stop the cycle (tumour suppressors such as p53 and Rb). A cell with broken checkpoints keeps dividing without growth signals, copies damaged DNA and can pass on the wrong number of chromosomes (aneuploidy). p53 is mutated in about half of all human cancers. Many cancer drugs attack dividing cells, for example by blocking the spindle.
Key takeaway: cancer cells divide because the brakes (checkpoints, tumour suppressors) fail and the accelerators (oncogenes) stay on.No. Mitosis is only one part of the cell cycle: the division of the nucleus, which takes about an hour in a typical human cell. The cell cycle is the whole sequence from one division to the next, including G1, S and G2. Cytokinesis, the splitting of the cytoplasm, is also separate from mitosis, although it usually starts during telophase.
Key takeaway: mitosis is a short part of the cell cycle; the cycle also includes interphase and cytokinesis.