Cell Cycle Checkpoints, Control and Cancer
Checkpoints hold a cell back at set points in the cycle until conditions and DNA are sound. Tumours follow when the genes that run those checkpoints stop working.
What a learner can do afterwards
- Names what each checkpoint is testing before the cell is allowed on.
- Distinguishes a gene that drives division from one that holds it back.
- Links a mutation in a control gene to uncontrolled division rather than to a faulty protein in general.
1 · Read
Your cells carry built in stop signs called checkpoints, and a cell may only pass when each test is satisfied. Skip enough of these tests and a tumour can start, which is why the checkpoints matter. The G1 checkpoint asks whether the cell is big enough and its DNA is undamaged. The G2 checkpoint asks whether DNA was copied fully and correctly. The spindle checkpoint, during mitosis, asks whether every chromosome is attached before they are pulled apart.
Signals from cyclins and kinases switch each stage on or off, and every border works like a locked gate. If a test fails, the cycle halts while repairs happen. If the damage is too severe to fix, the cell is ordered to die instead. That strict gating is why healthy tissue grows in an orderly way.
Two gene families run the gates from opposite sides. Proto-oncogenes encourage division only when it is needed, like an accelerator pressed at the right moment. Tumour suppressor genes hold division back, like brakes.
Cancer is division with the controls broken. A mutation can lock a proto-oncogene permanently on, like an accelerator stuck down, or knock out a tumour suppressor gene, like cut brakes. Either fault lets cells race past checkpoints and form a tumour. Most tumours need several such mutations stacked over years, not one single error.
Checkpoints halt the cycle until each test passes, and broken control genes let cells divide without limit.
Rewritten readings were written for this dataset.
More to read
Checks that regulate cell division
Checkpoints regulate a cell's progress through its cycle. G1 checks cell size and DNA damage. G2 checks that DNA replication is complete and that damage is repaired. During mitosis, the spindle checkpoint delays chromosome separation until chromosomes have proper attachments to opposite spindle poles.
Cyclins control the activity of cyclin-dependent kinases. Cyclin amounts rise and fall, while kinase activity changes to regulate transitions. A detected problem can pause the cycle for repair. These controls help healthy tissue grow in an organised way.
When growth controls are disrupted
Cancer involves cell growth and division escaping normal regulation. Mutations can turn proto-oncogenes, which normally promote needed division, into overactive oncogenes. Other mutations can disable tumour suppressor genes, removing restraints on division. Such changes can weaken checkpoint control.
The effect depends on the gene's role in regulating growth, not just on whether a protein is altered. When enough controls are disrupted, cells may divide uncontrollably and form a tumour. Cancer commonly develops through an accumulation of several mutations over years, rather than one mutation immediately causing disease.
Following the cell cycle in order
A dividing cell alternates between interphase and M phase. During interphase, G1 brings growth, S copies DNA, and G2 checks copied DNA and builds up supplies for division. M phase includes mitosis, which divides the nucleus, and cytokinesis, which divides the cell. Most cycling cells spend more time preparing in interphase than dividing.
Follow the order G1, S, G2, M. Checkpoints regulate specific transitions, including G1 before S, G2 before mitosis and the spindle checkpoint within mitosis. Cyclin-dependent kinase activity must reach the required level for major transitions. Pair each checkpoint with the condition it tests.
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