# The Cell Cycle and Mitosis
The cell cycle is the ordered sequence of events in which a cell duplicates its contents and divides. AP Biology focuses on cell cycle regulation, the role of checkpoints, mitosis mechanics, and how loss of control leads to cancer.
1. The Cell Cycle
Interphase (~90% of cycle)
- G₁ (Gap 1): Cell grows; organelles duplicate; cell carries out normal functions; G₁ checkpoint ("restriction point") — checks for adequate size, nutrients, growth signals, and DNA integrity
- S (Synthesis): DNA replication — each chromosome becomes two sister chromatids joined at centromere; centrosome duplicates
- G₂ (Gap 2): Final preparations; proteins for mitosis synthesised; G₂ checkpoint — checks DNA replication is complete and undamaged
- Some cells enter G₀ — a non-dividing state (e.g., mature neurons, muscle cells)
Mitotic (M) Phase
- Mitosis: division of the nucleus (PMAT)
- Cytokinesis: division of the cytoplasm
2. Mitosis — Detailed
| Stage | Key Events |
|---|---|
| Prophase | Chromosomes condense; spindle forms from centrosomes; nuclear envelope begins to break down |
| Prometaphase | Nuclear envelope fully breaks down; spindle fibres attach to kinetochores on centromeres |
| Metaphase | Chromosomes align at metaphase plate; spindle checkpoint — ensures all chromosomes attached |
| Anaphase | Centromeres split; sister chromatids pulled to opposite poles by shortening spindle fibres |
| Telophase | Chromatids arrive at poles; nuclear envelopes reform; chromosomes decondense |
Cytokinesis
- Animal cells: cleavage furrow (actin-myosin contractile ring pinches inward)
- Plant cells: cell plate forms from Golgi vesicles; becomes new cell wall
Result: Two genetically identical daughter cells
3. Cell Cycle Regulation
Cyclins and CDKs
- Cyclin-dependent kinases (CDKs): enzymes that drive the cell cycle; only active when bound to cyclins
- Cyclins: regulatory proteins whose concentrations fluctuate during the cycle
- Cyclin-CDK complexes phosphorylate target proteins, triggering progression through cycle phases
- Example: MPF (M-phase promoting factor) = cyclin B + CDK1 → triggers mitosis
Checkpoints
| Checkpoint | Location | What Is Checked |
|---|---|---|
| G₁ | End of G₁ | Cell size, nutrients, growth signals, DNA damage |
| G₂ | End of G₂ | DNA replication complete, no DNA damage |
| Spindle (M) | Metaphase | All chromosomes properly attached to spindle |
Growth Factors
- External signals (e.g., PDGF — platelet-derived growth factor) stimulate cell division
- Density-dependent inhibition: crowded cells stop dividing (contact inhibition)
- Anchorage dependence: cells must be attached to a surface to divide
4. Cancer — Loss of Cell Cycle Control
- Cancer results from mutations that disrupt normal cell cycle regulation
Proto-oncogenes → Oncogenes
- Proto-oncogenes: normal genes that promote cell growth
- Oncogenes: mutated versions that are constitutively active → promote uncontrolled division
- Example: Ras mutation → continuous growth signalling
Tumour Suppressors
- Tumour suppressor genes: normally inhibit cell division or promote apoptosis
- p53 ("guardian of the genome"): detects DNA damage → halts cell cycle or triggers apoptosis
- Mutations in p53 → damaged cells continue to divide → accumulate further mutations
Characteristics of Cancer Cells
- No density-dependent inhibition (grow over each other)
- No anchorage dependence (grow without attachment)
- Ignore checkpoint signals
- Avoid apoptosis
- Immortal (telomerase activation)
- Angiogenesis (stimulate new blood vessel growth)
- Metastasis: spread to other tissues via blood/lymph
Worked Example
Question: Explain how a mutation in the p53 gene could lead to cancer. (4 points)
Solution:
p53 is a tumour suppressor protein that acts at the G₁ checkpoint. When DNA damage is detected, p53 activates genes that halt the cell cycle, allowing time for DNA repair. If the damage is irreparable, p53 triggers apoptosis (programmed cell death) to prevent the damaged cell from dividing. A mutation in p53 that inactivates it means the cell cycle is not halted even when DNA is damaged. The cell continues to divide with mutations, which can accumulate over time. Additional mutations in proto-oncogenes or other tumour suppressors further remove growth controls, leading to uncontrolled cell division — cancer.
Practice Questions
- Describe the events of the S phase and explain its importance. (3 points)
- Explain the role of cyclin-CDK complexes in the cell cycle. (3 points)
- Compare cytokinesis in animal and plant cells. (2 points)
- Explain why cancer cells are described as 'immortal'. (2 points)
Answers
- During the S phase, each DNA molecule is replicated, producing two identical sister chromatids joined at the centromere. The centrosome is also duplicated. This is critical because it ensures each daughter cell will receive a complete and identical copy of the genome after mitosis.
Want to check your answers and get step-by-step solutions?
Summary
- Cell cycle: G₁ → S (DNA replication) → G₂ → M (mitosis + cytokinesis); regulated by cyclin-CDK complexes.
- Checkpoints (G₁, G₂, spindle) ensure the cell is ready before proceeding.
- Mitosis: PMAT → 2 genetically identical cells. Cytokinesis: cleavage furrow (animals) or cell plate (plants).
- Cancer: caused by mutations in oncogenes (overactive growth) and tumour suppressors (lost brakes); characteristics include immortality, metastasis, and evasion of apoptosis.