# The Importance of Mitosis & Apoptosis

**Mitosis** produces identical new cells for growth, cell replacement and tissue repair; **Apoptosis** is programmed cell death of old or damaged cells

## What is Apoptosis? - Apoptosis = programmed cell death (sometimes called natural cell death) - Old cells that have undergone many mitotic divisions (~50 divisions, varies by cell type) are systematically destroyed - Think of it like scheduled demolition of an old building - controlled, orderly, planned ### Processes Occurring During Apoptosis 1. **DNA condensation** - DNA becomes denser and more tightly packed - Like compressing files before deletion 2. **Nuclear envelope breakdown** - Nuclear envelope breaks down - Chromatin condenses further 3. **Vesicle formation** - Vesicles form containing hydrolytic enzymes - These act like demolition crews with specialized tools 4. **Phagocytosis** - Phagocytes engulf and digest the cell - Clean-up crew removes all debris

Apoptosis is a tidy, controlled process - unlike necrosis (accidental cell death) which causes inflammation and damage to surrounding cells

## Mitosis & Apoptosis in Body Plan Development - Both processes constantly **replace and destroy cells** throughout early organism development - They are **key mechanisms controlling body form** ### Why Apoptosis is Essential in Development - Some cells produced by mitosis early in development are **no longer needed** later - These surplus cells must be destroyed as part of normal development - **Example: Digit formation** - Fingers and toes initially develop as paddle-like structures (webbed) - Cells between digits undergo apoptosis to separate individual fingers/toes - Like a sculptor removing excess clay to reveal the final form

Without proper apoptosis during development, structures like webbed fingers would persist - highlighting how essential programmed cell death is to normal development

## Control of Mitosis & Apoptosis ### Gene Categories Controlling Mitosis | Gene Type | Function | Effect on Cell Division | |-----------|----------|------------------------| | **Proto-oncogenes** | Stimulate cell division | Increase mitosis | | **Tumour-suppressor genes** | Reduce cell division | Decrease mitosis | - Tumour-suppressor genes also **stimulate apoptosis** in cells with irreparable DNA damage - This acts as a safeguard - destroying potentially cancerous cells before they multiply

Think of proto-oncogenes as the accelerator and tumour-suppressor genes as the brake - both needed for controlled cell division

## Cell Cycle Checkpoints - Various **checkpoints** exist throughout the cell cycle - These ensure the cell is prepared for mitosis - Any DNA damage must be repaired before proceeding - Like quality control inspections on a production line ### Regulatory Proteins: Cyclins & CDKs **Two groups of proteins regulate cell cycle progression:** 1. **Cyclins** - Act as regulators - Different cyclins produced at different cell cycle stages - Respond to internal molecular signals 2. **Cyclin-dependent kinases (CDKs)** - Act as catalysts (once activated by cyclins) - Catalyse phosphorylation of target proteins - This activates or inactivates target proteins **How they work together:** - Cyclins activate CDKs - Activated CDKs phosphorylate target proteins - Target proteins either switch on or off - This ensures progression from one cell cycle stage to the next

**Phosphorylation** is the addition of a phosphate group to a protein, changing its shape and function

## Responding to Cell Stimuli - Genes controlling the cell cycle and apoptosis respond to both internal and external stimuli - This allows cells to adapt to changing conditions ### Internal Cell Stimuli **Internal factors that trigger apoptosis or affect the cell cycle:** - **Irreparable genetic damage** - DNA mutations that cannot be fixed - Like discovering structural damage too severe to repair - **RNA decay** - Breakdown of messenger RNA molecules - **Internal biochemical changes** - Oxidative reactions causing cellular injury - Accumulation of toxic metabolic byproducts - **Cyclin D production** - Signals readiness to progress through cell cycle

Cells with irreparable DNA damage must undergo apoptosis to prevent cancer - this is why tumour-suppressor genes are so important

### External Cell Stimuli **External factors affecting apoptosis and the cell cycle:** 1. **Cell signalling molecules** - **Cytokines** from the immune system - **Hormones** (e.g. growth hormone, insulin) - **Growth factors** (e.g. epidermal growth factor) - Like messages telling cells when to divide or die 2. **Harmful agents** - Viruses and bacteria - Harmful pollutants - Ultraviolet light - These can damage or destroy cells faster than they can be repaired/replaced **Cell responses to stressful external stimuli:** - Activate survival pathways (attempt to repair and continue) - Initiate apoptosis (controlled suicide to prevent further damage) - Like deciding whether to repair a damaged vehicle or scrap it entirely ## The Balance Between Mitosis & Apoptosis - Normal tissue maintains a **dynamic equilibrium** - Rate of new cell production (mitosis) ≈ Rate of cell death (apoptosis) - This balance ensures: - Tissues maintain proper size - Damaged cells are replaced - Organism develops correct body form **When the balance is disrupted:** - Too much mitosis + too little apoptosis = Tumour growth - Too much apoptosis + too little mitosis = Tissue degeneration - Like a bank account - deposits (mitosis) and withdrawals (apoptosis) must balance

Understanding how mitosis and apoptosis are controlled has huge implications for cancer treatment - many therapies aim to restore the normal balance

## Summary Table: Key Concepts | Process | Purpose | Control Mechanism | |---------|---------|------------------| | **Mitosis** | Produce identical cells for growth, repair, replacement | Proto-oncogenes (stimulate), tumour-suppressor genes (inhibit) | | **Apoptosis** | Remove old, damaged, or unnecessary cells | Tumour-suppressor genes, internal/external stimuli | | **Cell cycle checkpoints** | Ensure cell ready for division, DNA intact | Cyclins and CDKs | | **Internal stimuli** | Respond to cell's own condition | Genetic damage, RNA decay, biochemical changes | | **External stimuli** | Respond to environmental factors | Signalling molecules, pathogens, radiation |