# Cell Communication and Signalling
Cells communicate through chemical signals to coordinate activities within tissues, organs, and the whole organism. AP Biology (Unit 4) emphasises signal transduction pathways, types of cell signalling, receptor types, and how signalling errors can lead to disease.
1. Types of Cell Signalling
| Type | Distance | Speed | Example |
|---|---|---|---|
| Direct contact | Adjacent cells | Fast | Gap junctions, plasmodesmata, cell-cell recognition |
| Paracrine | Short range (local) | Fast | Growth factors, neurotransmitters |
| Endocrine | Long range (bloodstream) | Slow | Hormones (insulin, adrenaline) |
| Autocrine | Same cell or nearby same-type cells | — | Cancer cells stimulating own growth |
| Synaptic | Across synapse | Fast | Neurotransmitters (acetylcholine, dopamine) |
2. Signal Transduction Pathway
Three stages: Reception → Transduction → Response
Stage 1: Reception
- Signal molecule (ligand) binds to a specific receptor protein
- Ligand-receptor binding is specific (complementary shapes)
- Types of receptors:
- Membrane receptors: for water-soluble ligands that cannot cross the membrane
- G-protein-coupled receptors (GPCRs): activate G proteins → activate enzymes
- Receptor tyrosine kinases (RTKs): dimerize and phosphorylate each other → activate relay proteins
- Ligand-gated ion channels: open ion channels upon ligand binding
- Intracellular receptors: for hydrophobic ligands (steroids, thyroid hormones) that cross the membrane → directly activate gene expression
- Membrane receptors: for water-soluble ligands that cannot cross the membrane
Stage 2: Transduction
- Signal amplification: a cascade of molecular interactions amplifies the signal
- Phosphorylation cascade: kinases add phosphate groups to proteins (activating or inactivating them); phosphatases remove phosphate groups
- Second messengers: small molecules that relay signals inside the cell
- cAMP (cyclic AMP): produced by adenylyl cyclase from ATP; activates protein kinase A
- Ca²⁺: released from ER; activates many proteins including calmodulin
- IP₃ (inositol trisphosphate): triggers Ca²⁺ release from ER
Stage 3: Response
- The signal ultimately causes a cellular response:
- Gene expression changes (transcription factor activation)
- Enzyme activation/inhibition
- Cell division, differentiation, or apoptosis
- Ion channel opening/closing
- Cytoskeletal rearrangement
3. Signal Amplification
- One ligand binding can produce millions of product molecules
- Each step in the cascade amplifies the signal exponentially
- Example: Epinephrine → activates adenylyl cyclase → many cAMP → many protein kinase A → many enzyme activations → massive glycogen breakdown
4. Signal Termination
- Signals must be turned off to prevent continuous stimulation:
- Phosphatases remove phosphate groups from proteins
- Phosphodiesterase breaks down cAMP
- GTPase activity turns off G proteins (GTP → GDP)
- Receptor internalisation (endocytosis)
- Ligand degradation
5. Apoptosis — Programmed Cell Death
- Apoptosis is an orderly, genetically controlled process of cell self-destruction
- Important for: development (shaping fingers), immune system (removing self-reactive cells), eliminating damaged cells
- Triggered by internal signals (DNA damage) or external signals (death ligands)
- Caspases: proteases that carry out cell destruction
- Failure of apoptosis → cancer (cells that should die continue to grow)
6. Signalling Errors and Disease
- Oncogenes (mutated proto-oncogenes): produce overactive signalling proteins → uncontrolled cell growth
- Example: Ras protein stuck in active form → continuous growth signal
- Tumour suppressor mutations: loss of checkpoints (e.g., p53 → cells don't undergo apoptosis when damaged)
- Cholera: cholera toxin locks G protein in active state → continuous cAMP production → water loss → diarrhoea
Worked Example
Question: Describe how a water-soluble hormone like epinephrine triggers a cellular response. (5 points)
Solution:
Epinephrine cannot cross the cell membrane (it is water-soluble). It binds to a G-protein-coupled receptor on the cell surface (reception). This activates a G protein on the cytoplasmic side, which in turn activates adenylyl cyclase. Adenylyl cyclase converts ATP to cAMP (a second messenger). cAMP activates protein kinase A, which phosphorylates downstream enzymes in a phosphorylation cascade (transduction). Each step amplifies the signal. The final response is the activation of glycogen phosphorylase, which breaks down glycogen into glucose — mobilising energy for the "fight-or-flight" response. The signal is terminated by phosphodiesterase breaking down cAMP.
Practice Questions
- Compare G-protein-coupled receptors and receptor tyrosine kinases. (3 points)
- Explain why signal amplification is important. (2 points)
- Describe two mechanisms of signal termination. (2 points)
- Explain how a mutation in the Ras gene can lead to cancer. (3 points)
Answers
- GPCRs work through a G protein intermediary that activates effector enzymes (like adenylyl cyclase), often using second messengers (cAMP, Ca²⁺). RTKs dimerize when ligand binds and directly phosphorylate each other (autophosphorylation), then activate relay proteins directly. GPCRs activate a single pathway; RTKs can activate multiple pathways simultaneously.
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Summary
- Cell signalling: reception (ligand binds receptor) → transduction (signal relay via cascades/second messengers) → response.
- Receptor types: GPCRs, RTKs, ion channels (membrane); intracellular (for steroids).
- Second messengers: cAMP, Ca²⁺, IP₃ — amplify and relay signals.
- Signals are terminated by phosphatases, GTPases, and second messenger degradation.
- Signalling errors (oncogenes, loss of tumour suppressors) → cancer.