describe the fluid mosaic model of membrane structure with reference to the hydrophobic and hydrophilic interactions that account for the formation of the phospholipid bilayer and the arrangement of proteins

Fluid‑Mosaic Membranes – Cambridge IGCSE/A‑Level Biology (9700)

Learning Objective

Describe the fluid‑mosaic model of membrane structure, explaining the hydrophobic and hydrophilic interactions that drive formation of the phospholipid bilayer and the arrangement of membrane proteins. Include the roles of cholesterol, glycolipids/glycoproteins, lipid‑raft microdomains, anchored proteins and enzyme‑linked receptors, the five main transport mechanisms, and the key steps of cell‑signalling through membrane receptors.

1. Main Components of the Plasma Membrane

• Phospholipids – amphipathic molecules with a polar (hydrophilic) head group and two non‑polar (hydrophobic) fatty‑acid tails.
• Cholesterol – a rigid sterol that inserts between phospholipids; it modulates fluidity by preventing tight packing at low temperature and restricting excessive movement at high temperature.
• Glycolipids & Glycoproteins – carbohydrates covalently attached to lipids or proteins on the extracellular face; they act as cell‑recognition markers and antigens.
• Integral (transmembrane) proteins – contain one or more hydrophobic α‑helices that span the bilayer.
• Peripheral proteins – loosely attached to the inner or outer leaflet via electrostatic or hydrogen‑bond interactions.
• Anchored proteins – e.g., GPI‑anchored proteins that are tethered to the outer leaflet by a glycolipid anchor.

2. Spontaneous Formation of the Phospholipid Bilayer

In aqueous solution the opposing affinities of phospholipid regions drive self‑assembly:

1. Hydrophilic heads form hydrogen bonds and electrostatic interactions with surrounding water molecules.
2. Hydrophobic tails avoid water and associate with each other through van der Waals forces, creating a low‑energy interior – the hydrophobic core.

The result is a double‑layer with heads facing the extracellular fluid and the cytosol, and tails facing each other.

3. The Fluid‑Mosaic Model (Singer & Nicolson, 1972)

Fluid – phospholipids can laterally diffuse, rotate, and (rarely) flip‑flop, giving the membrane flexibility.

Mosaic – proteins are interspersed like tiles, each with a distinct function and varying mobility.

4. Non‑covalent Forces Maintaining Membrane Structure

• Hydrogen bonds – between polar head groups and water.
• Electrostatic attractions – between charged head groups and ions.
• Van der Waals forces – among fatty‑acid tails, stabilising the hydrophobic core.
• Hydrophobic effect – the entropic drive that forces water to exclude non‑polar tails, effectively pushing them together.

5. Classification & Functions of Membrane Proteins

6. Lipid Rafts – Ordered Microdomains

• Composed of sphingolipids, cholesterol, and associated proteins.
• Form less‑fluid “platforms” that concentrate signalling receptors (e.g., the insulin receptor) and GPI‑anchored proteins.
• Play a key role in organising signal transduction and endocytosis.

7. Factors Influencing Membrane Fluidity

8. Membrane Transport Mechanisms

All substances cross the membrane by one of the following five mechanisms:

1. Simple diffusion – small, non‑polar molecules (O₂, CO₂) move directly through the lipid core down their concentration gradient.
2. Facilitated diffusion – carrier or channel proteins assist polar or charged molecules (glucose, ions) down their gradient; no energy required.
3. Osmosis – water diffuses through the bilayer or aquaporin channels driven by a water‑potential gradient.
4. Active transport – pumps (e.g., Na⁺/K⁺‑ATPase) move ions against their electrochemical gradient using ATP.
5. Bulk transport – endocytosis (intake) and exocytosis (release) of large particles or volumes of membrane‑bound vesicles.

9. Cell‑Signalling Through Membrane Receptors (Key Terminology)

1. Ligand release – a signalling molecule (hormone, neurotransmitter) is released into the extracellular fluid.
2. Ligand transport – diffusion or carrier‑mediated transport brings the ligand to the target cell surface.
3. Receptor binding – the ligand fits a specific extracellular domain of a membrane receptor, causing a conformational change.
4. Signal transduction cascade – the conformational change activates an intracellular messenger system (e.g., G‑protein → ↑ cAMP, or receptor tyrosine kinase → phosphorylation cascade).
5. Cellular response – the cascade leads to a physiological change such as altered enzyme activity, gene expression, or ion flux.

Exam‑style example: Binding of adrenaline to a β‑adrenergic receptor activates a G‑protein, which stimulates adenylate cyclase → ↑ cAMP → activation of protein kinase → increased glycogen breakdown.

10. Practical Application & SA:V Ratio Link

11. Summary

The fluid‑mosaic model (Singer & Nicolson, 1972) explains how phospholipids self‑assemble into a bilayer driven by hydrophilic–hydrophobic interactions, creating a semi‑permeable barrier. Cholesterol modulates fluidity, while glycolipids/glycoproteins and lipid rafts provide surface identity and organise signalling complexes. Proteins are interspersed according to their affinity for the hydrophobic core (integral), the aqueous surfaces (peripheral), or a glycolipid anchor (anchored). These structural principles underpin the five membrane transport mechanisms and the basic steps of cell‑surface signalling, all of which are core to the Cambridge IGCSE/A‑Level Biology syllabus.