Double bond → kink → loose packing → fluid membrane. Cold-adapted cells carry more kinks.
The plasma membrane behaves like a liquid, not a wall: two layers of phospholipids with proteins drifting through them. Two facts explain most of what you'll be asked: the middle is oily, and the parts move.
Key terms
- Phospholipid — a lipid with a water-loving phosphate head and two water-fearing fatty acid tails.
- Fluid mosaic model — proteins studded through the bilayer (the mosaic), with lipids and many proteins drifting sideways (the fluid).
- Integral protein — set into the bilayer, often spanning it; the part in the core is nonpolar. Peripheral proteins sit on the surface.
- Cholesterol — a lipid wedged between phospholipids in animal membranes. It steadies fluidity: less runny when warm, less stiff when cold.
- Glycoprotein — a membrane protein with a sugar chain on the outer face. Sugar chains work as ID tags for cell recognition.
- Unsaturated tail — a fatty acid tail with one or more C=C double bonds. A double bond bends the tail into a kink.
How it works
- Heads like water and tails avoid it. So in water, phospholipids assemble into a bilayer on their own, tails tucked inside.
- That leaves a hydrophobic core: an oily layer between two watery surfaces. O2 and CO2 dissolve straight through it. Ions almost never cross it unaided.
- The sheet is fluid. Lipids and many proteins drift sideways all the time. Flipping from one layer to the other is rare.
- Fluidity depends on packing. Straight saturated tails pack tightly → stiffer membrane. Kinked unsaturated tails pack loosely → more fluid membrane.
- Cold pushes a membrane toward a stiff gel that traps its proteins. So many organisms build more unsaturated tails in the cold and more saturated ones in warmth.
Why it matters
The next few topics, permeability and transport, all start from this structure: an oily core that blocks charged particles, and proteins that let them through. Exam questions often give you data, not a definition. Labeled proteins mixing after two cells fuse? That's the fluid part. More unsaturated tails at colder temperatures? That's the packing rule.
Exam traps
| Trap | Actually |
|---|
| The membrane is lipid sandwiched between two rigid sheets of protein. | That model was dropped. Proteins sit scattered through a fluid bilayer, and many of them drift. |
| In the cold, cells add saturated tails to hold the membrane together. | They add unsaturated tails. The kinks keep the membrane fluid, so its proteins can still move and work. |
| Double bonds make tails polar, or let them hydrogen bond to each other. | Tails stay nonpolar either way. The double bond changes their shape, and shape sets how tightly they pack. |
| Cholesterol always makes a membrane stiffer. | It buffers. It stiffens a warm membrane and keeps a cold one from packing solid. |
Worked example
Researchers built artificial membranes with and without cholesterol and measured their fluidity (arbitrary units; higher means more fluid). Without cholesterol: 2 at 10 °C and 9 at 40 °C. With cholesterol: 4 at 10 °C and 6 at 40 °C. What does cholesterol do to membrane fluidity?
- Compare at 10 °C. Cholesterol raises fluidity from 2 to 4, so it keeps the cold membrane from stiffening.
- Compare at 40 °C. Cholesterol lowers fluidity from 9 to 6, so it keeps the warm membrane from getting too runny.
- Compare the swings. Without cholesterol, fluidity changes by 7 units across the range. With it, fluidity changes by only 2.
Cholesterol buffers fluidity. It narrows the swing between cold and warm instead of pushing fluidity one way.
Cholesterol wedges between phospholipids. In the cold, it breaks up tight packing. In the warmth, it holds moving tails back. The near-miss is 'cholesterol makes membranes stiffer.' That is true at 40 °C only, and the 10 °C data rule it out.