Locked-on switch → response with no signal. Missing switch → no response, unless a switch below it is locked on.
A signal molecule doesn't tell a cell what to do. It flips one switch, the receptor. Signal transduction is the relay inside the cell that passes that flip along, multiplies it, and ends in the cell's own response.
Key terms
- Ligand — the signal molecule. It binds only receptors whose binding site fits its shape.
- Receptor — a protein that changes shape when its ligand binds. Most sit in the plasma membrane.
- G protein — a relay switch. It is on while it holds GTP and turns itself off by hydrolyzing that GTP to GDP.
- Second messenger — a small molecule or ion, such as cyclic AMP (cAMP) or calcium ions, that spreads the signal through the cytoplasm.
- Protein kinase — an enzyme that adds phosphate groups to other proteins, switching them on or off. Phosphatases take the phosphates back off.
- Amplification — active enzymes each act on many molecules, so the numbers multiply. Output = starting number × every step's ratio.
How it works
- Reception. The ligand binds its receptor, and the receptor changes shape.
- In a G protein-coupled receptor pathway, the changed receptor makes a G protein swap GDP for GTP. The G protein switches on.
- The G protein turns on an enzyme, often adenylyl cyclase, which converts ATP into many cAMP molecules.
- cAMP activates a protein kinase, which phosphorylates the next protein, often another kinase. In this phosphorylation cascade, each kinase switches on many copies of the next protein.
- Response. The final targets change. In a liver cell, an enzyme starts breaking down glycogen to release glucose. In other cells, channels open or genes switch on.
- Shut-off. The G protein hydrolyzes its GTP, enzymes break down cAMP, and phosphatases remove phosphates. The response lasts as long as the switches stay on.
Why it matters
Exam questions often break one part of a pathway and ask what happens. A protein locked in its active form makes everything upstream of it irrelevant, so the response runs with no ligand. A missing protein blocks the response unless something below it is locked on. That logic explains many cancers. A growth-factor receptor or kinase stuck on tells a cell to divide with no growth factor present.
Exam traps
| Trap | Actually |
|---|
| The ligand carries the instructions for the response. | The receiving cell does. Two cell types can bind the same hormone yet hold different relay and target proteins, so they respond differently. |
| The response stops the moment the ligand leaves. | It stops when the switches reset. A G protein stays on until it hydrolyzes its GTP. Block that step and the response runs on. |
| Fewer receptors lower the ceiling but leave sensitivity alone. | Mostly the reverse. At each dose fewer receptors are bound, so the same response takes more ligand. The ceiling often barely moves. |
Worked example
Relay proteins P and Q carry a signal from a membrane receptor to a response, in an unknown order. Researchers test four cell lines with and without ligand. Normal cells respond only when ligand is present. Cells with P locked in its active form respond with or without ligand. Cells lacking Q never respond. Cells with P locked active and lacking Q never respond. Which protein acts first?
- Start with P locked on. Those cells respond without ligand, so active P is enough to drive every step after it.
- Now remove Q from those cells. If Q acted before P, the locked-on P would bypass the gap, and the cells would still respond.
- They stay silent. The signal from active P still has to pass through Q, so Q must come after P.
P acts first: receptor → P → Q → response.
A locked-on protein rescues losses upstream of it, never downstream. The near-miss is trying to order the pathway from the single mutants. Losing any required relay blocks the response by itself, so those results can't show order. Only the double mutant can.