Cell Communication and Cell Junctions
General Biology · Section 1.6 · 18 study cards
How cells send, receive and act on chemical signals, and the junctions that hold tissues together and let neighbours talk.
Practice this set → Spaced repetition, card by card. No account needed.
Method
Read every pathway as three stages
Almost every signalling question on this exam is really asking where in reception, transduction or response something happens. Before answering, place the item: a ligand and receptor are reception, kinases and second messengers are transduction, and a gene switching on or an enzyme becoming active is the response.
A procedure for tracing a pathway
- Ask whether the signal is hydrophilic or hydrophobic. Hydrophobic signals such as steroids cross the membrane and use an intracellular receptor; everything else needs a membrane receptor.
- For a membrane receptor, identify which of the three types it is: G protein-coupled, receptor tyrosine kinase, or ligand-gated ion channel. Each has a signature first move: a G protein swapping GDP for GTP, a dimer phosphorylating itself, or a gate opening.
- Follow the relay. Look for a second messenger such as cyclic AMP or Ca²⁺, then for a chain of kinases. Count the amplification points as you go, because each enzymatic step multiplies the signal.
- Name the response in concrete terms. Cytoplasmic responses change enzyme activity within seconds; nuclear responses change transcription and take minutes to hours.
- State how it stops. Every pathway has an off switch, and exam questions frequently attack the pathway there.
Junctions are a separate idea, so keep them separate
Junctions are structures, not pathways. Sort them by job: seal, fasten, or connect. Tight junctions seal, desmosomes fasten, gap junctions connect. Only the connecting ones move signal molecules, and plasmodesmata do that job in plants. If a question asks how two touching cells share a second messenger directly, the answer is gap junctions or plasmodesmata, not a receptor at all.
What examiners actually test
Expect three shapes of question: identify the receptor type from a description, predict what happens if one component is broken or permanently switched on, and explain why a tiny amount of hormone produces a huge effect. All three are answerable from the framework above rather than from memorised diagrams.
Definitions and theorems
Worked example
A person is startled and adrenaline is released into the blood. Liver cells respond within seconds by breaking glycogen down to glucose, yet the adrenaline concentration in blood is only about 10-10 molar. Trace the pathway from hormone to glucose and explain how so little hormone produces so large an effect. Then predict what happens in a liver cell treated with a drug that blocks phosphodiesterase.
Reception. Adrenaline is hydrophilic, so it cannot cross the membrane. It binds a G protein-coupled receptor on the liver cell surface, and the receptor changes shape.
G protein activation. The receptor binds an inactive G protein and causes it to release GDP and bind GTP. The activated G protein moves through the membrane to adenylyl cyclase.
Second messenger. Adenylyl cyclase converts many molecules of ATP into cyclic AMP. Cyclic AMP diffuses through the cytosol and activates protein kinase A.
Phosphorylation cascade. Protein kinase A phosphorylates and activates phosphorylase kinase, which phosphorylates and activates glycogen phosphorylase, the enzyme that cleaves glucose units from glycogen.
Amplification. Each enzyme in the chain acts on many substrate molecules before it is switched off, so the numbers multiply at every step: one receptor activates several G proteins, one adenylyl cyclase makes many cyclic AMP molecules, and so on. The result is roughly 108 glucose molecules released per hormone molecule bound.
Effect of the drug. Phosphodiesterase is the enzyme that destroys cyclic AMP. Blocking it means cyclic AMP is made but not removed, so protein kinase A stays active and glycogen breakdown continues long after adrenaline has gone. The response is prolonged and the cell can no longer report a change in hormone level.
Common mistakes
- Treating the signal as the instruction. Students write that the hormone tells the cell to divide. The hormone carries no such information; it only changes the shape of a receptor, and everything that follows is encoded in the receiving cell. This matters because it explains how one hormone produces different effects in different tissues.
- Confusing second messengers with signal molecules. Cyclic AMP and Ca²⁺ are inside the cell and are made or released in response to the first signal. The extracellular ligand never becomes the second messenger and usually never enters the cell at all.
- Saying steroid hormones use membrane receptors. Their whole point is that they are hydrophobic and diffuse through the bilayer to an intracellular receptor, which then acts as a transcription factor. If a question says the response was a change in gene expression that took hours, suspect an intracellular receptor.
- Mixing up desmosomes and gap junctions. Both join adjacent cells, but desmosomes are mechanical fasteners anchored to intermediate filaments and pass nothing, while gap junctions are open channels that pass ions and small molecules. If the question is about communication, desmosomes are never the answer.
- Forgetting termination. Questions about toxins and drugs almost always attack the off switch, not the on switch. When asked to predict the effect of a mutation that leaves a G protein unable to hydrolyse GTP, the answer is a permanently active pathway, not a dead one.
Practice it
Reading the method is not the same as being able to recall it under pressure. This set drills 18 cards one at a time and schedules each card separately, so the ones you keep missing come back sooner.