C2.1 Chemical signalling
Practice exam-style IB Biology questions for Chemical signalling, aligned with the syllabus and grouped by topic.
Question 1
What property of a receptor enables it to respond selectively to one signalling chemical?
A.
A membrane channel that remains open in the absence of ligand
B.
A hydrophobic surface that prevents ligands from dissociating
C.
A catalytic site that converts all signalling chemicals into products
D.
A binding site with complementary shape and chemical properties to the ligand
Question 2
A small protein secreted by an immune cell acts on neighbouring cells to alter gene expression. What functional category of signalling chemical is described?
A.
Steroid hormone
B.
Cytokine
C.
Neurotransmitter
D.
Calcium ion
Question 3
What causes bioluminescence genes to be expressed in a dense population of Vibrio fischeri?
A.
Individual cells measure the number of neighbouring bacteria by membrane contact
B.
Oxygen concentration falls and prevents receptor binding by the autoinducer
C.
Autoinducer accumulates and binds to receptor proteins that promote transcription
D.
Luciferase diffuses between cells and directly binds to bacterial DNA
Question 4
Which pair correctly matches a hormone with its chemical group?
A.
Epinephrine — protein
B.
Testosterone — steroid
C.
Glucagon — amine
D.
Insulin — steroid
Question 5
What explains why a hormone can have distant effects but only some cells respond?
A.
It diffuses through synaptic gaps, but only muscle fibres contain mitochondria
B.
It binds to DNA in every cell before entering the blood
C.
It is stronger than a neurotransmitter and therefore reaches all cells
D.
It is carried in blood, but only cells with its receptor transduce the signal
Question 6
What is a second messenger in a signal transduction pathway?
A.
A receptor protein that remains outside the target cell
B.
A small intracellular signalling molecule produced or released after receptor activation
C.
A DNA sequence that prevents transcription of target genes
D.
A blood-borne hormone that binds to the first receptor in a pathway
Question 7
Which target-cell effect is specified for progesterone in this topic?
A.
Opening acetylcholine receptors at neuromuscular junctions
B.
Maintenance of the endometrium by altering gene expression in endometrial cells
C.
Insertion of glucose transporters after binding to an insulin receptor
D.
Production of luciferase in *Vibrio fischeri*
Question 8
What is a key difference between a receptor binding a ligand and an enzyme binding a substrate?
A.
A receptor conveys information and usually releases the ligand unchanged
B.
An enzyme can bind only hydrophobic molecules inside the nucleus
C.
An enzyme has no specificity for the molecule that it binds
D.
A receptor always changes the ligand into a product faster than an enzyme
Question 9
Define ligand in the context of chemical signalling.
[1]
State one feature of a receptor binding site that contributes to ligand specificity.
[1]
Question 10
Compare the range of action of a hormone and a neurotransmitter. [2]
Question 11
The hormone epinephrine is also called adrenaline. Outline why two names persist for this hormone. [2]
Question 12
Which statement correctly compares transmembrane and intracellular receptors?
A.
Transmembrane receptors bind signals outside the cell; intracellular receptors bind signals that penetrate the plasma membrane
B.
Transmembrane receptors lack hydrophobic amino acids; intracellular receptors contain only hydrophobic amino acids
C.
Transmembrane receptors bind steroid hormones; intracellular receptors bind peptide hormones in blood
D.
Transmembrane receptors directly bind DNA; intracellular receptors always open ion channels
Question 13
What occurs when acetylcholine binds to its receptor in a postsynaptic membrane?
A.
Glucose transporter vesicles fuse with the postsynaptic membrane
B.
An ion channel opens and positive ions diffuse into the cell
C.
Adenyl cyclase converts cyclic AMP into ATP
D.
A steroid receptor binds DNA and promotes transcription
Question 14
What activates the alpha subunit of a G protein after a ligand binds to a G protein-coupled receptor?
A.
Tyrosine residues on insulin are phosphorylated
B.
GTP is hydrolysed to GDP before receptor binding
C.
The alpha subunit is released from DNA in the nucleus
D.
GDP is replaced by GTP on the alpha subunit
Question 15
What is the immediate effect of insulin binding to its receptor on a target cell?
A.
Diffusion of insulin through the phospholipid bilayer into the nucleus
B.
Binding of cAMP to the extracellular domain of the receptor
C.
Opening of an acetylcholine-gated sodium channel
D.
Activation of tyrosine kinase activity on the cytoplasmic side of the receptor
Question 16
How can an activated testosterone receptor increase production of a specific protein?
A.
The hormone–receptor complex binds DNA and promotes transcription of target genes
B.
The hormone binds ribosomes and directly catalyses peptide bond formation
C.
The receptor hydrolyses testosterone into amino acids for translation
D.
The receptor opens a membrane channel for positive ions to enter
Question 17
What is an example of negative feedback in reproductive hormone signalling?
A.
Increased testosterone inhibits GnRH and LH release, reducing further testosterone production
B.
Acetylcholine opens an ion channel and causes depolarization
C.
Autoinducer accumulation switches on luciferase transcription in dense bacteria
D.
Oestradiol near ovulation stimulates GnRH release and promotes further reproductive signalling
Question 18
In Vibrio fischeri, bioluminescence occurs mainly when bacterial density is high.
State the signalling molecule involved in quorum sensing.
[1]
Explain why light production is switched on only at high density.
[1]
Question 19
Distinguish between a hormone, a neurotransmitter and a cytokine by referring to their usual source or range of action. [3]
Question 20
Outline chemical diversity among hormones, giving one named example for each of three chemical groups. [3]
Question 21
Outline how receptor activation initiates a signal transduction pathway. [3]
Question 22
State the target cells specified for oestradiol in this topic.
[1]
State the target cells specified for progesterone.
[1]
State the type of receptor used by both hormones.
[1]
Question 23
Explain why acetylcholine receptors respond to acetylcholine but not to every small molecule in extracellular fluid. [3]
Question 24
The table compares four animal signalling chemicals by source, route and duration of response.
| Signal | Source cell/type | Signal nature | Route of movement | Distance to target | Response duration |
|---|---|---|---|---|---|
| P | Neurone terminal | Small soluble molecule | Across synaptic cleft | 0.02 µm | 1–10 ms |
| Q | Endocrine gland cell | Lipid-soluble molecule | Carried in blood | 0.1–1 m | 10 min–hours |
| R | Activated immune cell | Soluble protein | Through tissue fluid | 0.1–5 mm | Hours–days |
| S | ER or cell surface channel | Ca²⁺ ion | Diffuses in cytoplasm | 1–10 µm | 1–60 s |
Identify which signal is most likely to be a neurotransmitter.
[1]
Identify which signal is most likely to be a hormone.
[1]
Explain why a cytokine in the table is unlikely to cross the lipid bilayer directly.
[1]
Suggest one role for Ca²⁺ as an intracellular signal.
[1]
Question 25
A tissue releases a cytokine from a small cluster of immune cells. The graph shows cytokine concentration and receptor activation with distance from the release site.
Describe the relationship between distance and receptor activation.
[1]
Suggest why the effect is localized.
[1]
Explain why cells lacking the cytokine receptor do not respond even close to the release site.
[1]
Compare this with hormone transport in blood.
[1]
Question 26
What is the correct order of early events in epinephrine signalling in a liver cell?
A.
Epinephrine binds receptor → G protein activates adenylyl cyclase → cAMP is made
B.
Adenylyl cyclase binds DNA → ATP is phosphorylated → G protein enters blood
C.
cAMP binds epinephrine → receptor phosphorylates tyrosine → glucose transporters move
D.
Epinephrine enters nucleus → receptor binds DNA → luciferase is transcribed
Question 27
Why can nitrous oxide act differently from peptide neurotransmitters in tissues?
A.
As a calcium ion it depolarizes every target cell directly
B.
As a small gas it can diffuse rapidly through membranes and tissues
C.
As a protein it must bind only to ribosomes in the cytoplasm
D.
As a steroid it is transported only by blood plasma proteins
Question 28
Explain why insulin uses a transmembrane receptor rather than an intracellular receptor.
[1]
Explain why steroid hormones can bind intracellular receptors.
[1]
Question 29
The visual shows an acetylcholine receptor in a postsynaptic membrane.
State what happens to the receptor when acetylcholine binds.
[1]
Explain how this changes membrane potential.
[1]
Question 30
Outline how a G protein-coupled receptor conveys a signal into a cell after ligand binding. [3]
Question 31
Outline the pathway from insulin binding to increased glucose uptake by a target cell. [4]
Question 32
Explain how testosterone can alter gene expression in a target cell. [3]
Question 33
Distinguish positive feedback from negative feedback.
[1]
Outline one example of each in reproductive hormone signalling.
[1]
Question 34
The graph shows autoinducer concentration and relative luciferase mRNA in cultures of Vibrio fischeri grown from low to high density.
Describe the relationship between bacterial density and autoinducer concentration.
[1]
Identify the density region in which luciferase mRNA increases most rapidly.
[1]
Explain why luciferase mRNA remains low at low density.
[1]
Suggest why bioluminescence is advantageous only when many bacteria are present together.
[1]
Question 35
The graph shows membrane potential in a postsynaptic cell before and after acetylcholine is added, with and without a channel blocker.
Describe the effect of acetylcholine on membrane potential without the blocker.
[1]
Explain the ionic basis of this effect.
[1]
Suggest why the blocker prevents the response.
[1]
Question 36
The graph shows the amount of glucose transporter in the plasma membrane of muscle cells after exposure to insulin. A tyrosine kinase inhibitor was added to some cells.
Describe the effect of insulin without the inhibitor.
[1]
Compare the response with and without the inhibitor.
[1]
Explain why the inhibitor reduces glucose transporter movement.
[1]
State how increased transporter abundance affects glucose uptake.
[1]
Question 37
A steroid hormone was added to cultured target cells. The graph shows receptor location and target mRNA abundance over time.
Describe the change in target mRNA abundance after hormone addition.
[1]
Explain why the response is not immediate.
[1]
State the role of the activated receptor in the nucleus.
[1]
Suggest why blocking transcription prevents the response.
[1]
Question 38
Explain how binding of epinephrine to its receptor can lead to glycogen breakdown in liver cells. [4]
Question 39
Cells were treated with two signalling molecules. Molecule X caused a response only when added outside intact cells. Molecule Y caused gene transcription in intact cells and in isolated nuclei.
| Preparation | Molecule X response | Molecule Y response |
|---|---|---|
| Intact cells | Rapid cytoplasmic enzyme activation | Increased target-gene transcription |
| Membrane-permeabilized cells | No detectable enzyme activation | Increased target-gene transcription |
| Isolated nuclei | No detectable enzyme activation | Increased target-gene transcription |
Deduce which molecule is more likely to be hydrophobic.
[1]
Explain the evidence for your deduction.
[1]
Predict the receptor location for molecule X.
[1]
State one limitation of using these data alone to identify the chemical group of molecule Y.
[1]
Question 40
Liver cells were exposed to epinephrine with or without inhibitors of G protein activation and adenylyl cyclase. The table shows relative cAMP concentration and glycogen phosphorylase activity.
| Treatment | cAMP / rel. units | Phosphorylase activity / rel. units |
|---|---|---|
| Untreated | 1.0 | 1.0 |
| Epinephrine | 6.8 | 5.9 |
| Epinephrine + G protein inhibitor | 1.4 | 1.3 |
| Epinephrine + adenylyl cyclase inhibitor | 1.1 | 1.0 |
Identify the treatment expected to give the highest cAMP concentration.
[1]
Explain why inhibiting adenylyl cyclase lowers cAMP.
[1]
Explain why G protein inhibition also reduces cAMP.
[1]
Suggest why glycogen phosphorylase activity follows the cAMP pattern.
[1]
Question 41
The graph shows plasma testosterone concentration and relative GnRH and LH secretion in an experimental mammal after testosterone was increased artificially.
Describe the change in GnRH and LH secretion after testosterone increases.
[1]
Identify the type of feedback shown.
[1]
Explain how this feedback reduces further testosterone production.
[1]
Suggest why negative feedback is useful in hormone signalling systems.
[1]
Question 42
Outline the role of an autoinducer in bacterial quorum sensing.
[1]
Explain how quorum sensing controls bioluminescence in Vibrio fischeri and why this is an example of coordinated gene expression.
[1]
Question 43
Define positive feedback and negative feedback in signalling pathways.
[1]
Evaluate the roles of positive and negative feedback in reproductive hormone signalling.
[1]
Question 44
Outline how acetylcholine produces a rapid response in a postsynaptic cell.
[1]
Compare localized neurotransmitter signalling with distant endocrine signalling.
[1]
Question 45
Researchers compared a normal GPCR with two mutant receptors. The table shows ligand binding, GDP release from the G protein and effector enzyme activity.
| Receptor | Ligand bound / % normal | GDP release / % normal | GTP bound / % normal | Effector act. / % normal |
|---|---|---|---|---|
| Normal | 100 | 100 | 100 | 100 |
| Mutant 1 | 24 | 27 | 30 | 33 |
| Mutant 2 | 96 | 18 | 21 | 23 |
Identify the mutant most likely to have a defective ligand-binding site.
[1]
Identify the mutant most likely to bind ligand but fail to activate the G protein.
[1]
Explain why GDP release is important for signalling.
[1]
Suggest why effector enzyme activity is low when GDP release is low.
[1]
State one reason humans can respond to many different extracellular signals using GPCRs.
[1]
Question 46
Outline two similarities between transmembrane receptors and intracellular receptors.
[1]
Compare and contrast transmembrane receptors and intracellular receptors, including ligand properties, receptor structure or location, and outcome of activation.
[1]
Question 47
State the general mechanism by which steroid hormones enter target cells and activate receptors.
[1]
Discuss how steroid hormone signalling affects gene expression, using testosterone, oestradiol and progesterone as examples.
[1]
Question 48
State three chemical groups of hormones with one example of each.
[1]
Discuss why a wide range of chemical substances can function as signalling chemicals.
[1]
Question 49
Outline the role of phosphorylation in cell signalling.
[1]
Compare and contrast epinephrine signalling through a G protein-coupled receptor with insulin signalling through a tyrosine kinase receptor.
[1]
Question 50
Outline the general pattern of chemical communication from source cell to target-cell response.
[1]
Evaluate the importance of signal transduction pathways using examples from epinephrine, insulin and steroid hormone signalling.
[1]
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