Biology HL

1. 1.

   Compare how a water-soluble peptide hormone and a lipid-soluble steroid hormone can signal to target cells. Refer to membrane permeability, receptor location and the importance of receptor specificity.

   [4 marks] · no calculator

   Worked explanation

   1. Start with the ligand's chemical properties to predict whether it crosses the bilayer.
   2. Membrane receptor activation must be transduced inward, whereas an intracellular steroid-receptor complex can affect gene expression.
   3. Specific binding and downstream machinery determine a target response, not simply exposure to the hormone.

   Common mistake: A blood-borne hormone does not act identically on every cell; appropriate receptors and response machinery are required.

   Marking points

   • A water-soluble peptide generally cannot pass directly through the hydrophobic bilayer and binds a membrane receptor.
   • A lipid-soluble steroid can cross the bilayer and bind an intracellular receptor.
   • Activated intracellular steroid receptors can regulate transcription by interacting with specific DNA sequences.
   • Only cells with appropriate functional receptors/pathways respond; transport in blood does not mean every cell responds equally.

   Examiner tip: A blood-borne hormone does not act identically on every cell; appropriate receptors and response machinery are required.

2. 2.

   Adrenaline binds to a G-protein-coupled receptor on a liver cell. Explain the roles of the receptor, G protein and cAMP in conveying and amplifying the signal, and predict the effect of a receptor that cannot activate its G protein.

   [4 marks] · no calculator

   Worked explanation

   1. The extracellular ligand need not enter the cytoplasm to initiate an internal response.
   2. Trace information from receptor to G protein to cAMP, distinguishing the hormone from the second messenger.
   3. A failed coupling step interrupts the chain upstream of cAMP; ligand presence alone is insufficient.

   Common mistake: cAMP is made inside the responding cell; it is not adrenaline renamed after crossing the membrane.

   Marking points

   • Adrenaline binding changes receptor activity at the cell surface.
   • The activated receptor activates a G protein which stimulates the pathway producing cAMP.
   • cAMP is an intracellular second messenger; production of many messenger molecules and downstream enzyme activation can amplify the signal.
   • A receptor unable to activate its G protein reduces/prevents this response even if adrenaline still binds normally.

   Examiner tip: cAMP is made inside the responding cell; it is not adrenaline renamed after crossing the membrane.

3. 3.

   In a hypothetical insulin-responsive muscle cell, insulin binds normally but the receptor's tyrosine kinase activity is blocked. Explain the normal sequence leading to increased glucose entry and predict the effect of the block. Assume the glucose gradient favours entry.

   [4 marks] · no calculator

   Worked explanation

   1. Separate hormone recognition from activation of the intracellular receptor domain.
   2. More membrane transporters increase the capacity for glucose entry down the stated gradient.
   3. The block acts on signalling, not directly by removing extracellular glucose or making every existing transporter inactive.

   Common mistake: Insulin is not itself the glucose channel, and glucose entry through these transporters is not made uphill merely because signalling uses phosphorylation.

   Marking points

   • Insulin binds to its receptor in the plasma membrane.
   • Receptor activation normally causes intracellular tyrosine phosphorylation initiating a signalling sequence.
   • The sequence promotes insertion of vesicles carrying glucose transporters into the plasma membrane.
   • Blocking kinase activity reduces transporter recruitment and the insulin-stimulated increase in glucose entry despite ligand binding.

   Examiner tip: Insulin is not itself the glucose channel, and glucose entry through these transporters is not made uphill merely because signalling uses phosphorylation.

4. 4.

   Two hypothetical cells are exposed to the same extracellular peptide signal. Cell A has its specific membrane receptor; cell B lacks it. Predict their initial responses and explain why the presence of a receptor does not imply that every responding cell must produce the same final response.

   [3 marks] · no calculator

   Worked explanation

   1. Receptor specificity determines whether the cell can detect this signal through the stated route.
   2. Signal reception is distinct from subsequent transduction and cellular response.
   3. A receptor is necessary for this particular route but is not by itself proof that every later step works or that all target cells behave identically.

   Common mistake: Exposure to a hormone does not make every cell a target cell, and receptor presence alone does not determine one universal response.

   Marking points

   • Cell A can bind the signal and initiate receptor-mediated signalling if its downstream pathway is functional.
   • Cell B cannot initiate that specific receptor-mediated response without the receptor.
   • Different downstream proteins and gene-expression programmes can produce different responses even to the same signal.

   Examiner tip: Exposure to a hormone does not make every cell a target cell, and receptor presence alone does not determine one universal response.

5. 5.

   A hypothetical drug inhibits adenylyl cyclase without preventing adrenaline from binding its receptor. Predict the effect on cAMP production in a G-protein-linked pathway and explain how this illustrates the distinction between a first messenger and a second messenger.

   [3 marks] · no calculator

   Worked explanation

   1. Locate the inhibited step after receptor recognition rather than concluding the receptor cannot bind adrenaline.
   2. Adenylyl cyclase generates cAMP; inhibiting the enzyme reduces that production even if the earlier G-protein step occurs.
   3. Distinguish the extracellular ligand from the intracellular relay molecule and avoid claiming that every possible cellular signal is abolished.

   Common mistake: cAMP is not the extracellular hormone, and blocking one transduction step is not equivalent to blocking all receptor binding.

   Marking points

   • Adrenaline is the extracellular first messenger and can still bind the receptor in this scenario.
   • Inhibiting adenylyl cyclase reduces production of intracellular cAMP from ATP through this pathway.
   • cAMP is a second messenger that relays the signal inside the cell, so receptor binding need not lead to normal downstream activation.

   Examiner tip: cAMP is not the extracellular hormone, and blocking one transduction step is not equivalent to blocking all receptor binding.

Original, unofficial practice questions from SubjectScout — not official past-paper questions or complete syllabus coverage. Added English teaching explanations are AI-authored; independent teacher review is pending.