Cell Biology Quiz: Epithelial Transport
20 questions · exam conditions
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Epithelial TransportQuestion 1 of 20

Which experiment best shows that transport proteins are apically versus basolaterally polarized?

Measure ATPase in cell lysate
Measure total transporter mRNA
Compare apical vs basal uptake
Check cell shape by microscopy
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Cell Biology Quiz

Cell Biology Quiz: Epithelial Transport

Practice Epithelial Transport in Cell Biology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Epithelial Transport, giving you a quick way to practice the rules, question types, and explanations that matter most for Cell Biology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

Which experiment best shows that transport proteins are apically versus basolaterally polarized?

  1. Measure ATPase in cell lysate
  2. Measure total transporter mRNA
  3. Compare apical vs basal uptake (correct answer)
  4. Check cell shape by microscopy
Explanation: Transport proteins being polarized means they function only on one membrane domain, so the direct test is to compare uptake across the apical surface with uptake across the basal surface. Differential rates reveal which transporters sit where. Measuring total transporter mRNA is tempting, but mRNA levels or total protein in a lysate cannot show where a protein is actually localized and active.

Question 2

Blocking the basolateral Na/K pump stops apical Cl- secretion. Why?

  1. Na+ gradient drives Cl- entry (correct answer)
  2. Cl- channel uses pump ATP
  3. Tight junctions need pump ATP
  4. Pump sits on apical membrane
Explanation: Blocking the basolateral Na/K pump collapses the Na+ gradient that powers basolateral Na+-K+-2Cl- cotransport, so Cl- cannot enter the cell to be secreted apically. The Cl- channel uses its own electrochemical gradient, not pump ATP, and the pump sits basolaterally, not apically. The tempting wrong answer is that the pump directly supplies ATP to the Cl- channel, but ATP from the pump is not what drives Cl- exit.

Question 3

Tight junctions still seal, but their fence function fails; apical and basal proteins mix. Which is lost?

  1. Ion gradient generation
  2. Membrane ATPase activity
  3. Paracellular selectivity
  4. Vectorial solute transport (correct answer)
Explanation: Because the fence function fails, apical and basolateral membrane proteins mix, so epithelial cells can no longer transport solutes in one direction across the sheet; directional transport depends on the asymmetric placement of transporters. Paracellular selectivity is tempting, but that belongs to the seal/barrier function, and the seal is intact.

Question 4

Basal ouabain, not apical, blocks Na+-glucose uptake. What is the best conclusion?

  1. Na/K pumps are basolateral (correct answer)
  2. Glucose exit is basolateral
  3. Tight junctions block ouabain
  4. Na+ enters via basal side
Explanation: Ouabain blocks Na/K pumps, which maintain the Na+ gradient that drives apical Na+-glucose uptake. Basal ouabain works but apical ouabain doesn't, so the pumps must be on the basolateral side, out of reach of apical drug. The tempting wrong idea is that tight junctions block ouabain; that would explain access, but the real conclusion is about where the pumps are located.

Question 5

An epithelium absorbs glucose from lumen to blood. Which membrane arrangement is required?

  1. Pump apical, SGLT1 basal side
  2. Pump basal side, SGLT1 apical (correct answer)
  3. Pump apical, SGLT1 apical side
  4. Pump basal, SGLT1 basal side
Explanation: Glucose enters the cell against its gradient using SGLT1, which couples uptake to the Na+ gradient; that transporter must face the lumen, so it's apical. The Na+/K+ ATPase pump keeps intracellular Na+ low and must sit on the basolateral side, facing the blood. The tempting error is putting the pump apical with SGLT1 basal, which would move Na+ outward at the lumen and cannot drive luminal glucose uptake.

Question 6

A student observes that treating epithelial cells with cytochalasin D (which disrupts actin filaments) causes apical membrane proteins to appear in the basolateral membrane within 2 hours. However, basolateral membrane proteins do not redistribute to the apical membrane during the same time period. What is the most likely explanation?

  1. Apical membrane proteins have higher mobility than basolateral proteins because they lack cytoskeletal anchoring points in normal conditions
  2. Cytochalasin D specifically affects the trafficking machinery that delivers proteins to the apical membrane but not the basolateral membrane
  3. The actin cytoskeleton normally restricts lateral diffusion of apical proteins, while tight junctions independently prevent basolateral protein movement (correct answer)
  4. Apical membrane proteins are smaller molecules that can diffuse through tight junctions, while basolateral proteins are too large for this pathway
  5. The disruption of actin allows apical proteins to diffuse laterally around tight junctions, but an intact microtubule network still restricts basolateral protein movement
Explanation: When analyzing epithelial cell polarity, you need to understand how cells maintain distinct apical and basolateral membrane domains through two key mechanisms: tight junctions that form a physical barrier between domains, and the actin cytoskeleton that provides structural organization. The correct answer is C because epithelial cells use different mechanisms to restrict different membrane proteins. The actin cytoskeleton forms a dense network beneath the apical membrane that normally prevents apical proteins from diffusing laterally. When cytochalasin D disrupts these actin filaments, apical proteins lose their spatial restriction and can move to the basolateral membrane. However, tight junctions function independently of actin and continue to form a physical seal that prevents basolateral proteins from crossing into the apical domain. Option A is incorrect because both apical and basolateral proteins have cytoskeletal connections - the difference lies in which cytoskeletal elements restrict their movement. Option B misunderstands the mechanism; cytochalasin D affects the structural cytoskeleton, not trafficking machinery, and the effect is on protein redistribution after they've already reached the membrane. Option D incorrectly suggests that protein size determines movement through tight junctions, when actually tight junctions prevent lateral movement of membrane proteins regardless of size - they're embedded in the membrane, not passing through intercellular spaces. Remember: epithelial polarity depends on multiple independent barriers. When one fails (like actin disruption), others (like tight junctions) may still function, creating asymmetric effects on protein redistribution.

Question 7

A researcher observes that glucose transport across an epithelial cell layer requires the presence of sodium ions only on the apical side, while glucose appears in the medium on the basolateral side even when sodium is absent from that compartment. What is the most likely explanation for this observation?

  1. Glucose transporters are present only on the apical membrane and glucose diffuses through tight junctions to the basolateral side
  2. Sodium-glucose cotransporters are located on the apical membrane while glucose uniporters are located on the basolateral membrane (correct answer)
  3. The tight junctions are permeable to sodium but not glucose, creating a sodium gradient across the epithelium
  4. Glucose is actively transported by sodium-independent pumps on both apical and basolateral membranes simultaneously
  5. The epithelial cells consume glucose for metabolism, preventing its transport to the basolateral compartment
Explanation: When you encounter questions about epithelial transport, focus on how polarized cells use different transporters on their apical and basolateral membranes to move substances directionally across tissue barriers. The key observation here is that sodium is only required on the apical side, yet glucose appears on the basolateral side even without sodium in that compartment. This indicates a two-step transport process. On the apical membrane, sodium-glucose cotransporters (like SGLT1) use the sodium gradient to actively transport glucose into the cell against its concentration gradient. Once glucose accumulates inside the cell, it exits via facilitated diffusion through glucose uniporters (like GLUT1) on the basolateral membrane—a process that doesn't require sodium. This arrangement allows epithelial cells to transport glucose from low concentrations (apical) to high concentrations (basolateral), enabling absorption functions. Option A is incorrect because if glucose only entered apically and diffused through tight junctions, you wouldn't see the sodium dependency described. Option C misunderstands the setup—tight junctions are actually impermeable to sodium, and the observation isn't about sodium crossing the epithelium. Option D suggests active transport on both sides, but the basolateral glucose movement occurs without sodium, indicating passive transport rather than active pumping. Remember that epithelial transport questions often test your understanding of membrane polarity and how cells couple active and passive transport mechanisms. Look for clues about which side requires energy or specific ions—this reveals the transport mechanism at work.

Question 8

In kidney proximal tubule cells, Na⁺/K⁺-ATPase pumps are exclusively located on the basolateral membrane. If these pumps were instead distributed equally between apical and basolateral membranes, what would be the most immediate consequence for sodium reabsorption?

  1. Sodium reabsorption would increase because more pump molecules would be available to transport sodium out of the tubule
  2. Sodium reabsorption would decrease because apical pumps would compete with sodium channels for the same substrate pool
  3. Sodium reabsorption would cease because the sodium gradient driving apical sodium entry would be eliminated by apical pump activity (correct answer)
  4. Sodium reabsorption would remain unchanged because the total number of pump molecules per cell would be the same
  5. Sodium reabsorption would become bidirectional because pumps on both membranes would create opposing sodium gradients across the epithelium
Explanation: When you encounter questions about epithelial transport, focus on how membrane polarity creates directional transport across cell layers. The key principle is that transporters on opposite membranes work together to move substances from one side of the epithelium to the other. In normal proximal tubule cells, sodium reabsorption works through a two-step process: sodium enters the cell from the tubule lumen through apical sodium channels (driven by the low intracellular sodium concentration), then exits the cell into the bloodstream via basolateral Na⁺/K⁺-ATPase pumps. This creates a transcellular sodium transport pathway that removes sodium from the urine and returns it to circulation. If Na⁺/K⁺-ATPase pumps were placed on the apical membrane, they would actively pump sodium back into the tubule lumen while simultaneously creating high intracellular sodium levels. This would eliminate the concentration gradient that normally drives sodium entry through apical channels. Without this driving force, sodium couldn't enter the cell from the tubule, completely disrupting reabsorption. Answer C correctly identifies this mechanism. Answer A is wrong because having more pumps doesn't help if they're working against each other. Answer B incorrectly suggests competition for substrate rather than the actual problem of opposing gradients. Answer D misses that pump location, not just quantity, determines function—the spatial organization of transporters is crucial for directional transport. Remember: In epithelial physiology questions, always consider how transporter polarity creates the driving forces for directional movement. Disrupting this polarity typically eliminates transport function entirely.

Question 9

A mutation disrupts the sorting signal that targets a specific ion channel to the apical membrane of intestinal epithelial cells. If the channel now distributes randomly between apical and basolateral membranes, which functional consequence is most likely?

  1. The channel will function normally because ion gradients are the same across both membrane domains in polarized cells
  2. Epithelial barrier function will be compromised because channels in the basolateral membrane will create inappropriate leak pathways
  3. Channel activity will be enhanced because the protein can now access larger membrane surface area for increased expression
  4. Transcellular transport will be eliminated because proper vectorial ion movement requires asymmetric channel distribution between membrane domains (correct answer)
  5. Cell viability will be unaffected because tight junctions will prevent any functional consequences of the mislocalized channels
Explanation: When you encounter questions about protein sorting and membrane polarity, focus on how the asymmetric distribution of proteins drives directional transport across epithelial barriers. Epithelial cells maintain distinct apical and basolateral membrane domains with different protein compositions. This asymmetry is essential for transcellular transport - the directed movement of substances from one side of the epithelial barrier to the other. Ion channels positioned specifically on either the apical or basolateral membrane create the driving forces and pathways that enable vectorial (directional) transport. When a sorting signal is disrupted and channels distribute randomly, this carefully orchestrated asymmetry is lost, eliminating the cell's ability to transport ions directionally across the epithelium. Choice A is incorrect because ion gradients are actually different across apical and basolateral membranes - that's precisely what drives directional transport. Choice B misses the primary consequence; while barrier function might be affected, the most direct result is loss of directional transport capability. Choice C incorrectly assumes more channels equals better function, ignoring that proper localization matters more than quantity for epithelial transport. Choice D correctly identifies that transcellular transport depends fundamentally on asymmetric protein distribution. Without proper sorting, the epithelium loses its ability to create the coordinated ion movements necessary for functions like nutrient absorption or electrolyte balance. Remember: epithelial function questions often test whether you understand that location determines function. Asymmetric protein distribution isn't just organization - it's the mechanistic basis for directional transport across polarized barriers.

Question 10

In gastric parietal cells, H⁺/K⁺-ATPase pumps are located on the apical membrane facing the stomach lumen. During acid secretion, these cells also insert additional pump proteins from intracellular vesicles into the apical membrane. What would happen if these vesicles instead fused randomly with both apical and basolateral membranes?

  1. Acid secretion into the stomach would increase because more total pump proteins would be present in cellular membranes
  2. The cell would maintain normal function because H⁺/K⁺-ATPase activity does not depend on membrane location for proper operation
  3. Gastric acid production would decrease and cellular pH regulation would be disrupted due to inappropriate proton pumping directions (correct answer)
  4. Potassium homeostasis would improve because pumps in both membranes would provide better control over intracellular potassium levels
  5. The parietal cells would increase in size because membrane fusion events would add surface area to both apical and basolateral domains
Explanation: When you encounter questions about membrane proteins and cell polarity, focus on how protein location determines function and the consequences of disrupting normal cellular organization. Gastric parietal cells are highly polarized, with H⁺/K⁺-ATPase pumps strategically positioned on the apical membrane to pump protons into the stomach lumen while importing potassium from gastric juice. This creates the acidic environment needed for digestion. If vesicles containing these pumps fused randomly with both membranes, pumps on the basolateral side would pump protons out of the cell into the bloodstream while bringing potassium into the cell from blood. This would reduce net acid secretion into the stomach since some pumps would be working in the wrong direction. Additionally, pumping protons into the blood would disrupt the cell's pH regulation and could affect systemic pH balance. Option A incorrectly assumes more total pumps automatically means more acid production, ignoring that misdirected pumps would counteract stomach acid secretion. Option B fails to recognize that membrane sidedness is crucial—the same protein can have opposite physiological effects depending on which cellular compartment it faces. Option D misses the point entirely; while potassium movement would change, the primary issue is disrupted acid secretion and pH control, not improved homeostasis. Remember that in polarized epithelial cells, the apical and basolateral membranes have distinct functions. Protein mislocalization typically disrupts normal physiology rather than improving it, because cells evolved specific targeting mechanisms for optimal function.

Question 11

A research team measures the electrical resistance across an epithelial monolayer and finds it decreases significantly when extracellular calcium is removed. Simultaneously, they observe that a fluorescent tracer molecule that normally cannot cross the epithelium begins to appear on the opposite side. What is the most likely explanation?

  1. Calcium removal activates calcium-sensitive ion channels that increase membrane permeability to the tracer molecule through transcellular transport
  2. Loss of extracellular calcium disrupts tight junction integrity, creating paracellular leak pathways that reduce electrical resistance and allow tracer passage (correct answer)
  3. Calcium depletion causes cell shrinkage that opens mechanical gaps between cells, but tight junctions remain functionally intact
  4. Removal of calcium activates endocytic pathways that transport the tracer across cells through vesicular transcytosis mechanisms
  5. Calcium absence triggers apoptosis in scattered epithelial cells, creating discrete holes that account for both tracer passage and resistance changes
Explanation: When you encounter questions about epithelial barrier function, focus on the two main transport pathways: transcellular (through cells) and paracellular (between cells). The key clue here is the simultaneous decrease in electrical resistance and increased tracer permeability when calcium is removed. Tight junctions between epithelial cells are calcium-dependent structures that seal the paracellular space. These junctions contain proteins like claudins and occludins that require extracellular calcium to maintain their structural integrity. When calcium is depleted, these protein complexes destabilize, creating gaps in the normally tight seal between cells. This explains both observations: electrical resistance drops because ions can now leak between cells, and the fluorescent tracer can pass through these newly formed paracellular pathways. Answer A incorrectly suggests transcellular transport through ion channels, but ion channels wouldn't allow large tracer molecules to pass, and the mechanism doesn't explain the resistance change. Answer C describes mechanical gaps but claims tight junctions remain intact—this contradicts the calcium-dependence of tight junction stability. Answer D proposes transcytosis, which is an active transport mechanism that wouldn't cause the observed decrease in electrical resistance and doesn't explain why calcium removal would specifically activate this pathway. Remember that calcium depletion is a classic experimental technique to disrupt tight junctions. When you see "calcium removal + increased permeability + decreased resistance" together, think paracellular leak due to tight junction disruption. This combination of effects is the hallmark signature of compromised epithelial barrier integrity.

Question 12

An epithelial cell line grown on permeable filter supports shows robust transepithelial chloride secretion when stimulated with forskolin (which increases cAMP). This response is blocked when the apical medium contains a specific chloride channel inhibitor, but not when the same inhibitor is added to the basolateral medium. What does this suggest about the transport mechanism?

  1. Chloride channels are present only on the apical membrane, and chloride enters the cell through the basolateral membrane via a different transport mechanism
  2. The inhibitor cannot cross the tight junctions to reach chloride channels that are actually located on the basolateral membrane
  3. Forskolin specifically activates chloride channels on the apical side while having no effect on basolateral chloride transport proteins
  4. Chloride secretion requires coordinated transport involving basolateral chloride uptake followed by apical chloride channel-mediated efflux as the rate-limiting step (correct answer)
  5. The epithelial cells preferentially absorb the inhibitor from the apical medium, making it more effective when applied to that compartment
Explanation: When you encounter questions about epithelial transport, focus on the directional nature of secretion and which step limits the overall process. Epithelial chloride secretion is a coordinated, two-step process that moves chloride from the basolateral (blood) side to the apical (lumen) side of the cell. The key insight from this experiment is understanding what "rate-limiting step" means. Since the chloride channel inhibitor only blocks secretion when applied apically, this tells you that apical chloride efflux through channels is the bottleneck that controls the overall secretion rate. Chloride must first enter the cell from the basolateral side (likely through Na-K-2Cl cotransporters), then exit through apical chloride channels. The forskolin/cAMP stimulus activates these apical channels, making them the rate-limiting step, which is why answer D correctly describes this coordinated mechanism. Answer A is wrong because it ignores that inhibiting apical channels specifically blocks the rate-limiting step, not because basolateral chloride entry uses different proteins. Answer B incorrectly assumes the channels are basolateral when the evidence clearly shows apical channels control the process. Answer C misunderstands forskolin's mechanism - while forskolin does activate apical channels via cAMP, the question isn't about forskolin's selectivity but about which step limits transport. For epithelial transport questions, always consider the complete pathway from entry to exit, and remember that blocking the rate-limiting step eliminates the entire transport process, regardless of what happens at other steps.

Question 13

In a polarized epithelial cell, the Na⁺/K⁺-ATPase creates a potassium concentration of 140 mM inside the cell compared to 5 mM in the extracellular fluid. If potassium-selective channels are present only on the basolateral membrane, what is the predicted effect on the transepithelial electrical potential?

  1. The apical side will become positive relative to the basolateral side because potassium efflux through basolateral channels creates a diffusion potential (correct answer)
  2. The basolateral side will become positive relative to the apical side because potassium accumulation in the basolateral compartment increases local charge
  3. No transepithelial potential will develop because potassium channels are present on only one membrane domain of the epithelial cell
  4. The transepithelial potential will fluctuate because potassium channels undergo voltage-dependent gating in response to the concentration gradient
  5. The magnitude of the potential will equal the potassium equilibrium potential calculated from the Nernst equation using the given concentrations
Explanation: When analyzing transepithelial electrical potentials in polarized epithelial cells, you need to consider how ion gradients and selective membrane permeability create electrical differences across the entire epithelial layer. The Na⁺/K⁺-ATPase establishes a steep potassium gradient (140 mM intracellular vs. 5 mM extracellular), creating a strong driving force for K⁺ efflux. Since potassium-selective channels exist only on the basolateral membrane, K⁺ will flow down its concentration gradient from the cell into the basolateral compartment. This efflux leaves behind negatively charged proteins and other anions that cannot cross the membrane, making the cell interior (and by extension, the apical side) negative relative to the basolateral side where positive K⁺ ions accumulate. Option A correctly identifies this mechanism - potassium efflux through basolateral channels creates a diffusion potential that makes the apical side positive relative to the basolateral side. Option B incorrectly suggests the basolateral side becomes positive relative to the apical side, which contradicts the direction of the electrical gradient created by K⁺ efflux. Option C is wrong because a transepithelial potential will definitely develop - asymmetric distribution of ion channels is actually what enables epithelial cells to generate such potentials. Option D incorrectly focuses on voltage-dependent gating, but the question describes the steady-state condition where the concentration gradient, not voltage fluctuations, determines the potential. Remember: transepithelial potentials depend on both ion gradients and asymmetric channel distribution. The side losing positive ions becomes relatively negative.

Question 14

A researcher studying intestinal epithelial cells finds that amino acid absorption is completely abolished when both sodium and the amino acid are present only on the basolateral side, but absorption occurs normally when both are present on the apical side. However, when sodium is on the apical side and the amino acid is on the basolateral side, no absorption occurs. What does this pattern indicate?

  1. Amino acid transporters are present on both apical and basolateral membranes, but only the apical transporters are sodium-dependent
  2. Sodium-amino acid cotransporters are located exclusively on the apical membrane, and amino acid efflux occurs through basolateral uniporters (correct answer)
  3. The tight junctions are permeable to sodium but impermeable to amino acids, preventing substrate availability for transport
  4. Amino acid absorption requires sodium gradients that can only be established when both substrates enter through the apical membrane
  5. Basolateral amino acid transporters require sodium that must first be transported across the apical membrane to activate the basolateral transport system
Explanation: When you encounter questions about polarized epithelial transport, focus on the directional movement of substances and the specific location of different transporters on apical versus basolateral membranes. The experimental data reveals a classic pattern of transcellular amino acid transport. Normal absorption occurs when both sodium and amino acids are on the apical side because sodium-amino acid cotransporters are located exclusively on the apical membrane. These cotransporters use the sodium gradient (maintained by basolateral Na+/K+-ATPase) to drive amino acid uptake into the cell. Once inside, amino acids exit through separate, sodium-independent transporters (uniporters) on the basolateral membrane into the bloodstream. When both substrates are only on the basolateral side, no absorption occurs because there are no sodium-amino acid cotransporters on that membrane. When sodium is apical but amino acids are basolateral, transport fails because the cotransporter requires both substrates on the same side (apical) to function. Choice A is incorrect because amino acid transporters aren't functionally present on both sides—the basolateral transporters are uniporters, not sodium-dependent. Choice C wrongly focuses on tight junction permeability rather than transporter location and specificity. Choice D misunderstands the mechanism—the sodium gradient exists regardless of substrate location, but the cotransporter itself must be positioned where both substrates are available. Remember: In polarized epithelia, different membrane domains have distinct transporter types that work together to achieve directional transport across the tissue.

Question 15

In thyroid follicular epithelial cells, iodide is concentrated from the blood (basolateral side) into the follicular lumen (apical side) against a steep electrochemical gradient. This process requires ATP and is inhibited by ouabain, which blocks Na⁺/K⁺-ATPase. What is the most likely transport mechanism?

  1. Direct ATP-powered iodide pumps on both apical and basolateral membranes work in series to achieve the observed concentration gradient
  2. Basolateral sodium-iodide symporters use the sodium gradient created by Na⁺/K⁺-ATPase, followed by apical iodide channels for efflux into the lumen (correct answer)
  3. Apical ATP-dependent iodide pumps directly transport iodide from blood to lumen, with Na⁺/K⁺-ATPase providing general cellular energy maintenance
  4. Iodide enters through basolateral chloride channels and exits through apical iodide-chloride exchangers powered by the sodium gradient
  5. Transcytotic vesicles transport iodide across the cell, with Na⁺/K⁺-ATPase providing energy for vesicle fusion and trafficking processes
Explanation: When you encounter questions about transport across epithelial cells against gradients, think about secondary active transport mechanisms. The key clue here is that the process requires ATP and is inhibited by ouabain, which specifically blocks Na⁺/K⁺-ATPase. The correct mechanism involves a two-step process. First, Na⁺/K⁺-ATPase on the basolateral membrane creates a sodium gradient by pumping Na⁺ out and K⁺ in using ATP. This gradient then drives sodium-iodide symporters (NIS) on the basolateral membrane, which co-transport Na⁺ and I⁻ into the cell together. Finally, iodide exits through apical channels into the follicular lumen. This explains why ouabain inhibits the process—without the sodium gradient, the symporter can't function. Choice A is incorrect because direct ATP-powered iodide pumps don't exist in this system, and such a mechanism wouldn't explain the ouabain sensitivity. Choice C mislocates the ATP-dependent step—the primary active transport occurs basolaterally with Na⁺/K⁺-ATPase, not apically with iodide pumps. Choice D incorrectly describes the basolateral entry mechanism as passive chloride channels rather than the active sodium-iodide symporter that actually concentrates iodide against its gradient. The answer is B because it correctly identifies the coupling between primary active transport (Na⁺/K⁺-ATPase) and secondary active transport (Na⁺/I⁻ symporter). Remember: when ATP is required but the inhibitor targets Na⁺/K⁺-ATPase rather than the transported ion directly, look for secondary active transport mechanisms that depend on sodium gradients.

Question 16

A genetic mutation eliminates the expression of claudin-2 protein in intestinal epithelial cells. Claudin-2 normally forms paracellular channels selective for small cations like sodium. What would be the predicted effect on overall sodium absorption in the intestine?

  1. Sodium absorption would increase because transcellular transport would compensate for the loss of paracellular sodium movement
  2. Sodium absorption would decrease because paracellular sodium flux normally contributes significantly to total sodium uptake in the intestine (correct answer)
  3. Sodium absorption would remain unchanged because tight junctions normally prevent all paracellular ion movement regardless of claudin composition
  4. Sodium absorption would become more energy-efficient because all sodium transport would now occur through ATP-independent paracellular pathways
  5. The effect would depend on luminal sodium concentration, with high concentrations overcoming the loss of claudin-2 channels through increased transcellular transport
Explanation: When you encounter questions about tight junction proteins like claudins, focus on understanding how they regulate paracellular transport—the movement of substances between cells rather than through them. Claudin-2 creates selective paracellular channels that allow small cations like sodium to pass between intestinal epithelial cells. This paracellular sodium transport represents a significant portion of total intestinal sodium absorption, working alongside transcellular mechanisms (transport through cells via channels and pumps). When claudin-2 is eliminated, this important paracellular pathway is lost, reducing overall sodium absorption capacity. Answer B correctly identifies that sodium absorption would decrease because paracellular sodium flux normally contributes significantly to total sodium uptake. The intestine relies on both paracellular and transcellular routes for efficient sodium absorption. Answer A incorrectly assumes transcellular transport can fully compensate for lost paracellular transport. While some compensation might occur, it's unlikely to completely offset the loss of this major absorption pathway. Answer C contains a fundamental misconception—tight junctions don't prevent all paracellular movement. Their permeability depends entirely on their claudin composition, which is precisely what this question tests. Answer D reverses the energy relationships: paracellular transport through claudin-2 channels is actually the ATP-independent pathway, while transcellular transport often requires energy-dependent pumps. For cell biology exams, remember that claudin proteins determine tight junction selectivity and permeability. Different claudins create different paracellular transport properties—they're not just barriers but selective gatekeepers between cells.

Question 17

Researchers measure the transepithelial electrical resistance (TER) of cultured epithelial cells and find it increases 5-fold when extracellular chloride is replaced with an impermeant anion. Simultaneously, they observe that transcellular chloride transport (measured with radioactive ³⁶Cl⁻) is completely abolished. What is the most likely explanation?

  1. Chloride removal eliminates paracellular chloride leak pathways, increasing resistance, while transcellular transport stops due to lack of substrate availability (correct answer)
  2. The impermeant anion blocks chloride channels directly, preventing both paracellular leakage and transcellular transport through the same channels
  3. Chloride depletion causes tight junctions to close more tightly, increasing resistance, while simultaneously eliminating the driving force for transcellular chloride movement
  4. The replacement anion is larger than chloride and physically blocks paracellular pathways, while also preventing chloride binding to transcellular transporters
  5. Chloride removal disrupts the electrochemical gradients that normally drive both paracellular and transcellular ion movements across the epithelium
Explanation: When you encounter questions about transepithelial electrical resistance (TER) and ion transport, focus on the distinction between paracellular (between cells) and transcellular (through cells) pathways, and how substrate availability affects each. In this experiment, removing extracellular chloride creates two separate effects. The 5-fold increase in TER occurs because chloride ions normally leak through paracellular pathways between epithelial cells, providing a low-resistance shunt across the epithelium. When you eliminate chloride from the extracellular solution, this paracellular leak disappears, dramatically increasing the overall electrical resistance. Meanwhile, transcellular chloride transport stops completely because there's simply no chloride substrate available for the cellular transport machinery to move. Answer A correctly identifies both mechanisms: paracellular leak elimination increases resistance, while substrate unavailability stops transcellular transport. Answer B incorrectly suggests the impermeant anion directly blocks channels - but the effect is due to chloride absence, not channel blockade. Answer C wrongly claims tight junctions physically close tighter, when the resistance increase is actually due to eliminating the chloride leak current, not structural changes. Answer D incorrectly attributes the effects to physical blockade by a larger anion, but the key factor is chloride removal, not the replacement anion's size. For cell biology exams, remember that ion transport questions often test whether you can distinguish between loss of driving force (no substrate) versus active inhibition (channel blockers). Always consider both paracellular and transcellular contributions to epithelial electrical properties.

Question 18

An epithelial cell culture is treated with brefeldin A, which blocks protein transport from the endoplasmic reticulum to the Golgi apparatus. After 6 hours, researchers observe that established cell polarity is maintained, but newly synthesized membrane proteins fail to reach their correct membrane domains. What does this suggest about epithelial polarity maintenance?

  1. Epithelial polarity depends entirely on continuous protein synthesis and secretory pathway function for maintenance of membrane domain identity
  2. Once established, epithelial polarity is maintained by existing membrane proteins and cytoskeletal structures, independent of new protein delivery (correct answer)
  3. Brefeldin A selectively affects basolateral protein targeting while leaving apical protein sorting mechanisms intact through alternative pathways
  4. The secretory pathway is required only for initial polarity establishment but not for maintaining the concentration gradients that define membrane domains
  5. Epithelial cells can maintain polarity temporarily through protein recycling mechanisms that bypass the normal secretory pathway when it is blocked
Explanation: When you encounter questions about epithelial polarity and protein trafficking inhibitors, focus on distinguishing between what's needed to establish polarity versus what maintains it once formed. Brefeldin A blocks the ER-to-Golgi transport, essentially shutting down the secretory pathway for new proteins. The key observation here is that existing polarity remains intact even though newly made proteins can't reach their destinations. This tells you that once epithelial cells establish their apical-basal organization, they don't require continuous delivery of new membrane proteins to maintain that organization. The existing proteins already embedded in the appropriate membrane domains, along with established cytoskeletal networks and tight junctions, are sufficient to preserve the cell's polarized state. Option A is incorrect because the experiment directly shows that polarity maintenance doesn't depend entirely on continuous protein synthesis and secretory function—polarity persists despite blocking this pathway. Option C misinterprets the mechanism; brefeldin A blocks ER-to-Golgi transport globally, not selectively, and there aren't alternative pathways that bypass this block. Option D contains a grain of truth about initial establishment but incorrectly suggests the secretory pathway maintains concentration gradients, when the experiment shows existing structures handle maintenance. For cell biology exams, remember that established cellular architecture often has built-in stability mechanisms. Maintenance requirements are typically less demanding than establishment requirements—cells don't constantly rebuild their fundamental organization from scratch.

Question 19

A pharmaceutical company develops a drug that selectively opens potassium channels only when applied to the basolateral side of airway epithelial cells. When tested on cells that normally secrete chloride in response to cAMP elevation, what effect would this drug most likely have on chloride secretion?

  1. Chloride secretion would decrease because basolateral potassium efflux would depolarize the cell and reduce the driving force for apical chloride exit
  2. Chloride secretion would increase because enhanced basolateral potassium efflux would hyperpolarize the membrane and increase the driving force for apical chloride exit (correct answer)
  3. Chloride secretion would remain unchanged because potassium and chloride transport pathways operate independently in epithelial cells
  4. The effect would depend on extracellular potassium concentration, with high concentrations blocking chloride secretion and low concentrations enhancing it
  5. Chloride secretion would stop completely because potassium channel opening would eliminate the sodium gradients required for basolateral chloride uptake
Explanation: When you encounter questions about epithelial ion transport, focus on how membrane potential changes affect the driving forces for ion movement across both apical and basolateral membranes. In airway epithelial cells, chloride secretion depends on creating favorable electrochemical gradients. Normally, the Na⁺/K⁺-ATPase pump maintains a negative membrane potential, but opening additional basolateral potassium channels would enhance K⁺ efflux, making the membrane potential even more negative (hyperpolarization). This increased electrochemical driving force would promote greater chloride exit through apical CFTR channels, since chloride ions are driven out by both their concentration gradient and the more negative membrane potential. Answer B correctly identifies this mechanism - enhanced basolateral potassium efflux hyperpolarizes the membrane and increases the driving force for apical chloride exit, boosting secretion. Answer A contains a critical error: increased K⁺ efflux hyperpolarizes (doesn't depolarize) the cell, and this actually increases (not reduces) the driving force for chloride secretion. Answer C is incorrect because potassium and chloride transport are intimately connected through membrane potential. Changes in K⁺ permeability directly affect the electrochemical gradient driving Cl⁻ movement. Answer D misses the point entirely. The effect depends on the membrane potential change caused by K⁺ channel opening, not simply on extracellular potassium concentration. Remember: In epithelial transport questions, always consider how changes on one side of the cell affect the membrane potential and thus the driving forces for ion movement on the other side.

Question 20

Researchers studying gallbladder epithelial cells observe that water absorption is dramatically reduced when aquaporin water channels are blocked with mercury, but some water movement persists. The remaining water transport is eliminated when tight junctions are disrupted with EGTA (which chelates calcium). What does this suggest about water transport mechanisms?

  1. Water absorption occurs through both transcellular aquaporin-mediated transport and paracellular movement through tight junction pores, with aquaporins providing the major pathway (correct answer)
  2. Tight junctions contain water-selective channels that function independently of aquaporins, and both pathways contribute significantly to total water absorption
  3. Mercury treatment causes compensatory changes that redirect water transport from transcellular to paracellular pathways through tight junction modifications
  4. Aquaporins are located within tight junction complexes, and EGTA treatment eliminates water transport by disrupting the structural integrity of these channel proteins
  5. Water transport depends entirely on osmotic coupling to solute absorption, with aquaporins and tight junctions affecting solute rather than water movement directly
Explanation: When you encounter questions about cellular transport mechanisms, focus on distinguishing between transcellular (through cells) and paracellular (between cells) pathways, and understand how experimental interventions reveal which pathways are active. This experiment uses a classic approach: selectively blocking different transport mechanisms to determine their relative contributions. Mercury specifically blocks aquaporin water channels, dramatically reducing water absorption but not eliminating it completely. This tells you that aquaporins handle most water transport, but another pathway exists. When EGTA disrupts tight junctions by chelating calcium (essential for tight junction integrity), the remaining water transport disappears entirely. This confirms that the residual water movement was occurring paracellularly—between cells through tight junction pores. Answer A correctly identifies both mechanisms: aquaporin-mediated transcellular transport as the major pathway, plus paracellular movement through tight junctions as a minor but measurable contribution. Answer B incorrectly suggests tight junctions contain water-selective channels that function like aquaporins—they don't. Tight junctions are sealing structures with small pores, not specialized water channels. Answer C wrongly implies mercury causes compensatory changes. The experimental design shows mercury directly blocks aquaporins, revealing pre-existing paracellular transport rather than creating new pathways. Answer D mislocates aquaporins within tight junctions and suggests EGTA affects aquaporin structure. Aquaporins are transmembrane proteins distributed throughout the cell membrane, not concentrated in tight junctions. Remember: In transport physiology, most epithelial tissues use multiple pathways simultaneously. Look for evidence of parallel mechanisms when one pathway is blocked but function partially persists.