Plasma Membrane Structure, Fluid Mosaic Model (2A)
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MCAT Biological and Biochemical Foundations of Living Systems › Plasma Membrane Structure, Fluid Mosaic Model (2A)
A toxin inserts into the outer leaflet of the plasma membrane and crosslinks neighboring phospholipid head groups without directly binding proteins. Shortly after exposure, FRAP of a labeled transmembrane protein shows reduced lateral recovery. Under the fluid mosaic model, which explanation is most consistent?
The only possible cause is that the toxin removed cholesterol, since lipid crosslinking cannot alter fluidity.
Reduced lipid mobility can indirectly reduce protein lateral diffusion because proteins and lipids move within the same bilayer environment.
Crosslinking lipids converts the plasma membrane into a peptidoglycan-like wall that blocks all motion.
Crosslinking lipids should not affect protein mobility because proteins move independently of the lipid bilayer.
Explanation
This question assesses how lipid modifications affect protein mobility per the fluid mosaic model. The fluid mosaic model describes the membrane as a fluid bilayer where lipids and proteins intermingle and diffuse together. Crosslinking outer leaflet lipids reduces overall fluidity, indirectly slowing protein lateral diffusion. Choice D is correct because the shared bilayer environment links lipid and protein mobility. Choice B fails as proteins do not move independently; their diffusion depends on lipid dynamics. A transferable check is to use a toxin that crosslinks proteins instead, expecting similar fluidity reduction. Note that membrane asymmetry can influence such effects but does not negate the fluid mosaic.
A cultured mammalian cell line is shifted from 37°C to 15°C for 30 minutes. Researchers then use fluorescence recovery after photobleaching (FRAP) on a GFP-tagged transmembrane receptor and observe slower lateral recovery at 15°C. The team proposes this is consistent with the fluid mosaic model of the plasma membrane. Which conclusion is most consistent with the model and the observation?
The receptor’s slower recovery reflects decreased lateral mobility of membrane components as the lipid bilayer becomes less fluid at lower temperature.
The receptor’s slower recovery is best explained by the receptor leaving the membrane into the cytosol because proteins are not stable in bilayers at low temperature.
The receptor’s slower recovery indicates the bilayer has converted into a rigid cell wall-like lattice that prevents any protein diffusion.
The receptor’s slower recovery implies membrane proteins are fixed in place while only phospholipids diffuse laterally.
Explanation
This question tests understanding of how temperature affects membrane fluidity in the fluid mosaic model. The fluid mosaic model describes the plasma membrane as a dynamic lipid bilayer with embedded proteins that can diffuse laterally, influenced by factors like temperature. In this experiment, shifting cells to a lower temperature reduces the kinetic energy of membrane components, increasing bilayer viscosity. Choice D is correct because decreased fluidity at 15°C limits lateral mobility, leading to slower FRAP recovery of the receptor. Choice B is incorrect because the model does not suggest the bilayer becomes a rigid cell wall-like structure; it remains a fluid bilayer even if less mobile. To verify similar effects, check if warming the cells restores rapid recovery, confirming temperature-dependent fluidity. Remember that cholesterol can modulate these temperature effects by maintaining fluidity across ranges.
A neuron is exposed to a brief local cooling of its axonal membrane. Patch-clamp recordings show reduced conduction velocity without a change in ion channel expression. In the context of the fluid mosaic model, which explanation is most consistent with the observation?
Cooling increases bilayer fluidity, causing ion channels to detach from the membrane and stop conducting.
Cooling fixes all membrane proteins permanently in place, eliminating any conformational changes required for ion passage.
Cooling primarily thickens the cell wall, increasing electrical resistance across the axon.
Cooling reduces bilayer fluidity, which can alter channel conformational dynamics and local membrane protein mobility, slowing signaling.
Explanation
This question evaluates how membrane fluidity impacts neuronal signaling under the fluid mosaic model. The fluid mosaic model views the plasma membrane as a flexible lipid bilayer with mobile proteins, including ion channels crucial for action potentials. Local cooling of the axonal membrane decreases fluidity, affecting channel dynamics and protein mobility without altering expression. Choice D is correct because reduced fluidity slows conformational changes and diffusion, impairing conduction velocity. Choice B fails as cooling decreases, not increases, fluidity, and channels remain embedded rather than detaching. For verification, test if rewarming restores normal velocity, linking fluidity to function. Recall that membrane composition, like unsaturation, helps maintain fluidity in varying conditions.
A student predicts that flipping (transverse movement) of phospholipids between leaflets should occur as readily as lateral diffusion because the membrane is “fluid.” In a live-cell assay, spontaneous flip-flop is rare compared with lateral diffusion. Which reasoning best fits the fluid mosaic model?
Lateral diffusion is frequent because it preserves head group exposure to water, whereas flip-flop is slow because the polar head must cross the hydrophobic core.
Flip-flop is slow because the membrane is a rigid wall; lateral diffusion occurs only in the cytosol.
Flip-flop is slow because cholesterol always increases fluidity and prevents transverse movement.
Flip-flop is slow because all phospholipids are covalently attached to membrane proteins.
Explanation
This question addresses phospholipid movement dynamics in the fluid mosaic model. The fluid mosaic model views phospholipids as amphipathic molecules in a bilayer, allowing lateral diffusion but restricting flip-flop due to the hydrophobic core. Lateral diffusion is favored as it keeps polar heads aqueous, while flip-flop requires head groups to traverse the nonpolar interior, making it rare. Choice D is correct by explaining the energetic barrier to transverse movement. Choice B is wrong because the membrane is not a rigid wall; flip-flop is slow due to bilayer properties. A transferable check is to use flippases, which catalyze flip-flop, increasing its rate. Note that proteins can facilitate specific lipid movements.
A lab increases cholesterol in the plasma membrane of a mammalian cell and then measures passive permeability to water and small uncharged solutes at 37°C. Permeability decreases. Which statement is most consistent with the fluid mosaic model and these results?
Cholesterol can reduce free volume between phospholipids at 37°C, decreasing bilayer permeability to small solutes.
Cholesterol increases permeability by acting as a hydrophilic pore that conducts water.
Cholesterol decreases permeability only by removing all peripheral proteins from the membrane surface.
Cholesterol decreases permeability because it converts the bilayer into a cellulose-based barrier.
Explanation
This question evaluates cholesterol's influence on permeability under the fluid mosaic model. The fluid mosaic model describes the membrane as a semi-permeable bilayer where cholesterol modulates lipid packing and solute passage. Increasing cholesterol at 37°C tightens packing, reducing permeability to water and small solutes. Choice A is correct by linking cholesterol to decreased free volume and permeability. Choice B fails as cholesterol does not form hydrophilic pores; it integrates hydrophobically. For verification, deplete cholesterol and expect increased permeability. Recall that permeability also depends on lipid saturation and temperature.
A cell is gradually adapted to cold conditions over several days. Without changing total lipid amount, the cell increases the fraction of unsaturated fatty acyl chains in its plasma membrane. Which outcome is most consistent with the fluid mosaic model and the adaptive change?
The membrane maintains higher fluidity at low temperature because unsaturated chains reduce packing, supporting lateral mobility of proteins and lipids.
The membrane becomes a rigid protein sheet because unsaturated chains displace all phospholipids.
The membrane becomes less fluid at low temperature because unsaturated chains pack more tightly than saturated chains.
The membrane’s behavior is unchanged because fluidity is determined only by the number of integral proteins, not lipid composition.
Explanation
This question tests adaptive lipid changes for fluidity homeostasis in the fluid mosaic model. The fluid mosaic model depicts the membrane as adjustable, with lipid composition modulating fluidity against environmental stress. Increasing unsaturated chains introduces kinks, reducing packing and maintaining fluidity in cold conditions. Choice A is correct as it supports mobility preservation via composition changes. Choice B is incorrect because unsaturated chains decrease, not increase, packing compared to saturated. To verify, measure diffusion rates pre- and post-adaptation. Remember, such homeoviscous adaptation is common in poikilotherms.
Two populations of the same cell are compared: Population A has decreased cholesterol; Population B is unmodified. At 37°C, Population A shows increased lateral diffusion of a fluorescent lipid probe and increased membrane leakiness to small solutes. Which conclusion is most consistent with the fluid mosaic model?
Lower cholesterol can increase membrane fluidity and permeability at 37°C by reducing ordering of phospholipid acyl chains.
Lower cholesterol increases fluidity because cholesterol is a rigid protein that blocks lipid motion.
Lower cholesterol increases permeability because it converts the plasma membrane into a porous cell wall.
Lower cholesterol decreases fluidity at 37°C by preventing phospholipids from interacting, reducing permeability.
Explanation
This question evaluates effects of cholesterol depletion on fluidity and permeability in the fluid mosaic model. The fluid mosaic model posits cholesterol as a key regulator of lipid ordering, with depletion increasing fluidity at 37°C. Lower cholesterol in Population A reduces packing, enhancing diffusion and leakiness. Choice A is correct by connecting depletion to increased fluidity and permeability. Choice B is incorrect because depletion increases, not decreases, fluidity. For verification, add back cholesterol and expect reversal. Remember, optimal cholesterol levels balance fluidity and barrier function.
A researcher observes that a membrane protein’s extracellular domain can be cleaved by a protease added outside the cell, but the protein remains membrane-associated afterward. Which interpretation is most consistent with the fluid mosaic model?
The protein can be integral; cleavage of an exposed domain does not require removal from the bilayer, which remains a dynamic lipid matrix.
The observation implies the membrane is a rigid wall; protease access indicates pores formed by cellulose fibers.
The observation implies lipids are fixed and proteins freely exchange between membrane and cytosol after cleavage.
The observation proves the protein is peripheral, because integral proteins cannot have extracellular segments.
Explanation
This question probes protein topology and membrane dynamics in the fluid mosaic model. The fluid mosaic model allows integral proteins to have extracellular domains accessible to proteases while remaining embedded in the fluid bilayer. Cleavage removes the domain but leaves the protein membrane-associated. Choice A is correct, consistent with dynamic integral proteins. Choice B is incorrect as integrals can have extracellular parts. For verification, sequence the protein for transmembrane domains. Note that such cleavages can regulate protein function.
Cells are engineered to produce phospholipids with more saturated fatty acyl chains in their plasma membranes, without changing cholesterol levels. At 37°C, the cells show reduced uptake of a small hydrophilic dye that normally crosses slowly by passive diffusion. Based on the fluid mosaic model, which interpretation is most consistent?
The change implies the plasma membrane behaves like a rigid cell wall that blocks diffusion regardless of lipid composition.
More saturated acyl chains primarily increase the number of integral proteins, decreasing dye permeability.
More saturated acyl chains increase bilayer packing, decreasing membrane fluidity and lowering passive permeability to polar solutes.
More saturated acyl chains increase membrane fluidity by creating kinks, increasing dye permeability.
Explanation
This question tests the impact of lipid saturation on membrane permeability via the fluid mosaic model. The fluid mosaic model portrays the plasma membrane as a dynamic bilayer where lipid composition affects fluidity and barrier properties. Engineering more saturated chains enhances packing, reducing fluidity and passive diffusion of polar dyes. Choice D is correct because tighter packing decreases permeability without involving proteins or wall-like structures. Choice B is wrong as saturated chains increase packing, not fluidity via kinks, which are from unsaturation. A transferable check is to measure permeability with unsaturated lipids, expecting increased uptake. Remember, cholesterol can further modulate these saturation effects on fluidity.
In an experiment, cells are exposed to a drug that selectively extracts cholesterol from the plasma membrane. Immediately afterward, cells are cooled from 30°C to 5°C, and researchers observe an increase in membrane-associated protein clustering (reduced mixing) over minutes. Under the fluid mosaic model, which explanation best accounts for increased clustering after cholesterol extraction and cooling?
Clustering increases because all membrane proteins are integral and must aggregate when cholesterol is removed from the cytosol.
Cooling decreases lipid motion; without cholesterol to prevent tight packing at low temperature, the bilayer becomes less fluid and components mix less efficiently.
Cooling increases lipid motion; without cholesterol, the bilayer becomes hyperfluid and proteins cluster to avoid excessive diffusion.
Cholesterol extraction converts the plasma membrane into a cell wall, which forces proteins into fixed clusters.
Explanation
This question tests understanding of cholesterol's role in preventing membrane phase transitions in the fluid mosaic model. The fluid mosaic model describes membranes as dynamic structures where lipids and proteins can mix through lateral diffusion, with this mixing dependent on membrane fluidity. When cholesterol is extracted and cells are cooled from 30°C to 5°C, the membrane loses its fluidity buffer. At 5°C, phospholipids pack very tightly without cholesterol to space them apart, dramatically reducing membrane fluidity. This decreased fluidity reduces the lateral diffusion of both lipids and proteins, preventing efficient mixing and leading to protein clustering as components become less mobile. Choice B incorrectly claims cooling increases lipid motion, contradicting basic thermodynamics. Choice C incorrectly invokes cell wall formation, which doesn't occur in animal cells. The transferable insight: cholesterol prevents gel-phase formation at low temperatures, and its removal allows membranes to become highly rigid when cooled.