What Happens Next?
A protein-free lipid vesicle contains 300 mOsm/L of nonpenetrating solute. It is placed in 200 mOsm/L solution. Will it initially swell, shrink, or stay the same size? Explain.
It will swell. Water moves into the vesicle because the concentration of nonpenetrating solute is higher inside than outside.
Cells containing more Protein L also grow faster. Does this show that Protein L causes faster growth? Explain.
No. This is a correlation. Faster growth could increase Protein L, or another factor could increase both. A controlled manipulation of L is needed to test a causal role.
A membrane protein is released by high salt without dissolving the bilayer. Is this more consistent with a peripheral protein or a transmembrane protein? Why?
A peripheral protein. High salt can disrupt electrostatic interactions that attach it to the membrane surface. A transmembrane protein has hydrophobic regions embedded in the bilayer.
Oxygen enters a cell through the lipid bilayer, moving from higher to lower concentration. Is this simple diffusion, facilitated diffusion, or active transport? Explain.
Simple diffusion. Oxygen crosses the bilayer down its concentration gradient without a transport protein or direct ATP use.
Fix this explanation: "An intact plasma membrane guarantees that a cell can maintain homeostasis indefinitely, even without an energy supply."
An intact membrane is necessary but not sufficient for sustained homeostasis. Cells also need energy and functioning regulatory processes to maintain gradients, repair damage, and support metabolism.
Two otherwise identical membranes are at the same temperature. One has more cis-unsaturated fatty acid tails. Which is expected to be more fluid, and why?
The membrane with more cis-unsaturated tails. Their bends reduce tight packing between tails, generally increasing fluidity under these matched conditions.
A researcher wants to follow vesicle movement in living cells. Choose fluorescent live-cell imaging or conventional TEM, and explain your choice.
Fluorescent live-cell imaging. It can track labeled vesicles over time in living cells. Conventional TEM provides detailed ultrastructure from prepared, nonliving samples rather than continuous live movement.
A vesicle buds from the Golgi and then fuses with the plasma membrane. A protein's sugar chain faces the vesicle lumen. After fusion, does the sugar face the cytoplasm or the extracellular space?
The extracellular space. Membrane orientation is preserved: the vesicle's luminal surface becomes the extracellular surface after fusion.
A transporter moves Na+ and an amino acid into a cell together. The amino acid moves against its concentration gradient, powered by Na+ moving down its electrochemical gradient. Name the transport type and directional arrangement.
Secondary active transport by a symporter. Both solutes move in the same direction; the Na+ gradient supplies the energy for uphill amino acid transport.
Fix this explanation: "Internal membranes slow everything down, so removing them would always make a eukaryotic cell more efficient." Give two reasons.
Internal membranes maintain specialized conditions, such as different pH or ion concentrations, and separate potentially incompatible reactions. They also provide surfaces for membrane-based reactions. Removing them would disrupt these functions.
A cell's ATP supply falls sharply, but its ion gradients are initially unchanged. Will Na+-driven nutrient uptake necessarily stop at once? Predict the immediate and later effects.
Not necessarily. The existing Na+ electrochemical gradient can initially power uptake. Later, insufficient pumping allows the gradient to weaken, reducing the energy available for coupled nutrient transport.
A centrifugation pellet contains both a mitochondrial marker and an ER marker. Can the researcher call it a pure mitochondrial fraction? What do the results support?
No. The results support a mixed fraction or contamination with ER material. Marker detection helps identify components, but the pellet's presence alone does not establish purity.
Two matched FRAP experiments reach the same corrected recovery plateau of 85%. One reaches half of that recovery in 8 seconds; the other takes 30 seconds. What differs, and what is similar?
Recovery is slower in the second experiment, indicating slower effective mobility under the matched conditions. The estimated mobile fractions are similar at 85% within the observation period. Slower recovery alone does not imply a larger immobile fraction.
A carrier has Jmax = 80 units/min and Km = 2 mM. Use J = Jmax x S / (Km + S). Calculate J at S = 2 mM and explain what this reveals about Km.
J = 80 x 2 / (2 + 2) = 40 units/min. Km is the substrate concentration at which the transport rate is half of Jmax in this model.
Fix this explanation: "An organelle has a membrane, so it must have evolved from an engulfed bacterium." Name two more informative types of evidence.
A membrane alone does not establish endosymbiotic origin. More informative evidence includes phylogenetic relationships between organelle and bacterial genes and bacterial ancestry of organelle translation machinery. Independent lines of evidence should be considered together.
An acidic digestive compartment becomes nearly neutral. Its membrane is intact and its enzymes are still present. Predict the effect on digestion and propose one membrane-related cause.
Digestion by acid-dependent enzymes is likely to decrease. Reduced H+ pumping or increased H+ leakage could explain the loss of acidity. The observations alone do not distinguish these causes.
A fluorescently tagged receptor remains inside the cell instead of reaching the surface. Propose one comparison to test whether the tag caused this result, and predict a result that would support that explanation.
Compare the tagged receptor with the untagged receptor at similar expression levels, using an independent detection method. If the untagged receptor reaches the surface while the tagged version remains inside, that supports a tag-related disruption. Testing a different tag position can provide additional evidence.
Many coated membrane buds form but remain attached by narrow necks. Is the main observed failure in bending the membrane or separating the vesicle? Name one additional measurement that could help investigate it.
Separation of the vesicle is the main observed failure; budding has occurred. Measure recruitment or activity of relevant scission machinery, or directly follow bud release by imaging. This morphology alone does not identify the defective protein.
At 37 C, [K+]in = 100 mM and [K+]out = 10 mM. Use EK = 61.5 x log10(out/in). Calculate EK. If Vm is initially -80 mV, which way will K+ move through an open channel?
EK = 61.5 x log10(0.1) = -61.5 mV. K+ initially moves inward because Vm is more negative than EK; the net electrochemical force on K+ is inward.
Fix this explanation: "If a protein works inside mitochondria, its gene must be in mitochondrial DNA and it must be made inside the mitochondrion."
Many mitochondrial proteins are encoded in nuclear DNA, made on cytosolic ribosomes, and imported using targeting information and import machinery. A protein's working location does not necessarily identify where its gene is stored or where it is synthesized.
A cell has Vm = -75 mV and ECl = -45 mV. More Cl- channels open. Predict the initial direction of Cl- movement and the direction of the voltage change.
Cl- initially moves outward. Loss of negative charge depolarizes the membrane, moving Vm toward -45 mV. Opening Cl- channels does not always hyperpolarize a cell.
Reducing Protein T lowers nutrient uptake. Restoring normal T restores uptake. A mutant T does not restore uptake, but is barely detectable. Can you conclude that the mutated region directly transports the nutrient? Explain and give the next check.
No. Failure to rescue could reflect poor mutant stability or expression rather than loss of transport activity. First verify comparable protein abundance and appropriate localization. Even then, functional evidence is needed to distinguish direct transport from an indirect regulatory role.
Treatment moves phosphatidylserine to the outer cell surface, but a membrane-impermeant dye still cannot enter. Explain what changed and why this does not, by itself, prove that the membrane ruptured or that apoptosis is the only explanation.
Lipid asymmetry changed without detectable loss of the membrane's barrier to that dye. Surface PS can occur during apoptosis but also in other contexts. Additional apoptosis markers and time-course measurements are needed to identify the process.
At 37 C: K+ out/in = 12/120 mM; Na+ out/in = 120/12 mM. PK = 1, PNa = 0.1; ignore other ions and direct pump current. Calculate Vm = 61.5 x log10[(PK x Kout + PNa x Naout)/(PK x Kin + PNa x Nain)]. Is Vm equal to EK = -61.5 mV? Explain.
Vm = 61.5 x log10(24/121.2) = approximately -43.3 mV. It is more positive than EK because Na+ permeability also contributes. A membrane permeable to multiple ions need not sit at the equilibrium potential of any one ion.
Fix this explanation: "An archaeal genome contains genes related to eukaryotic membrane-remodeling proteins. This proves that the organism has a nucleus and can engulf bacteria." State what the finding supports and what remains unproven.
The finding supports evolutionary relationships and the possibility that some molecular components associated with eukaryotic functions predate eukaryotes. It does not establish a nucleus or phagocytosis. Cell imaging and direct functional experiments are needed to test those features.