How a membrane that blocks almost everything nonetheless moves exactly what the cell needs — by diffusion, by carriers and channels, by ATP-driven pumps, and by coupling one gradient to another. Plus the electrical consequences the lecture skipped but the exam won't: selectivity, membrane potential, and action potentials. Verified against Alberts, Molecular Biology of the Cell, 7th ed., Chapter 11.
Source: Chapter 11 (transport + electrical properties)Format: Scantron MCQStudy mode: click any option for full reasoning
correct answer + mechanism distractor = named misconception▲ amber = lecture diverges from textbook
§Introduction
A membrane's whole value is that it blocks things — but a cell that blocked everything would starve, poison itself, and lose every gradient it depends on. The problem this chapter solves is selective permeability: how to keep the hydrophobic bilayer as a near-perfect barrier to ions and polar molecules, while still moving glucose in, waste out, and building the ion gradients that power nerves, muscles, and nutrient uptake.
Two facts set up everything. First, what crosses unaided is dictated by hydrophobicity and size: small nonpolar molecules (O₂, CO₂, steroids) slip through the bilayer; water and small uncharged polar molecules trickle through slowly; and ions and sugars essentially cannot cross at all. Second, to move those blocked solutes the cell uses membrane transport proteins — either channels (pores that let appropriate solutes flow down their gradient) or carriers/transporters (which bind a specific solute and change shape to ferry it across). Transport is either passive (downhill, no energy) or active (uphill, requires energy — ATP or a coupled gradient).
The lecture covered the transport core and then spent considerable time on vesicular transport (endocytosis, exocytosis, phagocytosis, viral entry). Note a structural point flagged throughout: in Alberts, small-molecule transport is Ch. 11, but vesicular traffic is Ch. 13 — it moves cargo without crossing the bilayer, a different mechanism entirely. This guide also restores the electrical half of Ch. 11 the lecture omitted (channel selectivity, resting potential, action potentials), which is high-yield and contains two points where common phrasing — including the lecture's — is misleading. Those are flagged in amber.
◎Learning Objectives
What the exam will hold you responsible for
Rank molecules by bilayer permeability (hydrophobic ≫ small polar > large polar ≫ ions) and explain why in terms of hydrophobicity and size.
Distinguish channels from carriers mechanistically — weak interaction + open pore vs. specific binding + conformational change — and know both can be passive.
Separate passive from active transport, and define the electrochemical gradient (concentration + charge) that governs ion movement.
Explain the Na⁺/K⁺ pump cycle (3 Na⁺ out, 2 K⁺ in, ATP, phosphorylation, conformational change), why it's electrogenic, and that it consumes ~⅓ of a cell's ATP.
Describe coupled transport (symport/antiport) using Na⁺-driven glucose uptake, and the logic of chemiosmosis (active H⁺ pumping → passive flow drives ATP synthase).
Explain ion-channel selectivity via the carbonyl-oxygen filter — and why "pore size" is the wrong model (Na⁺ is smaller than K⁺).
Account for the resting membrane potential: dominated by K⁺ leak channels and the K⁺ gradient; the electrogenic pump contributes <10% directly.
Outline the action potential (voltage-gated Na⁺ then K⁺ channels) and the three modes of vesicular transport (phago-, pino-, receptor-mediated endocytosis), including the CFTR/cystic-fibrosis case.
1Why Transport Is Needed: Selective Permeability
The bilayer's hydrophobic core is the barrier, and it discriminates by two properties: hydrophobicity and size. A molecule must dissolve into the oily core to cross unaided — so nonpolar molecules pass, and polar/charged ones are blocked. The result is a permeability ranking you should be able to reproduce cold.
Relative permeability of a pure lipid bilayer. The smaller and more hydrophobic the molecule, the faster it crosses. Ions — regardless of their small size — are effectively blocked by charge, which is what makes controlled ion gradients possible. Textbook Fig. 11–1.
The permeability ranking (Figure 11–1)
Hydrophobic molecules — high permeability. O₂, CO₂, N₂, steroid hormones dissolve in the core and diffuse straight through. No protein needed.
Small uncharged polar molecules — intermediate. Water, glycerol, urea cross slowly. Small enough to squeeze through, but polar, so it's inefficient — cells add aquaporins to speed water specifically.
Large uncharged polar molecules — low. Glucose, sucrose barely cross; they need transporters.
Ions — essentially impermeable. Na⁺, K⁺, Ca²⁺, Cl⁻, H⁺, HCO₃⁻ cannot cross the bilayer at all — their charge makes dissolving in the hydrophobic core prohibitive. They require channels or pumps, and this near-total block is exactly what lets cells build steep ion gradients.
Textbook note. It's tempting to think "small = crosses easily." Correction: for ions, charge dominates over size. A bare Na⁺ is tiny, yet it cannot cross the bilayer, because stripping its water shell and inserting a charge into the hydrophobic core is enormously costly. This same logic returns in §6 (why the K⁺ channel selectivity filter is not a size sieve) — Na⁺ being smaller than K⁺ is exactly why a size model breaks. (Ch. 11, Fig. 11–1)Flag this for the exam.
2Two Protein Classes: Channels vs Carriers
Everything the bilayer blocks moves through one of two kinds of transport protein. The distinction is mechanistic and the exam leans on it hard.
Channels: weak interaction, an open pore
A channel forms a continuous pore across the bilayer. When open, it lets suitable solutes flow through, discriminating mainly by size and charge and interacting with them only weakly — the solute is not tightly bound. The lecture's analogy: a pet door sized for a cat lets in anything small enough, without "recognizing" each animal. Channels move solutes fast (millions/second) and are usually gated (they open/close in response to a signal), but the gating step is a conformational switch of the whole channel, not binding of the cargo.
Carriers (transporters): specific binding, conformational change
A carrier (transporter) works differently: it binds a specific solute at a binding site, then undergoes a series of conformational changes that expose that site first to one side of the membrane, then to the other — physically ferrying the solute across. Because it depends on specific binding and a shape change, a carrier is solute-specific and much slower than a channel. Glucose transporters are the classic example. Crucially, carriers can operate passively (facilitated diffusion) oractively (pumps are carriers coupled to energy).
Channel vs carrier. Channels are pores that let solutes flow through with weak interaction (fast, size/charge-selective). Carriers bind a specific solute and change conformation to move it (slow, highly specific). Only carriers can pump uphill. Textbook Figs. 11–3, 11–4.
◆ Misconception
"Channels and carriers are basically the same, just holes of different sizes." Fix: the mechanisms differ fundamentally. A channel is an open pore with weak solute interaction and no obligatory shape change per solute; a carrierbinds its solute and undergoes a conformational cycle to move each one. This is why carriers are specific and slow, can saturate (like an enzyme), and can be coupled to energy to pump — while channels cannot pump uphill. (Ch. 11, transporters vs. channels)
3Passive Transport & the Electrochemical Gradient
Passive transport is any movement down a gradient — it releases free energy and needs no energy input. It comes in two flavors, and confusing the second one with active transport is a top exam error.
Simple vs facilitated diffusion — both passive
Simple diffusion: the solute dissolves in and crosses the bilayer directly, down its concentration gradient, until concentrations equalize. No protein. Works only for the permeant molecules of §1 (O₂, CO₂, steroids; slowly, water).
Facilitated diffusion: the solute crosses through a channel or carrier, but still down its gradient and still with no energy input. The protein provides a path for solutes the bilayer blocks (glucose via GLUT carriers; ions via channels), but does not push them uphill.
The lecture's tell for "no energy needed": the couch potato / swimming with the current. Both simple and facilitated diffusion are downhill — the protein in facilitated diffusion changes the route, not the direction.
For ions: the electrochemical gradient
For an uncharged solute, direction depends only on the concentration gradient. For an ion, you must add the electrical gradient (the membrane potential). The combined driving force is the electrochemical gradient — the sum of (1) the concentration difference and (2) the voltage across the membrane. An ion can even move against its concentration gradient if the electrical force is strong enough (and vice versa). This is why "downhill" for an ion means "down its electrochemical gradient," not merely its concentration gradient.
Both are passive. Simple diffusion crosses the bilayer directly; facilitated diffusion goes through a channel or carrier. Both move solutes down their gradient with no energy — the protein changes the path, not the thermodynamics. Textbook Fig. 11–4.
◆ Misconception
"Facilitated diffusion uses a protein, so it must be active transport." Fix: using a transport protein does not make transport active. Facilitated diffusion is passive — solute moves down its gradient with no energy input. What defines active transport is moving a solute up its (electrochemical) gradient, which requires energy. Protein-mediated ≠ active. (Ch. 11, facilitated diffusion vs. active transport)
4Active Transport & Pumps
Active transport moves a solute up its electrochemical gradient — which costs energy, supplied either by ATP hydrolysis (primary active transport / pumps) or by another ion's downhill gradient (secondary active transport / coupled transport, §5). Only carriers can do this; channels cannot. The lecture's image: swimming against the current takes work.
The Na⁺/K⁺ pump — the master gradient-maker
The Na⁺/K⁺ ATPase is the exam's flagship pump. Per cycle it moves 3 Na⁺ out and 2 K⁺ in, both against their gradients, using one ATP. The mechanism is a phosphorylation-driven conformational cycle:
3 Na⁺ bind at high-affinity sites facing the cytosol.
This triggers ATP hydrolysis and phosphorylation of the pump.
Phosphorylation drives a conformational change that exposes the Na⁺ sites to the outside and lowers their affinity → 3 Na⁺ released outside.
2 K⁺ bind at newly exposed high-affinity sites facing outside; this triggers dephosphorylation.
Dephosphorylation reverts the conformation, exposing K⁺ sites to the cytosol and lowering their affinity → 2 K⁺ released inside.
Two consequences to memorize: because it moves 3 out for 2 in, the pump is electrogenic — it exports net positive charge, contributing to the inside-negative membrane potential (but only slightly, directly — see §7). And it is expensive: a typical animal cell spends ~⅓ of its ATP running this pump (more in neurons). The Na⁺ gradient it builds then powers nutrient uptake (§5) and pH regulation.
The Na⁺/K⁺ pump cycle. Na⁺ binding → phosphorylation → conformational change exports 3 Na⁺; K⁺ binding → dephosphorylation → imports 2 K⁺. Net export of positive charge makes it electrogenic. Textbook Figs. 11–11, 11–12.
Other pumps and their energy sources
Ca²⁺ pumps (Ca²⁺ ATPases) keep cytosolic Ca²⁺ extremely low by pumping it out of the cytosol (across the plasma membrane or into the ER), which is what makes a Ca²⁺ influx a usable signal.
ABC transporters — the largest family of membrane transport proteins — use ATP to pump a huge variety of small molecules; some drive multidrug resistance in cancer cells by exporting drugs.
ATP synthase runs the logic in reverse and is the key to chemiosmosis (below).
Chemiosmosis: coupling active and passive transport
The lecture's mitochondrial example ties active and passive transport together. A pump actively transports H⁺ across the inner mitochondrial membrane, building a steep H⁺ gradient. That stored gradient then drives H⁺ passively back through ATP synthase, whose rotation synthesizes ATP. So active transport spends energy to build a gradient, and passive flow through the synthase captures energy as ATP — a battery-and-turbine arrangement.
Textbook note. The lecture describes the H⁺-gradient/ATP-synthase process as "glycolysis... in the mitochondria." Correction: that process is oxidative phosphorylation (the electron-transport chain building the H⁺ gradient, ATP synthase making ATP). Glycolysis is cytosolic — it occurs in the cytoplasm, not the mitochondria, and doesn't use a membrane H⁺ gradient. The chemiosmotic coupling shown is real; the label "glycolysis" is wrong. (Ch. 11 chemiosmosis; Ch. 14 oxidative phosphorylation)Flag this for the exam.
5Coupled Transport (Symport & Antiport)
Cells rarely burn ATP directly to import each nutrient. Instead they use the Na⁺ gradient (already built and maintained by the Na⁺/K⁺ pump) as a rechargeable battery: let Na⁺ flow downhill through a carrier, and couple that to dragging a second solute uphill. This is secondary active transport, or coupled transport.
Symport vs antiport
Symport: the two solutes move in the same direction. Example: Na⁺-glucose symport in the gut and kidney — Na⁺ moving into the cell down its gradient powers glucose moving into the cell against its gradient.
Antiport: the two solutes move in opposite directions. Example: a Na⁺/H⁺ antiporter that imports Na⁺ while exporting H⁺ to regulate cytosolic pH.
The key insight: the energy for the uphill solute doesn't come from ATP at this carrier — it comes from the Na⁺ gradient, which the Na⁺/K⁺ pump paid for earlier with ATP. Poison the pump and the Na⁺ gradient collapses, and coupled glucose uptake stops too.
Na⁺-glucose symport. Downhill Na⁺ entry is coupled to uphill glucose entry through one carrier. The Na⁺/K⁺ pump (ATP) recharges the Na⁺ gradient — so glucose uptake is indirectly ATP-powered. Textbook Fig. 11–9.
6Ion Channels: Selectivity & Gating
Ion channels are not just holes — they are exquisitely selective and tightly controlled. This whole section is Ch. 11 material the lecture did not cover, and it contains one of the most-tested conceptual traps in membrane biology.
7The Membrane Potential
Every animal cell holds a voltage across its plasma membrane — the inside is negative relative to the outside (typically around −60 to −90 mV). This resting membrane potential is the battery behind nerve and muscle signaling. The lecture attributed it to the electrogenic Na⁺/K⁺ pump; the textbook is explicit that this is mostly wrong, and the distinction is exactly the kind of thing an exam targets.
K⁺ leak channels set the resting potential
Nearly all cells have K⁺ leak channels that are open at rest, making the resting membrane far more permeable to K⁺ than to any other ion. Here's the causal chain:
The Na⁺/K⁺ pump builds a steep K⁺ gradient (high inside).
Through the open K⁺ leak channels, K⁺ diffuses out down that concentration gradient.
Each K⁺ that leaves carries positive charge out, leaving the inside increasingly negative.
That growing negativity pulls K⁺ back in. Equilibrium is reached when the outward concentration force balances the inward electrical force — and the voltage at that balance point is the resting potential (the K⁺ equilibrium potential, quantified by the Nernst equation).
So the resting potential is essentially a K⁺ diffusion potential, set by the K⁺ gradient and the dominance of K⁺ permeability — not directly by the pump.
The resting potential is a K⁺ diffusion potential. Open K⁺ leak channels let K⁺ exit down its gradient, charging the inside negative until the electrical pull balances the concentration push. The pump's job is to maintain the K⁺ gradient, not to set the voltage directly. Textbook Fig. 11–22.
Textbook note. The lecture says the electrogenic Na⁺/K⁺ pump (3 out, 2 in) "creates" the inside-negative membrane potential. Correction: the textbook states the pump's electrogenic effect "seldom directly contributes more than 10%" to the membrane potential — the remaining ~90% depends on K⁺ leak channels and the K⁺ gradient. The pump is indispensable, but indirectly: it builds the K⁺ gradient that the leak channels then convert into voltage. Attributing the resting potential mainly to the pump's charge export is the error. (Ch. 11: "The Membrane Potential… Depends Mainly on K⁺ Leak Channels and the K⁺ Gradient")Flag this for the exam.
8Action Potentials & Signaling Channels
The resting potential is a charged battery; the action potential is how neurons and muscle cells discharge and recharge it to send a signal. This is the payoff of voltage-gated channels, and it's pure Ch. 11 that the lecture omitted.
The sequence: Na⁺ in, then K⁺ out
Trigger. A stimulus (e.g. a ligand-gated channel opening at a synapse) depolarizes the membrane — the inside becomes less negative.
Depolarization spike. If depolarization reaches threshold, voltage-gated Na⁺ channels snap open; Na⁺ rushes in down its steep electrochemical gradient, driving the inside sharply positive. This is all-or-none.
Repolarization. The Na⁺ channels quickly inactivate, and slower voltage-gated K⁺ channels open; K⁺ flows out, restoring the negative interior.
Propagation. The local depolarization triggers neighboring voltage-gated Na⁺ channels, so the spike travels along the membrane as a self-regenerating wave.
The Na⁺/K⁺ pump doesn't drive the spike (it's far too slow); it restores the gradients over time. The action potential itself is powered by ions rushing down gradients through voltage-gated channels.
The action potential. Voltage-gated Na⁺ channels open → Na⁺ influx → sharp depolarization; they inactivate as voltage-gated K⁺ channels open → K⁺ efflux → repolarization. Self-propagates along the axon. Textbook Figs. 11–28, 11–29.
9Vesicular Transport (Endo- & Exocytosis)
Textbook note. The lecture covered endocytosis/exocytosis under "transport of small molecules," but in Alberts this is Chapter 13 (Intracellular Vesicular Traffic), not Ch. 11. It's a genuinely different mechanism: vesicular transport moves cargo without crossing the bilayer — a membrane-bound pocket buds off, travels, and fuses elsewhere, delivering its contents by membrane fusion. Ch. 11 transport (channels/carriers/pumps) moves individual solutes through the bilayer. Keep the two mechanisms distinct, but expect this content on the exam since the lecture taught it here. (Alberts Ch. 13)Flag this for the exam.
Exocytosis and endocytosis
A vesicle is a membrane-bound pocket. Because it can fuse with the plasma membrane, it ferries material across the boundary without any solute ever dissolving through the bilayer:
Vesicular transport. Receptor-mediated endocytosis concentrates specific cargo via clathrin-coated pits; phagocytosis engulfs large particles; exocytosis fuses vesicles to release contents outside. Cargo never crosses the bilayer — it's carried inside a membrane compartment. Alberts Ch. 13.
Exocytosis: an intracellular vesicle fuses with the plasma membrane, releasing its contents outside the cell (secretion; also how proteins from the ER/Golgi reach the surface).
Endocytosis: the plasma membrane invaginates and pinches off a vesicle, bringing material into the cell.
Three modes of endocytosis
Phagocytosis ("cell eating"): uptake of large particles — bacteria, cell debris. Prominent in macrophages and neutrophils, which surround the particle with pseudopods and trap it in a phagosome that then fuses with lysosomes for degradation.
Pinocytosis ("cell drinking"): non-specific uptake of extracellular fluid and its dissolved solutes.
Receptor-mediated endocytosis:specific uptake of particular molecules (e.g. LDL) that bind surface receptors. The receptors cluster in a membrane patch coated on its cytosolic side by the protein clathrin; the coated pit deepens and buds off as a clathrin-coated vesicle, concentrating the target cargo.
Immune uptake and viral entry
Two applications the lecture stressed:
Opsonization (receptor-mediated phagocytosis): antibodies coat a bacterium; their Fc regions are recognized by Fc receptors on macrophages/neutrophils, triggering efficient engulfment. The interaction is indirect (via antibody) but highly specific and strong.
Enveloped virus entry: viruses like HIV carry surface attachment proteins (e.g. gp120) that recognize specific host receptors — determining which cells they infect. The viral envelope then fuses with the plasma membrane, delivering the virus inside. This mirrors normal vesicle fusion, exploited by the pathogen.
Medical case: cystic fibrosis and the CFTR channel
Cystic fibrosis is a genetic disease caused by a defective chloride channel, CFTR — an ATP-gated anion channel that lets Cl⁻ flow down its electrochemical gradient across epithelial cells lining the airways, gut, and reproductive tract. Mutation misfolds CFTR, disrupting Cl⁻ (and consequent water/salt) movement, so secretions that should be thin become thick, sticky mucus that clogs ducts — most damagingly in the lungs. It ties the whole topic together: a single malfunctioning membrane transport protein produces systemic disease, and gene therapy to restore functional CFTR is an active treatment avenue.
◆ Misconception
"Endocytosis is just another way small molecules cross the membrane, like a big channel." Fix: in vesicular transport, cargo is never dissolved through the bilayer. It is enclosed in a membrane vesicle that buds and fuses — the material ends up on the other side inside a compartment, not by permeating the lipid core. This is mechanistically distinct from channel/carrier/pump transport (and is why it can move huge cargo like whole bacteria). (Alberts Ch. 13)
✦Core Concepts — Rapid Review
Everything most likely to be tested, compressed. If any line isn't instantly familiar, reread that section.
Selective Permeability
Know. Small nonpolar molecules cross freely; small polar cross slowly; ions and large polar molecules need transporters.
Memorize. Order: nonpolar > small polar > large polar > ions · O₂/CO₂ free; ions strongly excluded
Channels vs Carriers
Know. Channels are gated pores — fast, passive only, and don’t show classic saturation. Carriers bind and change conformation — can be active and saturate (Km).
Memorize. Only carriers can pump (active) · Carriers saturate (Km/Vmax); channels don’t · Facilitated diffusion = passive carrier
Passive Transport & the Electrochemical Gradient
Know. Passive transport runs down the electrochemical gradient (chemical + electrical). For ions, equilibrium ≠ equal concentration — the membrane potential balances the concentration difference (Nernst).
Memorize. Electrochemical gradient = concentration + charge · Nernst equation · Equilibrium can hold at unequal concentrations
Active Transport & Pumps
Know. Active transport moves solutes against their gradient using ATP or a coupled ion gradient. The Na⁺/K⁺ pump moves 3 Na⁺ out / 2 K⁺ in per ATP and is electrogenic.
Know. Symport = both solutes same direction; antiport = opposite. The driving ion is usually Na⁺ or H⁺. Flipping a symporter’s orientation does NOT convert it to an antiporter.
Memorize. Symport vs antiport · Na⁺–glucose symporter (SGLT) · Coupling character is set by mechanism, not orientation
Ion Channels: Selectivity & Gating
Know. Ion channels are selective for particular ions and are gated — they open and close rather than staying permanently open.
Know. The potential comes from a tiny charge separation across the membrane capacitor. At rest, K⁺ leak channels dominate, so V sits near E_K; only a minuscule fraction of ions moves.
Every Alberts end-of-chapter problem for this topic, one multiple-choice item each. Click any option to check it instantly — the correct choice is marked Answer as lectured. No submit step; feedback is immediate.
11–1verdict + reasonClaim: "Transport by transporters can be either active or passive, whereas transport by channels is always passive." This is —
Size isn't the reason; channels simply lack an energy-coupling step. (Ch. 11)
Many transporters are active, e.g. the Na⁺/K⁺ pump. (Ch. 11)
Answer as lectured Transporters cycle through conformations that may be energy-coupled or not; channels only permit downhill flow. (Ch. 11)
Channels only permit passive (downhill) flow — they can't pump. (Ch. 11)
11–2verdict + reasonClaim: "A symporter would function as an antiporter if its orientation in the membrane were reversed (the cytosolic portion facing outside instead)." This is —
Answer as lectured Reversing orientation reverses the direction of both coupled solutes; they still move together, so symport stays symport. (Ch. 11)
Swapping sides reverses direction for both, not the coupling relationship. (Ch. 11)
The point isn't insertion; even reversed, coupled solutes co-transport. (Ch. 11)
Both solutes reverse together, so the same-direction coupling is preserved. (Ch. 11)
11–3verdict + reasonClaim: "Excitatory synapses generally cause a small hyperpolarization of the postsynaptic membrane, whereas inhibitory synapses cause a small depolarization." This is —
Inhibitory synapses hyperpolarize, not depolarize. (Ch. 11)
Hyperpolarization opposes firing; depolarization promotes it. (Ch. 11)
Excitatory inputs move it toward threshold (depolarize). (Ch. 11)
Answer as lectured Excitatory inputs move the membrane toward threshold (depolarize); inhibitory inputs move it away (hyperpolarize). (Ch. 11)
11–4verdict + reasonClaim: "Transporters approach saturation at high solute concentration once all their binding sites are occupied; channels do not bind the ions they conduct, so channel flux does not saturate." This is —
Channels open to conduct; they don't saturate because they don't bind. (Ch. 11)
Fast cycling doesn't remove the finite-site limit; they do saturate. (Ch. 11)
Channels lack discrete binding sites, so no carrier-like saturation. (Ch. 11)
Answer as lectured A transporter's binding sites give Michaelis–Menten saturation; a channel lets ions flow through, so it doesn't saturate that way. (Ch. 11)
11–5verdict + reasonClaim: "The membrane potential arises from charge movements that leave bulk ion concentrations practically unaffected, causing only a very slight discrepancy in the number of + and − ions across the membrane." This is —
A slight charge separation is precisely what creates the potential. (Ch. 11)
Ions do cross through channels; just very few are needed. (Ch. 11)
Only a tiny fraction crosses; bulk concentrations barely change. (Ch. 11)
Answer as lectured Charging the membrane to tens of millivolts moves so few ions that bulk concentrations are essentially unchanged. (Ch. 11)
11–6conceptRank Ca²⁺, CO₂, glucose, RNA, and H₂O by how readily they diffuse unaided through a lipid bilayer (fastest first).
Glucose is large and polar — slow, not fastest. (Ch. 11)
Answer as lectured Small nonpolar (CO₂) is fastest, small polar water next, large polar glucose slow, a bare ion very slow, giant charged RNA slowest. (Ch. 11)
A charged ion is among the slowest, not the fastest. (Ch. 11)
Nonpolar CO₂ beats water, and a bare ion crosses more readily than huge RNA. (Ch. 11)
11–7conceptHow can a molecule be at equilibrium across a membrane yet not be at the same concentration on both sides?
Answer as lectured At electrochemical equilibrium the concentration gradient is exactly offset by the voltage, so net flux is zero despite unequal concentrations. (Ch. 11)
Impermeability isn't equilibrium; the solute is permeant but balanced. (Ch. 11)
For charged solutes, voltage can balance a concentration difference. (Ch. 11)
That's active transport, not equilibrium; equilibrium needs no pump. (Ch. 11)
11–8conceptA membrane has a single passive transporter (Km = 0.1 mM). How effective is it at equalizing solute concentrations, for starting values of 0.01/0.05 mM vs 100/500 mM (inside/outside)?
Passive transport always drives toward equal concentrations. (Ch. 11)
Answer as lectured A passive transporter always moves solute down its gradient toward equal concentrations; only the rate saturates at high levels. (Ch. 11)
It still equalizes at high concentrations, just at a saturated rate. (Ch. 11)
It works below Km too, at low concentrations. (Ch. 11)
11–9concept · figure→conceptMicrovilli cover the absorptive surface of intestinal cells. What is their principal effect, and why does the geometry matter?
Answer as lectured More membrane area means more transporters and a higher absorption rate; many thin projections maximize area in a small footprint. (Ch. 11)
Membrane thickness is unchanged; area is what increases. (Ch. 11)
Their main role is amplifying absorptive surface. (Ch. 11)
The benefit is surface area for transport, not storage volume. (Ch. 11)
11–10conceptA cell exports H⁺ via an Na⁺–H⁺ antiporter, then exports the gained Na⁺ via the Na⁺/K⁺ pump. Do these two restore normal Na⁺ and H⁺ — and do they perturb anything else?
The antiporter exports H⁺ as intended; H⁺ is restored. (Ch. 11)
Answer as lectured H⁺ and Na⁺ return to normal, but the Na⁺/K⁺ pump adds K⁺ and moves net charge, shifting the K⁺ level and the membrane potential. (Ch. 11)
The pump is electrogenic and moves K⁺ — there are side effects. (Ch. 11)
They do restore H⁺/Na⁺; they don't simply cancel. (Ch. 11)
11–11conceptIn a vacuum, an ion in an electric field accelerates continuously (like free fall). In water it moves at constant velocity in the same field. Why?
The charge and force remain; drag balances the force. (Ch. 11)
Answer as lectured Drag grows with velocity until it exactly cancels the electric force, giving constant speed — like an object reaching terminal velocity. (Ch. 11)
There's still a force; the ion just reaches terminal velocity. (Ch. 11)
Newton's laws hold — drag supplies the balancing force. (Ch. 11)
11–12conceptA free peptide at 100 µM inactivates a "ball-and-chain" K⁺ channel whose N-terminus was deleted. The tethered ball explores a hemisphere of radius ~21.4 nm (the chain length). Is its effective local concentration near 100 µM?
The quantitative match is the point — it validates the tethered mechanism. (Ch. 11)
Confined to a tiny volume, one molecule is a real, high local concentration. (Ch. 11)
The confinement volume gives ~100 µM, not far lower. (Ch. 11)
Answer as lectured A single tethered ball confined to a ~21 nm hemisphere has a local concentration on the order of the 100 µM free peptide — supporting the model. (Ch. 11)
11–13conceptUsing V = 58 mV·log(Co/Ci) with squid-axon values (K⁺: 344 in / 9 out; Na⁺: 65 in / 430 out), the Nernst potentials come out ≈ −92 mV (K⁺) and ≈ +48 mV (Na⁺). Which matches the resting vs action potential, and why?
It's the reverse — EK is near rest, ENa near the peak. (Ch. 11)
Each value corresponds to the state dominated by that ion's permeability. (Ch. 11)
Answer as lectured At rest the membrane is mainly K⁺-permeable (near EK); at the action-potential peak it's mainly Na⁺-permeable (near ENa). (Ch. 11)
ENa corresponds to the spike peak, not rest. (Ch. 11)
11–14conceptResting potential −70 mV across a 5 nm bilayer gives a field of ~1.4×10⁵ V/cm. What does that reveal, and what happens if you apply the same 70 mV across two electrodes 1 cm apart?
The membrane field is enormous; 70 mV can't arc a 1-cm air gap. (Ch. 11)
Answer as lectured Field = voltage/distance, so the same voltage across a 5 nm membrane is enormous, but across 1 cm it's a negligible 0.07 V/cm. (Ch. 11)
The field (V/distance) differs hugely between 5 nm and 1 cm. (Ch. 11)
Field depends on thickness (V/distance); thinner means stronger. (Ch. 11)
11–15concept · figure→conceptPatch-clamp recording of acetylcholine-gated channels in rat muscle shows current steps of two distinct sizes. How many kinds of channel are present, and how can you tell?
Only two distinct step sizes appear — two types, not many. (Ch. 11)
Amplitude directly reports conductance, so the number of types is readable. (Ch. 11)
Answer as lectured Step size reflects single-channel conductance, so two distinct amplitudes mean two channel types. (Ch. 11)
Topic 4 — Transport of Small Molecules. Content verified against Alberts, Molecular Biology of the Cell, 7th ed. Textbook-only concepts (formerly badged 📖) have been removed for lecture-scope focus; textbook corrections are inlined as notes and flagged for the exam. Midterm 1 scope.