Chapter 12
How would disrupting the Na⁺/K⁺ pump affect both passive and active transport processes across the plasma membrane, including glucose uptake and membrane potential maintenance.
Secondary active transport (e.g., the Na⁺-glucose symporter) cannot function effectively, because it depends on the Na⁺ influx to drive glucose uptake against its gradient. Passive transport of ions becomes altered, as the diminished membrane potential reduces the driving force for Na⁺ and K⁺ movement through leak channels.
Over time, the cell swells and may lyse due to osmotic imbalance, since ion gradients that regulate water movement are lost.
Why can prokaryotic cells perform glycolysis and the citric acid cycle without mitochondria?
Both pathways occur in the cytosol and on the plasma membrane. Electron transport and ATP synthesis occur across the bacterial cell membrane instead of a mitochondrial membrane.
If the inner mitochondrial membrane became permeable to protons, how would this affect ATP synthesis and the overall efficiency of oxidative phosphorylation? Explain your reasoning.
ATP synthesis would plummet and oxidative phosphorylation would become inefficient because the proton gradient that drives ATP synthase would be dissipated.
How does the Na⁺/K⁺ pump establish and maintain the electrochemical gradients necessary for secondary active transport in animal cells?
The Na⁺/K⁺ pump (Na⁺/K⁺-ATPase) actively transports 3 Na⁺ ions out of the cell and 2 K⁺ ions in per ATP molecule hydrolyzed. This creates a steep Na⁺ concentration gradient across the plasma membrane (high Na⁺ outside, low inside) and contributes to a negative membrane potential. The energy stored in this Na⁺ gradient is then used to drive secondary active transport, such as the Na⁺-glucose symporter, which couples Na⁺ influx with glucose uptake against its concentration gradient. Thus, the Na⁺/K⁺ pump indirectly powers many nutrient and ion transport processes by maintaining the electrochemical gradient.
Explain how oxaloacetate functions both as a substrate and as a catalyst in the citric acid cycle.
Oxaloacetate combines with acetyl CoA to form citrate and is then regenerated at the end of the cycle, enabling the cycle to repeat
Both mitochondria and chloroplasts use an electrochemical gradient to drive ATP production. How do the sources of high-energy electrons differ between the two organelles, and what does this reveal about their evolutionary origins?
Mitochondria: Electrons come from the oxidation of food molecules (such as NADH and FADH₂ from the citric acid cycle).
Chloroplasts: Electrons come from the splitting of water molecules during photosynthesis, driven by light energy.
Evolutionary insight: This difference reflects adaptation to different energy sources — chemical energy (mitochondria) vs. light energy (chloroplasts) — but both use the same chemiosmotic principle, suggesting they evolved from a common ancestral mechanism that predated both organelles
A neuron carries a mutation in its voltage-gated Na⁺ channels located at the presynaptic terminal. These channels can still open to depolarize the membrane, but the mutation disrupts their normal inactivation process. Using your understanding of action potential propagation and Ca²-dependent neurotransmitter release, analyze how this mutation could influence:
The shape of the action potential?
The activity of voltage-gated Ca²⁺ channels at the presynaptic terminal?
The pattern of neurotransmitter release?
The mutation slows or prevents Na⁺ channel inactivation, causing a broader, prolonged depolarization and delayed repolarization. If the Na⁺ channels fail to inactivate properly, a steady inward Na⁺ current continues even after the peak of the action potential. This prolongs depolarization, delays K⁺-driven repolarization, and therefore broadens the action potential.
Prolonged depolarization keeps Ca²⁺ channels open longer, increasing Ca²⁺ influx at the presynaptic terminal
Greater and longer Ca²⁺ entry leading to excessive or asynchronous neurotransmitter release.
Cells oxidize glucose through dozens of tightly regulated enzymatic steps rather than in a single combustion event. How does disrupting the pyruvate dehydrogenase complex alter the overall energy yield?
The pyruvate dehydrogenase complex (PDC) converts pyruvate into acetyl-CoA, linking glycolysis to the citric acid cycle. If PDC is disrupted, pyruvate cannot enter the TCA cycle, and acetyl-CoA formation halts. As a result, cells lose access to the high ATP yield from oxidative phosphorylation, dropping from about 30 to 32 ATP per glucose to only the 2 ATP produced in glycolysis. Pyruvate instead accumulates and is reduced to lactate to regenerate NAD⁺, allowing glycolysis to continue but at a much lower efficiency. PDC disruption severely limits aerobic ATP production and forces the cell to rely on anaerobic metabolism.
Chemiosmotic coupling is described as an ancient process. What evidence from the structure or function of modern cells supports this claim, and why might this mechanism have been so strongly conserved through evolution?
Evidence: Both mitochondria and chloroplasts — and even some bacteria — use membrane-bound electron transport chains to create a proton gradient that drives ATP synthesis through ATP synthase.
The similarity of ATP synthase across species (structure and mechanism) suggests a shared ancestral origin.
Reason for conservation: Chemiosmotic coupling is an extremely efficient and versatile method for converting energy into a usable form (ATP), giving strong evolutionary advantage, so it was preserved across all domains of life.
Compare how the inner membrane of mitochondria and the thylakoid membrane of chloroplasts support their distinct energy-conversion processes. What structural features allow each to maintain efficient ATP synthesis?
The mitochondrial inner membrane’s impermeability preserves the proton gradient generated by the electron transport chain, while cristae increases surface area for ATP synthase. Thylakoid membranes separate light reactions from the stroma, generating a proton gradient for photophosphorylation. Both rely on compartmentalization and membrane-bound protein complexes to drive chemiosmotic ATP production.
Suppose Photosystem II in chloroplasts stopped functioning, but Photosystem I remained active. Predict how this would alter ATP and NADPH production and how carbon fixation would be affected.
Photosystem II is responsible for splitting water and providing electrons to the electron transport chain
Without PSII, no new electrons would enter the chain, and no oxygen would be produced.
Photosystem I could still run cyclic photophosphorylation (producing ATP only), but NADPH would not be produced.
Because the Calvin cycle requires both ATP and NADPH, carbon fixation would slow or stop, halting sugar production.