Exercises: Membrane transport

Distinguish between passive transport and active transport across the membrane, indicating which of them requires an input of ATP and in which direction substances move in each case.

What is simple diffusion? Give two examples of substances that enter or leave cells by this mechanism and explain what common characteristics they share.

Explain what endocytosis and exocytosis are and give a specific biological example of each of these processes.

Glucose enters most cells by facilitated diffusion. Explain what this mechanism consists of, which proteins are involved and how it differs from simple diffusion.

Observe the diagram of the sodium-potassium pump. State which ion corresponds to particles A and which to particles B, explain why this mechanism is considered active transport and what consequence the unequal exchange of ions has for the electrical charge of the membrane.

A white blood cell engulfs a bacterium to destroy it. What type of endocytosis does it carry out and what is the vesicle formed called? Briefly describe the process.

The uptake of $\text{K}^+$ in barley seedling roots in a hydroponic medium is analyzed. Upon adding dinitrophenol (DNP) to the culture—a substance that uncouples mitochondrial ATP synthesis without halting $\text{O}_2$ consumption—$\text{K}^+$ uptake stops immediately and the ion begins to slowly leak out of the root, so that the accumulated $\text{K}^+$ is progressively lost. Interpret these data by deducing the transport mechanism involved in $\text{K}^+$ uptake, justify why blocking ATP causes the dissipation of the accumulated electrochemical gradient, and predict what would happen to uptake if, in the absence of DNP, the temperature were lowered to $0\ \text{°C}$.

Ouabain is a drug that inhibits the $\text{Na}^+/\text{K}^+$ pump. Predict what will happen, in the medium term, to the sodium gradient of the cell and to the coupled transport of glucose that uses this gradient in the intestine, and reason your answer.

A patient suffers from a form of familial hypercholesterolemia due to a mutation in the LDL receptor gene. The mutated receptor is synthesized and inserted into the plasma membrane, where it is capable of binding circulating LDL normally, but lacks the cytosolic tail that interacts with adaptin and clathrin. As a consequence, cholesterol does not enter the cells and accumulates in the bloodstream, despite pinocytosis of extracellular solutes remaining intact. Justify what type of vesicular transport is blocked and why the cell cannot internalize the ligand, and reason whether a compensatory increase in pinocytosis would effectively compensate for this deficiency.