When the protein gramicidin is integrated into a membrane, an H+ channel forms and the membrane becomes very permeable to protons (H+ ions). If gramicidin is added to an actively respiring muscle cell, how would it affect the rates of electron transport, proton pumping, and ATP synthesis in oxidative phosphorylation? (Assume that gramicidin does not affect the production of NADH and FADH2 during the early stages of cellular respiration.)

Sort the labels into the correct bin according to the effect that gramicidin would have on each process.

[The following are some hints to help you approach the problem.]

You know that membranes treated with gramicidin become very leaky to protons. Consider these four questions (in this order) to help you evaluate how gramicidin alters oxidative phosphorylation.

Is a proton gradient across the inner mitochondrial membrane required for ATP synthesis during oxidative phosphorylation?

What effect does a membrane that is very leaky to protons have on the ability of the mitochondrion to maintain a proton gradient across that membrane?

What effect does the ability of the mitochondrion to maintain a proton gradient have on the rate of proton pumping?

How is the rate of electron transport related to the rate of proton pumping, and are these rates affected by the membrane being leaky to protons?

electron transport rate

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rate of oxygen uptake

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proton pumping rate

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size of the proton gradient

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rate of ATP synthesis

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increases

remains the same

decreases (or goes to zero)