In 1961, British biochemist Peter Mitchell proposed the chemiosmotic theory. Mitchell illustrated how the transfer of electrons in the electron transport chain resulted in the movement of hydrogen ions across the inner mitochondrial membrane. This ion transfer leads to the generation of a pH gradient and an electric potential across the inner mitochondrial membrane. The electrochemical H+ gradient drives the synthesis of ATP by coupling the energetically favorable re-entry of protons into the matrix and the ATP synthesis machinery. This process of ATP synthesis is known as oxidative phosphorylation
Which of the following, if true, would not support the chemiosmotic model?
A)Decoupling agents such as DNP block ATP synthesis.
B)The Krebs cycle's main function is to break down large molecules in order to reduce the electron carriers NAD+ and FAD+.
C)ATP synthesis is blocked when the physical continuity of the mitochondrial membrane is interrupted.
D)Synthesis of ATP is increased when the pH of the intermembrane space is lowered relative to the pH of the mitochondrial matrix.
[Show/hide explanation]
Ans:B
This question is asking you which three choices DO support the model. The fact that the Krebs cycle does indeed break down larger molecules to reduce NAD+ and FAD does not, in itself, lend support to the chemiosmotic model. Choices A, C and D are wrong because all three would support the chemiosmotic model by illustrating that an electrochemical gradient is necessary for ATP synthesis. Decoupling agents do not permit ion exchange across ATP-synthase membrane pumps; the physical continuity of the membrane is necessary for the constant flow of hydrogen ions and for the interaction of proteins involved in the ETC; and, ATP synthesis depends upon a hydrogen ion gradient across the inner mitochondrial membrane. These are the reasons why choices A, C, and D support the chemiosmotic model, which invokes all of these ideas to account for mitochondrial ATP synthesis.
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My Q: Ok, Kerb's cycle does produce NADH and FADH2 but how can that not support the oxidative phosphorylation? Does any one follow the logic of the solution?
Which of the following, if true, would not support the chemiosmotic model?
A)Decoupling agents such as DNP block ATP synthesis.
B)The Krebs cycle's main function is to break down large molecules in order to reduce the electron carriers NAD+ and FAD+.
C)ATP synthesis is blocked when the physical continuity of the mitochondrial membrane is interrupted.
D)Synthesis of ATP is increased when the pH of the intermembrane space is lowered relative to the pH of the mitochondrial matrix.
[Show/hide explanation]
Ans:B
This question is asking you which three choices DO support the model. The fact that the Krebs cycle does indeed break down larger molecules to reduce NAD+ and FAD does not, in itself, lend support to the chemiosmotic model. Choices A, C and D are wrong because all three would support the chemiosmotic model by illustrating that an electrochemical gradient is necessary for ATP synthesis. Decoupling agents do not permit ion exchange across ATP-synthase membrane pumps; the physical continuity of the membrane is necessary for the constant flow of hydrogen ions and for the interaction of proteins involved in the ETC; and, ATP synthesis depends upon a hydrogen ion gradient across the inner mitochondrial membrane. These are the reasons why choices A, C, and D support the chemiosmotic model, which invokes all of these ideas to account for mitochondrial ATP synthesis.
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My Q: Ok, Kerb's cycle does produce NADH and FADH2 but how can that not support the oxidative phosphorylation? Does any one follow the logic of the solution?