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Post by mgarc805 » Sun Jul 28, 2019 12:12 pm

I understand that the introduction of a membrane spanning protein to the inner membrane of the mitochondria will dissipate the protein gradient (C) but wouldn't that also mean that the electron transport chain stops functioning (B).
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Re: AAMC FL 2 BB Q20

Post by NS_Tutor_Mathias » Mon Jul 29, 2019 1:14 pm

I assume you mean the proton gradient. And yes, correct - it relies on impermeability of the inner mitochondrial membrane, so suddenly making it permeable will dissipate the proton gradient.

The electron transport chain only relies on three broad components:
1. Electron donors
2. Functioning enzymes
3. Terminal electron acceptors

And point 1 wouldn't even commonly be considered a deficiency in the ETC, but more a lack of input into it. But in this scenario, nothing is preventing the ETC from functioning like normal - it may even still be pumping protons (why not?), it's just that all it's activity will be for naught: Every time it establishes a slight proton gradient, that gradient would be lost again to diffusion across the membrane. ATP synthase in turn would not be able to generate much ATP, if any, since the proton motive force would be virtually absent.

But, if our terminal electron acceptor, for example oxygen, is still present, then the ETC will continue to function - taking high-energy electrons from NADH and FADH2, using that energy to pump out protons, and finally donating those electrons to oxygen. The only thing that changes is that this now doesn't result in the production of ATP anymore, however the transport chain is working perfectly.

This is an excellent question for thinking about the relationship and dependency of different mechanisms, and in which ways they do and also do not interact.
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