ATPsynthase (TBR passage question)

[yestomeds]

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Hello, this is from the old TBR "metabolic pathways"
Book II, passage #1 (p. 229, answers on p. 257).

I thought I understood the e-transport chain and ox. phosphorylation, but maybe not 100%.

Question 2. You have this drug/poison thing that ultimately binds to ATPsynthase to deactivate it. Okay, thats easy.
What I thought was that the electron transport chain is coupled to the work the ATP synthase (ADP and Pi --> ATP generator). As in, the ETC requires the final e acceptor to be an oxygen (to ensure that it works, to ensure that each complex can successively be reduced, to allow for e- carriers to be oxidized etc. etc.). It is this last part that can make it stop working, and NOT the ATP synthase membrane protein thing that can make it stop working...?
So how does ATP synthase disruption (caused by this drug) lead to "the proton gradient formed by electron transport and proton pumping can no longer be relieved."
And thus "the result is that cells ever to anaerobic metabolism" (instead of proceeding to Krebs/ETC, they go off and make lactate after glycolysis) <-- this logic I get. I do not get the stuff in gray.

(Answers on p.257 - question 2, answer choice C).

Thank you everyone.

 

[Quinoline]

I believe the proteins in the ETC create a H+ gradient on their own and are independent of ATP synthase. I don't think the many proteins in the ETC are joined to each other, nor are they joined to ATP synthase, although diagrams often show them all right next to each other.

 

[bee17]

The "relief" of the proton gradient is what drives ATP synthase. If protons (pumped out through the membrane by the ETC) cannot come back through the membrane via the membrane protein part of ATP synthase, than ATP synthase can't make ATP, and oxidative respiration will not happen.

 

[yestomeds]

Right, so what I'm saying is that yep, if the proton gradient, achieved by the ETC) is disrupted, then the ATP synthase cannot function.
What I think (?) the answers section is saying is that it the ATP synthase is inhibited (thanks to the drug), THEN the proton gradient formed by the ETC can no longer be achieved. i.e. they are talking about a cause-effect relationship but in a backwards manner from what we are.

HOPE that makes sense? 🙄 Anyone with advice/knowledge?

 

[Quinoline]

In your original quote you said when the ATP synthase is inhibited the proton gradient can't be relieved, which I think makes sense by your forward logic. But your last post said that the proton gradient can't form when ATP synthase is inhibited, is that what the key actually says? If so, I do not understand either.

 

[yestomeds]

In your original quote you said when the ATP synthase is inhibited the proton gradient can't be relieved, which I think makes sense by your forward logic. But your last post said that the proton gradient can't form when ATP synthase is inhibited, is that what the key actually says? If so, I do not understand either.

Yes sorry, my original post was a bit long. I did say that as in I was trying to logically lay out what would make sense (which it does, as we all agree!).
Yes, the last part of what you typed, I did re-iterate the issue I had (which was buried in my long first post) - the fact that I think they are saying because ATP synthase is inhibited, THEREFORE the proton gradient is also affected. That seemed to be the answer choice.

If you or anyone is studying this topic, its TBR book II, "Metabolic Pathways."
p.229, passage #1, question 2.
(Answers on p.257 - question 2, answer choice C).

 

[bee17]

I don't have that book. If it says that disrupting ATP synthase in this way prevents the proton gradient from being relieved, that is correct. If it says that it prevents the proton gradient from forming, check the errata for the book.

 

[desertrat12]

I'm a bit confused as to what your actual question is, however if I understand it you are saying that the book claimed that once ATP synthase was inhibited then the proton gradient can't be achieved? I believe your thinking is right in the sense that the proton gradient can't be relieved due to the non functioning nature of the ATP synthase, however your other question I don't have an exact answer for. As far as I understand it the whole proton gradient is achieved with just complex 1,3,4 for NADH and 2,3,4 for FADH2, and ATP synthase is just a benefactor of the proton gradient. Without knowing the exact question or explanation for the answer, I am wondering if what they meant was the energy that is gained from the protons moving down their concentration and electrical gradient can't be achieved. Aka, the proton gradient is still there but the energy from it can't be achieved. Or perhaps they were referring to what would happen if no protons were pumped back into the matrix and there would be less protons to pump back out? I'm not sure..

 

[bee17]

If you want an exact answer, you will have to tell us how exactly your book explained the way the drug interacts with ATP synthase.

 

[Jepstein30]

They are coupled in the sense that the ETC proteins generate the H+ gradient.. and ATP synthase is one of the primary proteins that uses it. If you stop ATP synthase from working, you're no longer using that gradient and it eventually 'builds' up to the point where the ETC proteins can't pump protons against it... so they stop working.

You can still 'achieve' the proton gradient if you inhibit ATP synthase.. you just have nothing using it so ETC eventually stops pumping protons (electrical gradient is too high).

Based on the wording you've provided, the book isn't claiming that the proton gradient is affected (it's not).. but that the ETC proteins stop working (they do.. they've done their job in generating the proton gradient and are waiting for things to use it or 'relieve' it). Not making ATP anymore so switch over to anaerobic respiration.