Why hasn’t it been tested yet? Can they test it? Wouldn’t it be exciting?
Generally speaking such changes in function are really just the byproduct of the types of mutation that occur, which either turn out to be beneficial, or at least inconsequential and therefore not at a disadvantage. There are many papers detailing studies of the change in functions of proteins. I’ve cited one earlier in this thread.
See for example:
Tyler N. Starr, Lora K. Picton, and Joseph W. Thornton. Alternate evolutionary histories in the sequence space of an ancient protein. Nature. 2017 Sep 21; 549(7672): 409–413. doi: 10.1038/nature23902
Abstract
To understand why molecular evolution turned out as it did, we must characterize not only the path that evolution followed across the space of possible molecular sequences but also the many alternative trajectories that could have been taken but were not. A large-scale comparison of real and possible histories would establish whether the outcome of evolution represents a unique or optimal state driven by natural selection or the contingent product of historical chance events1; it would also reveal how the underlying distribution of functions across sequence space shaped historical evolution2,3. Here we combine ancestral protein reconstruction4 with deep mutational scanning5–10 to characterize alternate histories in the sequence space around an ancient transcription factor, which evolved a novel biological function through well-characterized mechanisms11,12. We found hundreds of alternative protein sequences that use diverse biochemical mechanisms to perform the derived function at least as well as the historical outcome. These alternatives all require prior permissive substitutions that do not enhance the derived function, but not all require the same permissive changes that occurred during history. We found that if evolution had begun from a different starting point within the network of sequences encoding the ancestral function, outcomes with different genetic and biochemical forms would likely have resulted; this contingency arises from the distribution of functional variants in sequence space and epistasis between residues. Our results illuminate the topology of the vast space of possibilities from which history sampled one path, highlighting how the outcome of evolution depends on a serial chain of compounding chance events.
Can be accessed for free here: Alternate evolutionary histories in the sequence space of an ancient protein
With respect to how an organism can lose one of the functions of ATPase, eukaryotes actually have both the F-type and V-type ATPase/ATP-synthetases. As a byproduct of the endosymbiosis between archaea and bacteria that gave rise to the current relationship with mitochondria living inside eukaryotic cells, the mitochondria are fully responsible for making ATP with their F-type ATP-synthases, while vacuolar V-type ATPases have lost this ability. So in essence, the loss of function for ATP synthesis by V-ATPase was compensated for by the presence of mitochondrial endosymbionts that continued to make it, and over time specialized for it.
This general phenomenon is ubiquitous in molecular evolution, even down to the level of individual protein functions. Many enzymes are known to have had so-called “promiscous” ancestors, which acted as catalysts for several similar chemical reactions. As genes encoding such enzymes were some times duplicated (meaning more copies of that same gene came to exist), this in turn could compensate for the loss of some of the functions in both copies, eventually leading to the specialization in both copies towards a more narrow set of substrates. If the enzyme originally catalyzed reactions A and B, then a duplication of the enzyme would allow the specialization towards A for one of the copies, and towards B for the other one. For either enzyme looked at in isolation the function A, or B, would be lost.
There are many papers similar to the one we have discussing, where scientists have used ancestral protein reconstruction to see how such functional partitioning of promiscous ancestors into separate enzymes have happened. See for example:
Voordeckers K, Brown CA, Vanneste K, van der Zande E, Voet A, Maere S,
Verstrepen KJ. Reconstruction of ancestral metabolic enzymes reveals molecular
mechanisms underlying evolutionary innovation through gene duplication. PLoS
Biol. 2012;10(12):e1001446. DOI: 10.1371/journal.pbio.1001446
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It certainly would but they probably can’t. One of the reasons for that is that as gene or protein sequenes become increasingly different due to time having passed since their shared ancestor, the odds that any given observed difference between them is the result of multiple mutations to the same residue increases. This makes it impossible to infer with any appreciable certainty what the ancestor state was. So the information required to infer the ancestral state is actually lost.
It could be that one protein mutated K->M->Q, and the other mutated K->L at the same position. You now have no information that the ancestor was K, all you see is L and Q.
There are some statistical methods scientists can employ to assess how likely it is that the sequences they observe have suffered multiple consecutive hits to the same residue.
Very few pre-LUCA proteins have been resurrected (there’s a few exceptions), and scientists generally don’t bother trying for things that old for that very reason. Of course it would be interesting, but ultimately it’s a science and we want to be testing something we can have appreciable assurance really represents the ancestral state closely enough. There’s no use performing an experiment to see how an entity works which you can be relatively confident doesn’t even correctly represent what the ancestor was.
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Did the function evolve?
In terms of the complexity of the structure that performs it, yes.
Ultimately the function originated by evolution too, yes.
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But in the specific case of the discussed paper did the function of V-ATPase per se evolve?
No. [“Post must be at least 5 characters” so this is my filler]
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Do Anc3 and Anc11 have any known functionality for V-ATPase that wasn’t in their ancestor Anc3-11?
Do Vma3 and Vma11 have any known functionality for V-ATPase that wasn’t in their ancestors Anc3 and Anc11?
Does Vma16 have any known functionality for V-ATPase that wasn’t in its ancestor Anc16?
How did the V-ATPase function originate?
Perhaps you already answered it at post #40, where you wrote:
Admittedly this is still very speculative.
Though you used a term that did not seem quite acceptable when I used it in my comments. 
C’est la vie, mon ami. 
Have a good weekend.
What is different about them compared to their ancestor from a functional perspective is their co-dependence. Apparently the Anc16, Anc3, and Anc11 proteins interface with each other in a way that means for the hexameric ring to properly function, if Anc11 is present, it won’t work unless Anc3 is also present, because something in Anc3 has changed in a way that Anc11 compensates for.
That means somewhere on the protein where they interface with each other, their surface has changed in a way that make them dependent on each other to properly function in the hexameric ring.
Do Vma3 and Vma11 have any known functionality for V-ATPase that wasn’t in their ancestors Anc3 and Anc11?
No, they’re different only in their co-dependence.
Does Vma16 have any known functionality for V-ATPase that wasn’t in its ancestor Anc16?
No.
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Yes, the ultimate origin of ATPase/ATP synthase is still speculative. The paper I references details some evidence which indicates that it emerged through the associating of two distinct protein complexes. One was (before ATPase) apparently a protein translocase (a sort of transport protein that pumps molecules in and out of cells) sitting in the membrane. The other was a cytosolic RNA helicase of some sort.
The evidence cited implies that these two distinct protein complexes became associated (it isn’t known why) by one binding to the other through an intermediate. The intermediate is proposed to be a translocated protein or RNA molecule. This proposed mechanism of association is just speculation.
I have no issue with the statement that some things are speculative. Some.
There are things we have very good evidence for, and things we don’t. It would not be reasonable to dismiss the entire field of evolutionary biology, or all inferences about the past, as being merely or equally speculative.
The points discussed here provide two good examples of each. Some sets of inferences are supported by very good evidence, and thus gives us reasonable confidence in the conclusions. Others are very openly admitted to still be speculation, and will have to be tested in time if and when possible.
Thank you sir. Have a nice weekend.
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Adaptation (microevolution) is generally accepted by many, but many macroevolutionary statements seem speculative, because they often seem puffing up very modest results.
Regarding the interesting 2012 V-ATPase paper you cited and explained so well, a known biochemistry professor* highlighted the following points:
Random mutation is superb at degrading genetic material, which sometimes is helpful to an organism.
The most glaringly obvious point -in the cited paper- is that this is evolution by degradation. All of the functional parts of the system were already in place before random mutation began to degrade them. Thus it is of no help to anyone who requires a mechanism that will construct new, functional systems.
What’s more, the mutated system presented in the paper is not even advantageous; it is neutral, according to the authors.
The title of the paper and news reports emphasize that the “complexity” of the system has increased. But increased complexity by itself is no help to life — rather, life requires functional complexity.
We all look at the same issues from radically different perspectives. That’s why we seem to talk past each other. That could turn unproductive at some point.
However, the latest discoveries in biology research don’t seem to support the macroevolution idea. Future discoveries will make things even harder to explain using outdated ideas devoid of evidences. For many years the knowledge gaps in biology have been filled with “just-so” macroevolutionary stories, but as those gaps get reduced by new discoveries made in the ongoing research, some scientists have realized that it’s time to look for better explanations. The scientists grouped under the so-called “third way of evolution” are an example of the new trends.
Not too long ago somebody asked “where’s the evo in evo-devo?” because apparently at a recent gathering of the evo-devo field of biology the agenda was disproportionally loaded with interesting devo presentations, but serious evo articles (specially macroevolutionary) were rare at best. It doesn’t take a rocket scientist to see that the fictional character Humpty Dumpty is real in cellular biology.
As we see everyday around us, functional complexity is designed by conscious agents that understand meaning and purpose. The same applies to biology.
Let’s enjoy the fascinating discoveries biology researchers are making practically every day and let’s apply the newly acquired knowledge to improve public healthcare.
(*) identity available upon request
Ahh I see you came back to edit your post 12 times after you posted it days ago. Funny.
I’ll take that as commentary. I don’t even see it’s relevance. Nothing about evolution below or above the species level has been mentioned in this thread so why you feel the need to start talking about that is really very odd indeed.
It has that distinct smell of a desperate need to declare and assert that “OMG NOTHING HAS BEEN PROVEN YOUR BACTERIA DIDN’T TURN INTO A GIRAFFE”.
You started the thread talking about ATP and ATPsynthase, I contributed a reference that details how it became more complex over time. Whether this lead to the formation of a new species or not is completely irrelevant to the discussion.
Regarding the interesting 2012 V-ATPase paper you cited and explained so well, a known biochemistry professor* highlighted the following points:
Random mutation is superb at degrading genetic material, which sometimes is helpful to an organism.
The most glaringly obvious point -in the cited paper- is that this is evolution by degradation. All of the functional parts of the system were already in place before random mutation began to degrade them.
Unsurprisingly Michael Behe said something actually false. A duplication of one of the components, so that there were three genes instead of two, happened first. Necessarily. You can’t degrade a new component that has yet to come into existence. So only after the number of different components increased, could they degrade in such a way that made both of them necessary.
Thus it is of no help to anyone who requires a mechanism that will construct new, functional systems.
It isn’t purported to be an example of a “new” functional system.
Of course, that depends on what anyone actually means by new. Creationists hate having to define their terms, so I have decided to do it for them: If it’s different from what it was before, then it’s new. If it’s slightly bigger, slightly smaller, slightly darker, slightly longer, slightly thinner, slightly more curved, if it has changed in ANY measurable way, then I say it’s new. That goes for physiological, mental, behavioral, and molecular changes of any and all kinds, whether in quality or quantity. Changing a T nucleotide into a G nucleotide is change, and therefore new. An ever so slightly taller person is different, so also new. Duplication means there is now more, so it’s different form what it was before, so also new.
There we go, “new” has now been defined and any measurable change now qualifies as new.
With respect to new information: New information is any change in a sequence such as a polymer like DNA, or a string of abstract symbols used in writing (including it’s length, or the order of arrangement of monomers or symbols within it) that wasn’t there before. If it wasn’t there before, it’s new. So any mutation is new information. All duplications are new information. All substitutions are new information. All deletions are new information, because they all constitute change that wasn’t there before.
Using this simple, intuitive definition of what would be “new”, all mutations cause new information and new functions. If creationists don’t like this definition, they’re going to have to come up with one they think is better.
What’s more, the mutated system presented in the paper is not even advantageous; it is neutral, according to the authors.
So what? It’s still an example of increased complexity. This is how you can have a system that only requires a few components to function, change into a system that requires more components to function by evolution.
Must all evolutionary change result in increased relative fitness? Why?
The title of the paper and news reports emphasize that the “complexity” of the system has increased. But increased complexity by itself is no help to life — rather, life requires functional complexity.
And it’s functional. It retained it’s overall function while growing more complex in it’s number of different required components.
What does it mean to say that life “requires functional complexity”? Is Michael Behe saying that all living organisms need to become ever more diverse in their functional capacities, otherwise they will go extinct? Or then it isn’t evolution? As usual Mike’s complaint here doesn’t even make sense.
However, the latest discoveries in biology research don’t seem to support the macroevolution idea.
This is molecular evolution we are looking at. Whether speciation happened is irrelevant.
Of course, the latest discoveries in biology research ONLY and CONCLUSIVELY supports macroevolution to such an extent that to think otherwise can only be an expression of ignorance.
Future discoveries will make things even harder to explain using outdated ideas devoid of evidences. For many years the knowledge gaps in biology have been filled with “just-so” macroevolutionary stories, but as those gaps get reduced by new discoveries made in the ongoing research, some scientists have realized that it’s time to look for better explanations. The scientists grouped under the so-called “third way of evolution” are an example of the new trends. As we see everyday around us, functional complexity is designed by conscious agents that understand meaning and purpose. The same applies to biology.
What a beautiful statement of belief.
(*) identity available upon request
It’s Michael Behe. Though it’s irrelevant who says what. What matters is what the evidence shows. It only ever shows evolution, and Michael Behe is forced to engage in silly rhetorical games about what counts as “new” or “novel” and “complexity” and “information” to try to distract from the fact that this molecular machine became more complex through simple evolutionary mechanisms like mutation.
One could probably render the evolution of the entire biospheres current diversity through Behe’s “devolution” rhetoric:
Whales “devolved” from terrestial mammals by “losing” the function of walking and running, “losing” the spaces in the flesh between their digits, “losing” their noses, “losing” the position of the blowhole in the front of their skull, “losing” the small amount of bone on the top of the skull where the blowhole is now located (there used to be bone covering that space, now it’s gone, so it was “lost” or “degraded”), and so on and so forth. There isn’t any kind of evolutionary change that couldn’t be described in this silly type of “loss” rhetoric.
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There was no new complex functionality created. The functionality was already there.
It was well explained in my comment. That’s why I edited it several times to make sure it was understood. Read it again, carefully. You may want to ask specific questions about a particular part of the text that you don’t understand within the comment, as I did with yours in this conversation. Thanks.
The papers you cited just puffed up very modest results. Gross extrapolation associated with delusional wishful thinking.
Nice try, but no, thanks. Give it another try.
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Since any change in functionality IS new functionality, according to the only one of us who has bothered defining “new”, you are demonstrably wrong.
If you don’t like the implications of that definition of new applied to these results, you can of course stick to whatever definition of new you are instead emotionally comfortable with.
The functionality was already there.
The function performed by the V-ATPase structure (ATP hydrolysis driving vacuolar acidification) was already there, but the way in which it is performed by parts of the structure (the hexameric membrane channel ring), and the degree of it’s compositional complexity, was not.
It was well explained in my comment. Read it again, carefully.
Your comment did not contain explanations, it contained rhetorical arguments and evaluations. It was nothing but an attempt to render the results of the evolutionary process into phrases that sound less impressive.
Clearly, since you felt the need to even do that, days after my last post, you must in some sense actually have found them impressive, otherwise you would not have felt so compelled to find a way to express them in more diminutive terms.
The papers you cited just puffed up very modest results. Gross extrapolation associated with delusional wishful thinking.
I appreciate your willingness to express in so uncertain terms how it impacts you emotionally.
Nice try, but no, thanks. Give it another try.
I’ll leave you to post some nice thank you post, then modify it 12 times several days later into some exposition of creationist rhetoric to get your concluding last words in about how it all feels to you and hasn’t proved anything.
Thank you for your time and interest.
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You haven’t proven anything yet either.
Citing papers that puff up very modest results doesn’t prove much, if anything at all.
That one of the components was replaced by another similar type through degradation?
Big deal. That happens all the time in all biology. But it won’t take you beyond the limits of microevolution.
I see that pawas has taken off his mask. Progress.
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Considering how his very first post on this website was a classic creationist talking point, I can’t say this unmasking is all that revealing. Wearing body paint, but was still naked.
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Guys, please bear with me. I’ve been assigned the difficult task of boosting the Alexa ranking of this website. I’m forced to write provocative comments in order to heat up the conversations and attract more visitors. 
BTW, you have been helpful in trying to boost the Alexa ranking too. Well done! Thanks for your support.
Too bad that other folks didn’t join the conversation. Maybe next time?
Confessing to being a troll will not increase your popularity.
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