Withiut watching the video: specified mutations selected in advance
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Yes, but the discussion in the video was about generation of new function. Yes, mutations can accumulate, but evolution is primarily about improvement in fitness, that is where the difficulty is, and the limit of about two mutations on the way to a new function, or supplying a new function.
I don’t think so! You don’t put your doggie in jail, when they pee on the carpet. They are not considered criminals, as sane humans are when they break the law.
But people with out-of-body experiences, especially those who lose consciousness, or even lose brain activity, would disagree with you.
Sure. Given the source and the limit of 2, it seemed likely the number originally came from Behe & Snoke. But the qualifications about prespecification, population size, etc. seem to have gotten lost along the way. And since Tour is so insistent that origin of life researchers are responsible for misunderstandings about their work, I was curious how this particular telephone chain had gone.
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I see. And how does one identify a mutation on the way to a new function? With a long enough time horizon, how could we rule out any mutation from this category?
In the case of HIV-1, resistance to several different antivirals has resulted from one or more mutations. Beyond that, I suppose it depends on how granular one wants to get about function. Is evading immunity induced by a particular vaccine a new function or enhancement of an existing one? Efficient human-to-human transmission?
That is an interesting over- and underestimate of viral capabilities. Viruses can’t make copies of themselves; they need features of their host cells to do that. At the same time, many of them are capable of functions beyond replication, such as modulating host immune response or host behavior. And the popularly named giant viruses have their own genes for various metabolic functions.
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You don’t understand the meaning of the term “fixation,” do you?
We’re talking about how they evolve. You don’t understand the meaning of the term “fixation,” do you?
Lots. HIV even evolved an entirely new protein. Mike Behe claimed that it hadn’t, and was humiliated by a graduate student. Note that the student was, and remains, a virologist. Mike Behe, like so many IDcreationists, pretended to be an expert in a field not his own.
Sounds familiar, no?
It’s hard to know if your incredible ignorance or your incredible arrogance dominates. Maybe it’s a metaphorical seesaw.
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They are untrained in the subjects they are pretending to be experts in, yes.
They do not. They routinely lie about the evidence itself, as do you. If they had evidence, they’d be publishing that evidence in the primary literature.
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No. Adaptation is about improvement in fitness, but not all of evolution is adaptation. Much of molecular evolution is actually genetic drift and various related neutral processes.
That literally doesn’t make sense. Its blatantly idiotic. How do you know that one or more of those neutral mutations aren’t potentially enabling new functions at a later time? If you admit hundreds of neutral mutations can accumulate in relatively few generations, then why can’t, say, 20 of those enable new functions?
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No, that’s not in the video, in several examples, bacteria were allowed to evolve under pressure, and the mutations that then occurred were examined. No mutations were selected ahead of time.
But the video (did you watch it?) has numerous examples of this limit, drawn from non-ID sources, papers where the conclusion, or examination of the paper shows that the limit of about 2 mutations is real. So this is not ID people quoting and requoting other ID people.
Again, please watch the video, what seems to happen in experiments where two residues are altered, and no fitness is gained by restoring just one of the altered residues, is that evolution gives up, and disables production of the result entirely. So as not to waste resources in making a defective result, this provides a small fitness advantage. So time is not your friend.
I tend to think of function as being something like ATP synthase, something that does something constructive. Or restoration of altered residues, that is generally what is attempted in limit-of-evolution experiments. Per the video!
Certainly, so I said “basically”. And if I catch a cold and my nose starts running, I’m not going to call that a function of the virus. An effect of the virus, is what I would say. And as far as modulating host immune response, did you mean like AIDS does? If so, again I would say this is also an effect, surely it’s not somehow beneficial for a virus to weaken a host, or kill it.
And I wasn’t well-versed in giant viruses, so I now need to know if they can acquire new functions in around two mutations. The conclusion of the above-mentioned limit doesn’t vanish, just because viruses can have other functions than replication (using the host).
Apparently there’s been another conference, this time at Balliol College.
IIRC, we were struggling to come up with a definition of the Third Way. I think Larry just nailed it:
The Third Way of Evolution is a strange organization composed of mavericks who think they’re not getting enough attention
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Cite the papers then. This should be funny.
Anyone else wanna take bets on whether the papers show a limit of 2 mutations?
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A number of comments have been sent back for revision, either for cause or to allow edits edit in light of new context.
You know the drill - make things easier to moderate by moderating yourselves.
I second the challenge.
And let’s not forget how @lee_merrill views challenges to which there is no response…
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Here’s the first one. It’s by Ann Gauger from BIO-Complexity. Wow, we’re off to a great start!
Next:
Doesn’t look to promising to Tour and Stadler’s case.
The third is an oldie. ID’ers have been misconstruing and misrepresenting this study for years. The really funny thing is that it explicitly refutes one of Behe’s arguments. Not sure if Stadler and Tour mention that.
Next:
https://www.cell.com/cell/fulltext/S0092-8674(25)00506-9
This one shows that rice plants were able to develop cold tolerance thru epigenetic changes. Interesting. Not sure how that shows anything about a “two mutations” limit. Lee? Can you explain?
Another one:
https://www.nature.com/articles/ncomms11607
From what I saw, Stadler didn’t like this one because the adaptations weren’t as “innovative” as he wanted them to be. Can’t argue with that? Can you?
Anyway, I haven’t read these or watched the video in depth. Just providing the articles for others to do with as they wish.
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I don’t believe you.
I’m right not to believe you, because your next post describes an experimental attempt at reversing the alteration of two residues - which is selecting the mutations to look for ahead of time
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I don’t. They may be from ID sources instead.
(One is apparently from bio-complexity. So much for non- ID sources)
(Jacques Cousteau voice): “Two minutes later:”
IOW, they were waiting to see if a specified mutation occurred. Huh.
Here is the relevant part of the previous discussion:
You asked me to explain how the claim “My brain atoms made me do it” would “fly in court”, but that is not something I ever claimed would happen. That you seem to think that, in order to support my argument, I need to demonstrate that it would fly in court only demonstrates that you don’t understand what I am saying.
Yes, primarily for two reasons. If QM is not determined but indeterminate, all that could do is make our actions random. If our actions are random, however, it is difficult to argue that they are free.
Also, even if determinism is not true at the quantum level, that does not mean it is not still true at the higher levels (e.g, physical brain processes) that pertain to our actions.
Because there are believed to be situations in which a perso’ns mind is being influenced by illness or other factors such that they ought not be held responsible for their actions. This does not support your argument that a rational mind could not have been produced by evolutionary processes.
And I have explained why I do not find that evidence at all convincing. You have not demonstrated that you understand my counterarguments, never mind providing a meaningful response.
It should be obvious, but whatever: You start by saying psychiatrists do not concern themselves with the source/cause of a patient’s thinking, then conclude by saying we decide whether thinking is irrational based on whether is has an unreasoning source/cause.
Does that help?
Wrong again. e.g.In cognitive psychotherapy, we will try to help the patient enlist their capacity for rational thought to counteract the irrational thoughts that might be part of their condition.
Not really, that’s not the main disagreement here. In theory, our minds could be produced by immaterial causes that are still deterministic, and in my view free will could still exist.
All that requires is the ability to distinguish a human brain from, say, a boulder or a coffee table. Do you understand the differences between those things?
And yet you insist we take seriously the whacky conspiracy theories proposed by Axe, Tour, Behe et al. There’s that hypocrisy, again.
Tour is not an evolutionary biologist. He is a chemist who, several years ago, publicly proclaimed that he does not understand evolution, and proceeded to spend the rest of his time proving this to be correct.
Stadler is not an evolutionary biologist, but a biomedical engineer.
Behe is a trained biochemist, but has a twenty year history of making dishonest and incompetent claims about evolution, so he has no credibility on the subject.
I dismiss that video for the same reason you dismiss the video on the hollow moon. The difference is I have spent considerable time researching the claims made by Tour, Behe et al so I am confident they have nothing worthwhile to say. How much time have you spent researching the Hollow Moon Theory?
Based on what I have already read by the two of them, I really doubt that would be a productive use of my time. Thanks, but no thanks.
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As I mention above, the very first paper they discuss is an ID paper, not published in a real journal but on an ID website.
So maybe he question is: Did you watch the video?
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I have little appetite for watching more than an hour of video that, based on past experience with the host, is unlikely to represent the current state of knowledge of the topic. Also, the video is not my introduction to the topic; I’m already skeptical of the two mutation limit because of everything else I know about biology and evolution.
Fortunately, the video is organized around a slide show, so I can scrub through it and find out what papers they are referencing and the written commentary. That’s the best I can offer.
Before I dig into the video contents, a few follow-ups to your comments.
Those are two widely divergent concepts of function, the latter of which doesn’t actually sound like a concept of function. Also, “restoration of altered residues” is attempted in the first paper discussed in the video (which we will come back to), but is not a general approach among them all or in the field in general.
So you meant “a virus can basically copy itself, and that’s about it” as opposed to “a virus can copy itself, and that’s basically about it”? Still seems a stretch, but I suppose that is closer.
Good, because that’s a function of your immune and respiratory systems.
HIV-1 is certainly one virus that modulates the host immune response, perhaps more dramatically than most. But other viruses do this also, include SARS-CoV-2, as way to reduce or delay the immune response and thus prolong the virus’ window for replication. To give more time to the video contents, allow me to just point you to a reference.
Agreed that the mere fact that some viruses have metabolic functions doesn’t tell us anything about viral evolution or evolution generally; that was just me being a virus nerd and sharing interesting facts.
Now, to the video’s cited papers & two mutation limit.
Early on, we get a slide with the title “Scientists recognize that it is extremely difficult to demonstrate evolutionary innovation” with quotes from four papers supporting this thesis. Already we are not off to a great start. It is always easy to find quotes from the introductions of papers describing some challenge, some understudied topic or unanswered question. That’s all by way of setting up the actual research which addresses that topic or question. And indeed, all four quotes are from the respective introductions.
The four papers:
In which are investigated the properties of a phage protein that accumulated 7 mutations in the process of evolving the ability to use a new receptor. While the mutations are engineered into the viruses in this paper, they are based on the mutations that occurred without intervention in this paper, which is also discussed in the review the fourth quote comes from.
This paper is discussed later in the video. The experimental evolution portion involves changes in the expression of two genes; the molecular basis for these changes is not characterized and so could be as few as two mutations (not one, since the two expression patterns don’t change simultaneously).
A variety of lineages exhibiting a variety of novel traits are characterized in this paper; the different clones average 4 mutations each, with a max of 9. These include indels and structural variants as well as SNPs.
This is a review paper discussion a range of experimental evolution work. In addition to the phage paper mentioned already, just scanning the table summarizing the reviewed papers turns up this paper in which strains accumulate 1-6 mutations during the experiments.
Now, because I didn’t listen to the commentary of the hosts, I don’t know whether the specific limit of 2 mutations was their message or if that was your takeaway. But the first four cited papers certainly don’t support that particular conclusion.
As for the papers discussed in depth, the first one does indeed deal with the ability to evolve two mutations: Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness But this is precisely the scenario that @Roy guessed–they introduced two mutations into a protein and waited to see if those specific mutations would be reversed. Reversion mutations can happen, and indeed the experiment showed that when introduced singly, the mutations were reverted. But in general, evolutionary innovation does not require such precision–any way to achieve a given function or improve fitness will do.
Incidentally, while you may not be aware, this work was done at the Biologic Institute and published in BIO-Complexity, so in the case of this paper featuring in the video, it is ID folks referencing ID research. And the first reference in this paper is the Behe & Snoke paper I alluded to, which involves theoretical work regarding two specified mutations.
This is also the one paper that matches your description of how “limits-of-evolution” research is carried out and the typical results thereof. But it stands out as being the only paper that expects a prespecified outcome at the level of particular mutations.
The rest of the papers are not ID publications; on that you are correct. Next up is Phenotypic and molecular evolution across 10,000 generations in laboratory budding yeast populations. The hosts evidently spend all their time discussing a single reversion mutation which arose in that research. Did they ever mention the upwards of 400 other mutations that became fixed in the study populations during the experiments? Or the fact that while fitness increases slowed, they did not approach an asymptote, at least in all cases?
Then they mention Random sequences rapidly evolve into de novo promoters, evidently to make the point that sure, random mutation and selection can find some functions as long as they are simple enough. Do they ever explain why they don’t discuss other work on evolution from random sequences to functional proteins?
Then we get Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution. This is theoretical work again relating to two specific mutations. Do the hosts ever give any evidence that such a combination was necessary for human evolution when discussing the >100M year wait time? Or the fact that, if the first mutation is neutral, there’s no requirement that they both happen in the lifetime of a given species?
Then they mention Inheritance of acquired adaptive cold tolerance in rice through DNA methylation to point out that sometimes novel phenotypes don’t require any genetic changes.
Then they go into detail on Adaptive evolution of complex innovations through stepwise metabolic niche expansion, evidently to point out that the novel metabolic phenotype resulted from the overexpression of genes rather than de novo creation of new enzymes.
Finally they bring up Real-Time Evolution of New Genes by Innovation, Amplification, and Divergence to criticize it for involving so much experimental design to achieve the outcome. But did they mention how many mutations occurred in the different genes?
Overall, the sources do not support anything so precise as a two mutation limit on evolution. If there is a general theme to the results cited, it is that extent complex organisms are not the best model for studying the evolution of entirely new functional proteins, because the chances are much greater that novel phenotypes are more readily achievable by tweaking existing proteins and pathways. From an evolution perspective, this is a feature, not a bug. Look at how much novelty is just a few steps away!
If one is interested in how a new enzyme might evolve in a way that looks more like “from scratch” there are better types of experiments to do, and they have been done. Oh, and since they kept showing a contrast of common descent versus separate creation, there are better, more direct ways of testing for that too, better than asking whether anything evolved in a laboratory experiment satisfies the criteria for a patent.
(Sorry for anyone disappointed that I did this work instead of other parties, but I had already started down the path and didn’t want to throw away what I had done.)
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