ID theorists publish new paper in Journal of Theoretical Biology

_{Denyse O'Leary

August 19, 2021

Darwinism, Intelligent Design, Mathematics}

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On the improbability of Darwinian claims:

A new peer-reviewed paper in the Journal of Theoretical Biology, “On the waiting time until coordinated mutations get fixed in regulatory sequences,” is authored by three key scientists in the intelligent design (ID) research program: Ola Hössjer, Günter Bechly, Ann Gauger. The paper is part of the “Waiting Times” project, spurred by Discovery Institute as part of its ID 3.0 initiative, and it investigates a question of vital interest to the theory of intelligent design: How long does it take for traits to evolve when multiple mutations are required to give an advantage? A previous peer-reviewed publication from this team appeared as a chapter in the 2018 Springer volume Stochastic Processes and Applications. This latest paper is lengthy, technical, and math intensive. In other words, it’s not for the fainthearted, but it’s open access and free to read here.
Casey Luskin, “In Mainstream Journal, ID Theorists Explore “Waiting Times” for Coordinated Mutations” at Evolution News and Science Today (August 18, 2021)

We hope the journal isn’t intimidated by Darwin’s Outrage Machine, Inc. Just think, some people are now allowed to bring this up. And not just as an inhouse titter, followed promptly by dismissal of the question.

Ola Hössjer, Gunter Bechly, and Ann Gauger, are competent scientists who happen not to be Darwinists. It’ll be interesting to see what happens now. More from Luskin:

This paper develops a complex mathematical model for calculating the waiting time for the evolution of a trait that requires L nucleotides in order to function. Although this is strictly a methodological paper, one potential application could be the evolution of regulatory regions which control the expression of a gene. Changes to transcription are thought to be important to evolving new body plans or biological systems. Regulatory regions such as enhancers or promoters may have a length of 1000 nucleotides, and for expression to occur special proteins called transcription factors must bind to these regulatory regions at binding sites, which may be 6 to 10 nucleotides in length.
Casey Luskin, “In Mainstream Journal, ID Theorists Explore “Waiting Times” for Coordinated Mutations” at Evolution News and Science Today (August 18, 2021)

It’s like just hoping that random guesses on a multiple choice exam will net you 100% and that is what you need to graduate.

A friend comments that the paper basically shows that if many mutations must be coordinated to enable a new feature, Darwinism won’t do it. Note: Dense mathematics warning.

Update updated: Apparently, the disclaimer below applies only to an earlier article: “The Journal of Theoretical Biology and its co-Chief Editors do not endorse in any way the ideology of nor reasoning behind the concept of intelligent design. Since the publication of the paper it has now become evident that the authors are connected to a creationist group (although their addresses are given on the paper as departments in bona fide universities). We were unaware of this fact while the paper was being reviewed. Moreover, the keywords “intelligent design” were added by the authors after the review process during the proofing stage and we were unaware of this action by the authors. We have removed these from the online version of this paper. We believe that intelligent design is not in any way a suitable topic for the Journal of Theoretical Biology.”

Neither paper was retracted. A friend asks us to have pity on the poor editors who are like deer among the wolves, when it comes to dealing with Darwin mob. Very well. We shall. Kudos to them for publishing something despite the mob.

Note: Facebook is now subjecting posts from Uncommon Descent to inhouse review as “selling” something, so they may no longer be visible. You may need to come to this page yourself to see the news. If you voted for this, rejoice and be glad. Otherwise, think again. We may need to start reporting here on the valiant efforts to curb irrational Big Tech censorship. Note: They seem to have stopped doing it for the last couple of posts. But just remember, they don’t work for you. They work for a Big Guy. Stay tuned.

Comments

Oops it's been a couple weeks. That said: Querius wrote:
Silver Asiatic, That was kind, but don’t hold your breath. -Q
It seems you were right. Bob wrote:
Right, but the paper I’m citing undermines this by showing that their scenario is unrealistic for the specific problem they are looking at: you don’t need 6 or 7 specific mutations to get a binding site.
The authors gave a list of complex adaptions in the paper which were examples of the problems they were looking at. I fail to see where they say that 6 or 7 specific mutations were required to create a simple binding site.
All of it? it shows the target space to get regulatory function is much much larger than Hössjer et al./i> assume.
Well that's an assumption Yona, et al. make, but they didn't actually demonstrate it and stated as much in the paper.
Although the evolved promoters likely have no regulation, we hypothesize that such crude promoters might play an important role in the evolution of the transcriptional network, as newly activated genes do not necessarily require the regulated/induced expression in order to confer significant advantage
Essentially, the researchers are aware of the limitations of their work and implications thereof. In other words, it's not something they demonstrated, they couldn't do that. They hypothesized it might be a start, or the typical "stepping stone" or so to speak. There is, however, more to say. What is great about the kind of model Hössjer et al. did is that even if they weren't aware of Yona, et al., which they were, and even if they didn't incorporate that information, which they did, (or would if it had been something probabilistically surprising - which it wasn't.) all Yona, et al. really demonstrated was what could be already probabilistically modeled anyway, so it makes no difference.Yarrgonaut_{September 16, 2021
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Silver Asiatic, That was kind, but don't hold your breath. -QQuerius_{August 31, 2021
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Bob
SA – if you actually asked me to educate you, I would write a short post to explain what you asked about. No entrapment.
That's a good deal and is greatly appreciated. I'd just ask that if you think you have something that would benefit the discussion then please add it.Silver Asiatic_{August 31, 2021
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SA - if you actually asked me to educate you, I would write a short post to explain what you asked about. No entrapment. My response to LCD was a bit dismissive, because it wasn't what we were discussing and it's a fairly common creationist talking point. So I didn't want to engage and make the thread worse.Bob O'H_{August 31, 2021
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Bob O'H
I was assuming some minimal knowledge of genetics and evolution. If you don’t understand, just ask. I don’t like writing long posts, because they take more time for everybody, and it’s also less likely that we’ll stick to the main point: there will be too many side issues that can be brought up.
Again, Bob - you appear to have entrapped us in a circle. We are invited to ask you to educate us on genetics and evolution, but you don't like writing long posts because they "take more time for everybody". On the contrary - I think almost all of us would appreciate a long post where you spell our your views in great detail. That's what this site is about.Silver Asiatic_{August 31, 2021
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Bob O'H:
I guess you’re just going to repeat that now, rather than respond to what I wrote.
I have exposed what you have posted as pure nonsense. Try to keep up. The discussion has always been about multiple mutations- always. The fact that binding sites were used is for ease of demonstration. That you are too dim to grasp that is on you. It is all linked. the multiple mutations for gene regulation and the multiple mutations required to get a duplicated gene and then to form a new protein fold from that. The math is more difficult for gene sequences. So they use binding sites. Again, I don't expect you to understand that.ET_{August 31, 2021
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Bob O'H
LCD – Here’s a link that should help
Sending us to Google where we can learn that mutations are random and mutations are not random and that we really don't know either way. Whatever we choose will line up with your answer to that question?Silver Asiatic_{August 31, 2021
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Querius #74 Exactly! He is just wasting everybody's time. Reasoning with these people is a hopeless business. One of the reasons why a few very good contributors and commentators have gone away. I confess I recently reappeared and got dragged into this thread trying to reason with Bob O'H, which was a complete waste of time.EugeneS_{August 31, 2021
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Bob O'H LCD – Here’s a link that should help: https://lmgtfy.app/?q=are+mutations+random
Ok ,you have no clue if mutations are random (this is just a necessary materialistic religious belief ). What about the mechanisms of checking and repairing DNA, are they random ?Lieutenant Commander Data_{August 31, 2021
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LCD - Here's a link that should help: https://lmgtfy.app/?q=are+mutations+random Querius - I was assuming some minimal knowledge of genetics and evolution. If you don't understand, just ask. I don't like writing long posts, because they take more time for everybody, and it's also less likely that we'll stick to the main point: there will be too many side issues that can be brought up. ET - I guess you're just going to repeat that now, rather than respond to what I wrote.Bob O'H_{August 30, 2021
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Bob- Learn how to read. And at least try to respond to what I post. yes it does pertain to any and all multiple mutations. “Waiting for TWO Mutations” was an attempt to refute Behe. Yet Behe NEVER discussed binding site evolution is the book the paper was responding to. They used binding sites for ease of demonstration. And recombination is a design mechanism. Read “Not By Chance”. All. Multiple. Mutations. And the logic and reasoning are right there, too, Bob. So obviously you are the problem.ET_{August 30, 2021
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ET - we're not discussing Behe's paper, though. Please try to keep up.Bob O'H_{August 30, 2021
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ET – no it doesn’t pertain to all and multiple mutations. They ignore, for example, recombination.
And once again in reply, the unsupported assertion is shot down. But don't worry, you'll see more such vacuous responses in brand new threads using the same form:
"No, the reference doesn't apply to [TopicVariable], they [ignore/don't understand/misunderstand], for example, [natural selection/global warming/quantum mechanics/recombination/statistical regression analysis]."
One has come to expect that the subsequent reply to several long responses that debunk such unsupported assertions will take the following form:
"No, this is completely unconvincing. You need to brush up on [random term]."
If you challenge the reference to the random term with another long post, you won't get a response because the mission to waste your time has been accomplished. Just my opinion. -QQuerius_{August 30, 2021
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Do not exist random mutation everything is preset. Can somebody present an argument on proving that a mutation is random? :)))
There is no agreement on the extent to which metabolism could develop independently of a genetic material. In my opinion, there is no basis in known chemistry for the belief that long sequences of reactions can organize spontaneously — and every reason to believe that they cannot. The problem of achieving sufficient specificity, whether in aqueous solution or on the surface of a mineral, is so severe that the chance of closing a cycle of reactions as complex as the reverse citric-acid cycle, for example, is negligible. The same, I believe, is true for simpler cycles involving small molecules that might be relevant to the origins of life and also for peptide-based cycles. (Orgel 1998, 494–495)
Lieutenant Commander Data_{August 30, 2021
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Bob- yes it does pertain to any and all multiple mutations. "Waiting for TWO Mutations" was an attempt to refute Behe. Yet Behe NEVER discussed binding site evolution is the book the paper was responding to. They used binding sites for ease of demonstration. And recombination is a design mechanism. Read "Not By Chance".ET_{August 30, 2021
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ET - no it doesn't pertain to all and multiple mutations. They ignore, for example, recombination.Bob O'H_{August 30, 2021
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Wow. Bob the claim pertains to any and all multiple mutations, duh. They just used binding sites for ease of demonstration. So you're not even able to use basic logic and reasoning. And yes, you should be afraid.ET_{August 30, 2021
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Yarrgonaut -
I don’t see anywhere that Hössjer et al. assume that it must always be the case that multiple changes are required to obtain any functionality. They say rather that it is necessary specifically for complex adaptions of a species.
Right, but the paper I'm citing undermines this by showing that their scenario is unrealistic for the specific problem they are looking at: you don't need 6 or 7 specific mutations to get a binding site.
Considering that the study you cited dealt only with a very simple promoter, wherein the repressor was deleted, and the mutS gene was also deleted to increase the mutation rate, can you point to any particular point where the cited study contradicts the conclusion of the study in the original post?
All of it? it shows the target space to get regulatory function is much much larger than Hössjer et al./i> assume. ET - we're not discussing multiple mutations generally, we're discussing the evolution of regulatory sequences (the title of the paper is On the waiting time until coordinated mutations get fixed in regulatory sequences). So you're not addessing the point, I'm afraid. EugeneS - I have no idea what you are on about, sorry. Can you explain?Bob O'H_{August 30, 2021
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Bob O'H Can you do better than using the good old true Scotsman fallacy? I am not impressed.EugeneS_{August 29, 2021
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Earth to Bob O'H- The alleged evolution of trichromatic vision involved MULTIPLE, just-so, mutations. It is a real world example that refutes your nonsense that only one is required. All alleged gene duplications that led to new protein folds are real world examples requiring multiple coordinated mutations. The alleged evolution of bacterial flagella involved multiple coordinated mutations. The paper I linked to says that is way out of the reach of blind and mindless processes. And papers like that exist because you and yours don't have anything beyond stories. These are real world examples that refute your nonsense of one mutation is all that is required.ET_{August 28, 2021
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Eugene wrote:
Yes. The so called ‘directed evolution’, which is, in reality, intelligent selection in camouflage. BTW, this OP by GPuccio is a treasure. Darwinists either do not appreciate or conceal the real challenge in front of them, i.e. the sheer vastness of the sequence space, the existence of about 2000 substantially different and unrelated protein superfamilies, and the limited probabilistic resources available to evolution.
Yes, that definitely articulates the ID argument and in particular on functional proteins very well. I have yet to see anything in the way of a substantial rebuttal to it. Bornagain,
Thanks Yarrgonaut for adding more detail. I appreciate it.
I read through again and realized I was being a bit redundant I did think this deserved more discussion though. :) Bob,
Indeed, that’s the point. It undermines the assumption of the Hössjer et al. by showing that there are a lot of sequences that can act as promotors. Yes, they are not complicated but that also means that it is relatively easy for them to evolve some functionality (i.e. comparable to the wild type), whereas Hössjer et al. assume there have to be several changes to get any functionality.
I don't see anywhere that Hössjer et al. assume that it must always be the case that multiple changes are required to obtain any functionality. They say rather that it is necessary specifically for complex adaptions of a species. Their paper says:
We study how the waiting time distribution depends on the number of genes, the mutation rate, the length of the binding sites, the length of the regulatory sequences, and the way in which the targeted binding sites are coordinated for different genes in terms of selection coefficients.
They find:
the expected waiting time increases exponentially with m, for a selectively neutral model, when back-mutations are possible.
This isn't an argument from irreducible complexity, it's an argument about the amount of time necessary for complex adaptions. Considering that the study you cited dealt only with a very simple promoter, wherein the repressor was deleted, and the mutS gene was also deleted to increase the mutation rate, can you point to any particular point where the cited study contradicts the conclusion of the study in the original post?
The cited paper has relevance to the ID argument, but it doesn't have any relevance as a counter argument.
It's irrelevant as a counter-argument, that doesn't mean it doesn't have useful information.Yarrgonaut_{August 28, 2021
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ET - I don't think Rick Durrett know much about trichromatic vision. Certainly the paper you cite doesn't provide any evidence about it. Actually, I've never met Rick Durrett but the evil side of me wants to drag him into a lab to see what he would do.Bob O'H_{August 28, 2021
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And Bob, the ONLY reason probability arguments are used with respect to evolution by means of blind and mindless processes is due to the fact that there aren't any real world examples of such processes doing what evolutionists claim they did. You and yours have nothing beyond whatever single, isolated mutations can wrought.ET_{August 28, 2021
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ET @62, I'd blame might be called "ideological poisoning." While ID promoters have a variety of beliefs about God, Darwinist fundamentalists are becoming the "flat earthers" of biology who don't understand that their Norwegian Blue parrot is not "pinin' for the fjords." It's dead as is their 19th century theory! https://www.youtube.com/watch?v=vZw35VUBdzo -QQuerius_{August 28, 2021
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Wow. Learn how to read. AGAIN- the alleged evolution of trichromatic vision involved a gene duplication followed by specific changes to the duplicated gene. What part of that don't you understand? And that example stands for all alleged gene duplications. Clearly you have reading issues. Or perhaps you are just dishonest. Either way all you are doing is proving that you don't have a clue and shouldn't be called a scientist.ET_{August 28, 2021
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ET - where do you provide this example? Not @58, clearly: that's a paper with a model and not a real world example.Bob O'H_{August 28, 2021
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Earth to Bob O'H- I provided an example in which multiple mutations were required in the real world. Clearly you don't know anything about the real world as there are millions of such examples. Your willful ignorance still isn't an argument. And that is all you have.ET_{August 28, 2021
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ET - and the point of citing the paper I did was to point out that you don't need multiple mutations, so the Hössjer et al. paper seems to have little to no relevance to the real world.Bob O'H_{August 28, 2021
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Wow. Earth to Bob O'H- I have already explained it. The paper in the OP pertains to MULTIPLE mutations. The paper you referenced pertains to ONE. Again, what part of that don't you understand? Then there is the paper Waiting for TWO Mutations- written by evolutionists trying to refute Behe. Yet all they did was expose evolutionism for the nonsense that it is. The alleged evolution of trichromatic vision involved multiple mutations. All alleged gene duplication events that led to new protein folds require multiple mutations. Universal common descent required multiple mutations- but that is moot as mutations are impotent with respect to producing the diversity of life.ET_{August 27, 2021
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There is some comprehension issue here. This paper does support and, very strongly, the belief that wild types are globally optimized.
OK, so why did you cite it when I asked for evidence for your claim that wild types are optimised? I hope you can understand how i might be confused. You made what was, to me, a strange comment, and when asked for evidence to back it up you presented something that doesn't back it up.Bob O'H_{August 27, 2021
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