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ID theorists publish new paper in Journal of Theoretical Biology

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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
Bob, There is some comprehension issue here. This paper does support and, very strongly, the belief that wild types are globally optimized. Nobody in the world is capable of proving that, so you are knowlingly requesting the impossible. However, there is very solid ground under the belief that they are globally optimized. The paper does not claim that explicitly. However, for someone looking for this sort of evidence what is said there is enough. In the lab, using realistic assumptions and library size, they could only achieve 40% of the wild type peak. To achieve more they need a much larger library and more sophisticated techniques which will blur the distinction between the capabilities of evolution per se, which is what they really want to demonstrate, and the capabilities of intelligently guided search. I do not think you are unbiased. I think you are willfully commiting the true Scotsman fallacy.EugeneS
August 27, 2021
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ET - if the paper I linked to doesn't have anything to do with the paper in the OP, then you should easily be able to explain both of these: (1) why it is irrelevant that a perfect match isn't needed (and indeed a lot of sequences can act as binding sites). The issue is whether the paper is relevant to the real world, of course. (2) why the authors of the paper in the OP cited the paper I cited, if it is irrelevant.Bob O'H
August 27, 2021
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Bob, stop doubling down on your dishonesty. The paper you linked to doesn't have anything to do with the paper discussed in the OP. What is wrong with you?ET
August 27, 2021
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EugeneS - that paper doesn't say anything about wild types being a global optimum. Do you have a reference that supports what you claim?Bob O'H
August 27, 2021
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Querius, I agree. I do not think that Bob O'H is genuinely interested. I am just posting stuff that helped me get to where I got to as regards creating a mental picture of evolution, in the hope that it can help others.EugeneS
August 27, 2021
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Bob Experimental Rugged Fitness Landscape in Protein Sequence Space http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000096 This paper is hard evidence for what I am saying. That is, of course, if you are interested. The authors honestly report that in their evolution experiment they could get to about 40% of a wild peak. In the OP by GPuccio (see the link in one of my comments above), this paper is discussed at length. Darwinian evolution does not work even in a computer simulation. What works (the so called evolutionary algorithms) is artificial selection, i.e. guided search for solutions. In reality, evolution also faces huge challenges to do with random selection and genetic drift. For a mutation to be fixed, it needs to provide a statistically significant selective advantage. That is a real killer. See here: https://uncommondescent.com/evolution/gamblers-ruin-is-darwins-ruin/ On average, Darwinian evolution does not work. It can work, in corner cases (when noise is not a huge problem). But on average it just doesn't. That is reality.EugeneS
August 27, 2021
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EugeneS, Here's a tip: No amount of "your" evidence will satisfy Bob O'H that won't be challenged, misunderstood, objected to, and scoffed at. It's a fool's errand. Can you imagine that there will ever be a response such as, "Yes, that's really strong evidence. I can see what you mean. Thank you." There are references in some of Bornagain77's posts (and others here) that have provided information that I didn't know about. I appreciate cogent discussion but find it pointless to argue with parrots and chatbots. -QQuerius
August 26, 2021
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EugeneS -
And once again, there is strong evidence to believe that wild types are globally optimal.
Really? Can you provide your evidence for this?Bob O'H
August 26, 2021
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Bob is trying to be pedantic with my word choice again, so to be crystal clear, I will quote directly from the paper, "We find that ~60% of random sequences can evolve expression comparable to the wild-type with only one mutation, and that ~10% of random sequences can serve as active promoters even without evolution."
Random sequences rapidly evolve into de novo promoters – 2018 How new functions arise de novo is a fundamental question in evolution. We studied de novo evolution of promoters in Escherichia coli by replacing the lac promoter with various random sequences of the same size (~100?bp) and evolving the cells in the presence of lactose. We find that ~60% of random sequences can evolve expression comparable to the wild-type with only one mutation, and that ~10% of random sequences can serve as active promoters even without evolution. https://www.nature.com/articles/s41467-018-04026-w
There are no two way about it, THAT is a huge “jump’ in functionality (10% to 60%) with only one (supposedly) ‘random’ mutation to a completely random sequence. Something certainly does not smell right, and such a jump in functionality, with a supposedly completely ‘random’ mutation to a supposedly completely random sequence, certainly does not fit into the Darwinian paradigm. Something else definitely must be at play. ‘Something else’ that falsifies the ‘bottom-up’ materialistic presuppositions of Darwinian evolution and validates Intelligent Design. (Cell Cognition?; i.e. J. Shapiro) And, as I have already shown in post 34, we have very good reason to believe that some type of 'cell cognition' is directly involved in genome repair.bornagain77
August 26, 2021
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Bob O'H:
the point is that if single mutations are enough, and if there are multiple possible sequences, then the paper is irrelevant for the real world.
Wow. You have serious issues. Again, the paper was discussing scenarios in which MULTIPLE, COORDINATED mutations are REQUIRED. What part of that are you too dim to understand? For example the evolution of colored vision requires multiple, coordinated mutations. You can't get it with just one. And there are millions of such examples.ET
August 26, 2021
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Bob All these questions are interrelated. If you do not see the big picture, such cross references really help. While I may not know all the necessary biological details, I think I can fully appreciate the combinatorial search challenges evolution is facing. The general flaw in any evo "demonstrating" paper like this one is, as I said ealrier, that the playing field is not level but biased to favor certain scenarios, steer events towards or even control the outcome. And once again, there is strong evidence to believe that wild types are globally optimal. Even in a lab setting it is incredibly hard to achieve global optimality, given fair conditions for evolution.EugeneS
August 26, 2021
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ET - the point is that if single mutations are enough, and if there are multiple possible sequences, then the paper is irrelevant for the real world. ba77 -
Bob, without one ‘random’ mutation, the random sequences had 10% functionality compared to wild type., with one (supposedly) ‘random’ mutation, they had 60% functionality compared to wild type.
No, I'm afraid you've mis-understood the paper. That's not what it showed. Unless you are going to torture the definition of "functionality" beyond recognition.Bob O'H
August 26, 2021
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Why have people dug their heels in with Darwin? And if so, why in the world would they come here and dialogue, being confronted with truth every day? I guess it's admirable in one way, but also very frustrating. Bob, Sev, ChuckyD.... what would you rate your confidence in the theory of evolution to accomplish the diversity of life?zweston
August 25, 2021
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Bob, without one 'random' mutation, the random sequences had 10% functionality compared to wild type., with one (supposedly) 'random' mutation, they had 60% functionality compared to wild type. THAT is a huge "jump' in functionality with only one (supposedly) 'random' mutation to a random sequence. Something certainly does not smell right, and such a jump in functionality, with a supposedly completely 'random' mutation to a completely random sequence, certainly does not fit into the Darwinian paradigm. Something else definitely must be at play. 'Something else' that falsifies the 'bottom-up' materialistic presuppositions of Darwinian evolution and validates Intelligent Design. (Cell Cognition?; i.e. J. Shapiro) Bob offers this following caveat for rigidly testing for fitness,,,,: "putting these strains back into a natural environment over a extended period of time would probably kill them",,, And that is precisely my point BOB, if you guys can NEVER actually empirically demonstrate that unguided, mindless, Darwinian processes are capable of creating something new over and above what already exists, then you guys simply have no real time experimental evidence for Darwinian evolution. PERIOD!
Darwin vs. Microbes (Where’s the substantiating evidence for Darwinian evolution?) https://docs.google.com/document/d/16umLl1dnEuGcRfGqErD_XzZXVbOxcAJmIRPaF7PBOVg/edit
All empirical evidence that is put forth by Darwinists after that primary failure of Darwinists to validate their theory with actual substantiating evidence, is just pointless navel gazing after that fact, Your present cited paper is especially included in that pointless navel gazing metaphor BOB! i.e. Without a empirical demonstration of Darwinian processes creating something new over and above what already exists, YOU'VE GOT NOTHING BOB!!!
John 1:3 Through him all things were made; without him nothing was made that has been made.
bornagain77
August 25, 2021
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The paper discussed in the OP pertains to multiple required mutations. It cannot be refuted by showing that in some instances it only takes one mutation to produce a promoter from an existing sequence that wasn't. Not only that there isn't any evidence that the mutation mutations in Bob's linked paper were due to blind and mindless processes. Bob is question begging by calling them random.ET
August 25, 2021
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EugeneS - you seem to want to discuss something other than the Hössjer et al. paper. Fine, but please be careful not to confuse the issues. ba77 - I don't think you understand the paper. There was no "jump from 10% to 60% functionality in a ‘random’ sequence with ONLY one “random’ mutation". 60% of the random sequences had functionality comparable to the wild type after only one mutation. And putting these strains back into a natural environment over a extended period of time would probably kill them: the strain used is artificial, and was designed so that it is easier to follow expression of the lac operon.Bob O'H
August 25, 2021
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Bob claims "Functional peaks were achieved." Again, my bet is that if they more realistically mimicked what wild-type bacteria actually experience in a natural environment over a extended period of time, instead of using a ‘comfy’ artificial laboratory environment to see if the mutated bacteria are as fit as the wild-type bacteria, then they would see small declines in fitness for the mutated bacteria when compared to the wild-type bacteria. After all, we are talking about only a very small segment of DNA being replaced with a random sequence. i.e. as with the jump from 10% to 60% functionality in a 'random' sequence with ONLY one "random' mutation, there is much that is suspect with this experiment that simply does not fit into the Darwinian narrative, but does fit with the ID narrative of cells being designed with (very) sophisticated repair mechanisms.bornagain77
August 25, 2021
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BTW it is exactly the same issue of the capabilities of evolution vs the capabilities of intelligent selection which is at the core of the so called evolutionary algorithms. These algorithms in reality have nothing to do with Darwinian evolution, as any unbiased developer who has actually worked with them would acknowledge. But we hear the same equivocation, even in cases like this https://ti.arc.nasa.gov/m/pub-archive/1244h/1244%20%28Hornby%29.pdf It looks as if the domain knowledge is not needed as soon as you have the magic wand of evolutionary algorithms.EugeneS
August 25, 2021
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Bob Again, finding a peak by evolution is no big deal, provided it is close enough to this peak already and it can do so in the amount of time available to it. In this sense, you are preaching to the converted. However, what you keep, I suspect intentionally, out of your responses, is the fact that it is the amount of the functional information that is of relevance in terms of design detection. If you had carefully read GP's post, you would have remembered that he deals with the question of island size. Saying it is an archipelago is equivalent to saying it corresponds to low functional complexity. You haven't even started debunking ID. ID is about high functional complexity and high specificity. Are you suggesting that it is possible to implement OS Linux in a 100 lines of source code?EugeneS
August 25, 2021
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Bob O'H:
It undermines the assumption of the Hössjer et al. by showing that there are a lot of sequences that can act as promotors.
Where do you get those random sequences from? And why did evolutionary biologists publish "Waiting for TWO Mutations" that basically agrees with the issue at hand?ET
August 25, 2021
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Bob O'H:
The promotor sequences that evolved are new promotors for the lac operon. That would usually fit teh definition of a de novo promotor.
You are an equivocating coward, Bob. You cannot demonstrate the new promoter evolved by means of blind and mindless processes. That is what is being debated. Why do you think your willful ignorance is an argument?ET
August 25, 2021
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EugeneS -
=fit the definition of a de novo promotor.= You can call it whatever you like, the main point though is whether it demonstrates enough functional complexity to warrant inference to design, as you already know I am sure.
Good. Although what you think of as the main point is what the Hössjer et al. paper was looking at.
I repeat my point: if the system is already in a functional island, it is not surprising that it can find other peaks.
This is only of marginal relevance to the paper, but I guess you have to go with what you have.
Most likely, these “de novo” peaks are suboptimal, i.e. net function has probably degraded.
They're about as sub-optimal as the wild type. But the Hössjer et al. paper assumes that the sequences have no function, which is a bit more than being sub-optimal.
Again, this is no secret to the ID folks.
I guess they forgot to mention it to Hössjer et al. then.
Evolution can find other islands in the vicinity, given enough probabilistic resourcesv. But I would not hold my breath.
The Yona et al. paper shows that they don't need much in the way of "probabilistic resources": 10% of random sequences have a function comparable to the wild type, and 60% are within one mutation of that function. Basically, this is an archipelago.
The functional peaks in wild types are most probably globally optimal. Indeed, they cannot be achieved in a lab setting under the most generous but realistic assumptions.
Functional peaks were achieved. This is precisely what Yona et al. did. I've no idea if the WT was globally optimal or not, and I'm not sure that it matters, at least in an evolutionary sense.Bob O'H
August 25, 2021
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at 32 Bob states that, "If your argument is (as you state @ 19) ” whatever functionality was inherent in the deleted segment is being compensated for by other parts of the genome”, why does functionality only return in some of the strains? The rest of the genome is the same, so the redundancy you posit will be present in all strains." Well, I could very well be wrong in my assumption about genetic redundancy, (and if I am wrong I will be, unlike Darwinists, happy to admit my mistake and learn from it). But I still don't think that I am that far off the mark by appealing to 'genetic redundancy' (which is, as already noted, incompatible with Darwinian evolution), as a contributing factor for such a dramatic 'rate of return' for functionality, (10% to 60%), from, (supposedly), completely random sequences. Specifically, they "find that ~60% of random sequences can evolve expression comparable to the wild-type with only one mutation, and that ~10% of random sequences can serve as active promoters even without evolution", That, by itself, tells me that something else very mysterious must be going on in the cell in order to have such a dramatic increase in compensation for any lost functionality from the random sequences. In other words, with such a dramatic jump from 10% functionality to 60% functionality with only one mutation, then the burning question now becomes, "exactly how does the rest of the cell "know" exactly where to mutate the inserted random sequence with only one mutation in order to have such a dramatic increase in compensation, (I.e. 10% to 60%), for any lost functionality?" Surely, contrary to Darwinian presuppositions, the mutation cannot be a completely random affair but must instead be a purposely 'directed' mutation in order to achieve such a remarkable jump from 10% functionality to 60% functionality with only one mutation. If the mutation to the random sequence were truly a random affair, as Darwinists presuppose, then the 'rate of return' should have been much lower than the jump from 10% to 60%. Obviously, the cell must somehow 'know' exactly where to mutate the random sequence in order to achieve such a dramatic jump in functionality, (10% to 60%). To repeat, a truly random mutation to a completely random sequence would, obviously, have been expected to have a much lower 'rate of return' for functionality. And such 'cell cognition', (as James Shapiro of "The Third Way" has termed such examples as this), is simply completely incompatible with the reductive materialistic presuppositions of Darwinists. Indeed, and specifically, Shapiro calls cell cognition "far outside the mainstream" and says that such "vital properties",,, "has been among the most fiercely disputed topics in the history of science",,,
Barbara McClintock, Genome Self-Repair and Cell Cognition: - James Shapiro - 2012 Excerpt: Repair was an example of action by what McClintock came to call “smart cells.”,,, This kind of thinking was indeed far outside the mainstream. It is the reason that the neurobiologist and bacterial behavior researcher, Dennis Bray, comments,, that McClintock was the first biologist to ask what a cell knows about itself.,,, McClintock apparently wanted to draw special attention to the most challenging problems in biology: cognition and purposeful action by living cells. As she knew well from her long experience with 20th Century genetics and cell biology, whether life has special “vital” properties that separate it from inorganic matter has been among the most fiercely disputed topics in the history of science. In its early days, molecular biology promised to provide us with an explanation of life in terms of physics and chemistry. However, since the 1960s it has succeeded instead in amazing us with the richness and sophistication of intra- and inter-cellular control and communication networks. https://www.huffpost.com/entry/barbara-mcclintock_b_1223618
Perhaps the most dramatic, even 'miraculous", example of this 'vital principle' of cell cognition is the following example where the author compared the ability of D. radiodurans to reassemble its genome, after being shattered by radiation, to Jesus raising Lazarus from the dead.
Extreme Genome Repair - 2009 Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal.,,, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319128/
And the following study found that such 'miraculous' cell cognition is not limited to D. radiodurans, but that such 'miraculous raising from the dead' cell cognition is a widespread ability that is present in e-coli as a whole, (which happens to be the exact organism that the researchers used in the paper you cited)
In the lab, scientists coax E. coli to resist radiation damage - March 17, 2014 Excerpt: ,,, John R. Battista, a professor of biological sciences at Louisiana State University, showed that E. coli could evolve to resist ionizing radiation by exposing cultures of the bacterium to the highly radioactive isotope cobalt-60. "We blasted the cultures until 99 percent of the bacteria were dead. Then we'd grow up the survivors and blast them again. We did that twenty times," explains Cox. The result were E. coli capable of enduring as much as four orders of magnitude more ionizing radiation, making them similar to Deinococcus radiodurans, a desert-dwelling bacterium found in the 1950s to be remarkably resistant to radiation. That bacterium is capable of surviving more than one thousand times the radiation dose that would kill a human. http://www.news.wisc.edu/22641
So in conclusion Bob, while I very well could be wrong about 'genetic redundancy', I still don't think that I am that far off the mark when I appealed to 'genetic redundancy'. There is something very mysterious that is going on in the cell in order to compensate for any loss of functionality that the inserted random sequence took away from the cell. The 'directed' single mutation to the random sequence that increased functionality from 10% to 60%, by itself, tells us that far more is going on in the cell than just the cell, willy-nilly, mutating the random sequence as is presupposed in Darwinian thought.bornagain77
August 25, 2021
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Bob =fit the definition of a de novo promotor.= You can call it whatever you like, the main point though is whether it demonstrates enough functional complexity to warrant inference to design, as you already know I am sure. I repeat my point: if the system is already in a functional island, it is not surprising that it can find other peaks. Most likely, these "de novo" peaks are suboptimal, i.e. net function has probably degraded. Again, this is no secret to the ID folks. Evolution can find other islands in the vicinity, given enough probabilistic resources. But I would not hold my breath. The functional peaks in wild types are most probably globally optimal. Indeed, they cannot be achieved in a lab setting under the most generous but realistic assumptions. The main logic of design inference as applied to protein functionality is: 1. register a sudden increase in functional information. 2. measure the positive functional information delta. 3. compare it against what evolution is capable of (in the most optimistic scenario for evolution). If the functional information delta exceeds the capabilities of evolution, we can safely rule it out. As simple as that.EugeneS
August 25, 2021
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ba77 @ 21 -
To be more clear in what I was saying I admit that I should have used the term ‘replace’ instead of ‘delete’, but that is a minor and trivial point compared to the overall point that I was making. i.e. The experiment is nowhere near being the proof for functionality that Bob imagines it to be!
If your argument is (as you state @ 19) " whatever functionality was inherent in the deleted segment is being compensated for by other parts of the genome", why does functionality only return in some of the strains? The rest of the genome is the same, so the redundancy you posit will be present in all strains. EugeneS @ 24 -
Starting from a functional whole, deliberately breaking something and watching how it recovers, is not enough to claim that something has appeared de novo.
Why not? The promotor sequences that evolved are new promotors for the lac operon. That would usually fit teh definition of a de novo promotor. Yarrgonaut @ 25 -
Reading Bob’s paper, I don’t think they even did that. It looks like all they did is delete the repressor and switch the promoter to a random sequence to evolve another sequence of TATAAT and TTGACA. Given 100 base pairs, that shouldn’t be too hard.
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.Bob O'H
August 25, 2021
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Thanks Yarrgonaut for adding more detail. I appreciate it.bornagain77
August 24, 2021
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Yarrgonaut, 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.EugeneS
August 24, 2021
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Yes, this is it. Exactly as I anticipated. They start from something really complex, degrade the initial complexity, find it still works and, voi la, evolution did it.
Well part of it worked anyway. HahahaYarrgonaut
August 24, 2021
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Just to head off a potential lame comment from a Darwinist being something like "but it still evolved" - referring to my point about wait times. In this situation, we're talking about a very very small handful of base pairs, which should be pretty low hanging fruit, and even at that a waiting time was necessary. For situations that require mucho regulation, or something like functional proteins, that's a whole different ball game.Yarrgonaut
August 24, 2021
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For interested readers, the OP I referred to up this thread is here: https://uncommondescent.com/intelligent-design/defending-intelligent-design-theory-why-targets-are-real-targets-propabilities-real-probabilities-and-the-texas-sharp-shooter-fallacy-does-not-apply-at-all Among other things, it deals in detail with the rugged functional landscape in the space of protein linear sequences, which is relevant to this discussion. Bob O'H was around at UD at the time it was published and I am sure must have read and probably even discussed it.EugeneS
August 24, 2021
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20
AM
PDT
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