ID theorists publish new paper in Journal of Theoretical Biology

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

Silver Asiatic, That was kind, but don't hold your breath. -Q Querius

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

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

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

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

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

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

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

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

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

ET - we're not discussing Behe's paper, though. Please try to keep up. Bob O'H

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. -Q Querius

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

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

ET - no it doesn't pertain to all and multiple mutations. They ignore, for example, recombination. Bob O'H

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

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

Bob O'H Can you do better than using the good old true Scotsman fallacy? I am not impressed. EugeneS

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

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

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

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

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 -Q Querius

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

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

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

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

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

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

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

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

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

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

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

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

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. -Q Querius

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thanks Yarrgonaut for adding more detail. I appreciate it. bornagain77

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

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. Hahaha Yarrgonaut

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

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

Yarrgonaut, =the promoters evolved in our library are of very low complexity= 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. EugeneS

BA,

The main flaw in Bob’s paper is that, number one, they never evolved anything over and above the original wild type bacteria, and they, therefore, never really demonstrated that Darwinian evolution has the capacity within itself to create anything above and beyond what already exists in the wild-type bacteria."

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. Regarding using it as a response to the ID paper mentioned above, note the authors say:

"the promoters evolved in our library are of very low complexity, as most of the activating mutations involved no additional factors but the two basic promoter motifs. 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."

In other words, the assumption in this paper - that newly activated genes do not need to be regulated to offer significant advantage - is essentially the opposite of what the new ID paper is trying to test - How long does it take for traits to evolve when multiple mutations are required to give an advantage? In short, it is perfectly irrelevant. Except for:

...in the two cases, RandSeq29 and RandSeq40, we observed that predicted promoters in the random sequences were not active before evolution until the activated mutations occurred downstream to their TATAAT element, but did not create a promoter motif.

It appears that there wasn't any expression until both the promoter, and the downstream mutations were in place. Ironically, this paper, which was touted on Panda's Thumb as evidence against the above paper, demonstrated the very reality that the paper was discussing - that the wait times, even at a very very low level of complexity aren't imaginary. Yarrgonaut

I actually had a look at it. Starting from a functional whole, deliberately breaking something and watching how it recovers, is not enough to claim that something has appeared de novo. An old poodle trick. EugeneS

Bob Of course, it is your choice. I think that in good conscience a lot of people have tried their best for years to explain to you where they believe you are making mistakes. And yet... So I can say exactly the same thing in return: is it worth investing my time in these comments? ET # 22 That is exactly why I am not even bothering to look into all this stuff because it is bound to be the same old poodle tricks. "Give us another 5 years and we will..." whereas in the actual fact, all they are doing is intelligent selection. My favorite slogan is, the best refutation of Intelligent Design nonsense has been provided by the researchers from the Institute of Protein Design. EugeneS

The paper Bob linked to is a perfect example of a cell repairing itself because it was intelligently designed to do so. ET

Bob claims, "they didn’t delete sequences, though" Yet they replaced "the lac promoter with various random sequences". How you replace something without first removing and/or deleting it I have no idea. 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! Bob is, IMHO, being overly pedantic since he simply has nothing else to hang his hat on in that experiment. bornagain77

ba77 - they didn't delete sequences, though. So I've no idea what you mean. Bob O'H

Bob, they assumed that the (small) sequence they deleted could not be compensated for by other parts of the genome and/or by information in the cell body. In fact, It is far, far, more likely that whatever functionality was inherent in the deleted segment is being compensated for by other parts of the genome, i.e. ''genetic redundancy', than it is that some random sequence just so happened to have the functionality necessary to be a lac promoter. That much is, or should be, just plain common sense. As mentioned in post 10, the failure of Darwinists to take 'genetic redundancy' into consideration led them to, for years, severely underestimate the minimal genome size required for life.

Minimal genome should be twice the size – 2006 Excerpt: “Previous attempts to work out the minimal genome have relied on deleting individual genes in order to infer which genes are essential for maintaining life,” said Professor Laurence Hurst from the Department of Biology and Biochemistry at the University of Bath. “This knock out approach misses the fact that there are alternative genetic routes, or pathways, to the production of the same cellular product. “When you knock out one gene, the genome can compensate by using an alternative gene. “But when you repeat the knock out experiment by deleting the alternative, the genome can revert to the original gene instead. “Using the knock-out approach you could infer that both genes are expendable from the genome because there appears to be no deleterious effect in both experiments. http://www.news-medical.net/news/2006/03/30/16976.aspx

In other words, contrary to what Darwinists believe, it is turning out that the genome is not some cobbled together, piecemeal, affair, but that the genome is instead best viewed as being, more or less, an integrated whole where all the 'pieces' contribute to the functionality of the whole. Here is a semi related note to that effect:

Theory Suggests That All Genes Affect Every Complex Trait - June 20, 2018 Excerpt: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis. But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way,,, One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out. Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000. https://www.quantamagazine.org/omnigenic-model-suggests-that-all-genes-affect-every-complex-trait-20180620/

i.e. So much for Dawkins' entire 'selfish gene' concept! bornagain77

ba77 -

And even, via genetic redundancy, their one claim to have established functionality for random sequences is very much questionable.

Why? What mistakes did the authors make in the paper? Bob O'H

Earth to Bob O'H- the paper didn't have anything to do with blind and mindless processes. You are equivocating, again. ET

Whatever Bob. You got no evidence for you worldview. PERIOD! And even, via genetic redundancy, their one claim to have established functionality for random sequences is very much questionable. VERY questionable. So I really have no idea what you think the big deal is with that paper. You, as an evolutionist, simply have nothing solid to hang your hat on in that paper! bornagain77

ba77 -

actually is not what I want the paper to be about, it is about the fact that the results of the experiment are nowhere near showing that the unguided, mindless, processes of Darwinian evolution are capable of creating anything new, over and above, what already exists.

But that's not what the paper was investigating, though. The work described in the paper had a specific aim, and the paper describes those results. You're criticising the paper because it didn't show what it wasn't trying to show. I guess I could take the same approach and criticise you because you haven't provided a road map to peace in Afghanistan in this thread. Bob O'H

Bob. actually is not what I want the paper to be about, it is about the fact that the results of the experiment are nowhere near showing that the unguided, mindless, processes of Darwinian evolution are capable of creating anything new, over and above, what already exists. It is also not a minor failing that the authors just so happened to forget about 'genetic redundancy' which is now known to be ubiquitous within life. These are NOT minor failings for their experiment, nor is such a consistent lack of empirical support a minor failing for a theory that falsely claims to be as well established as Gravity. Again, It has nothing to do with my personal preferences and has everything to do with the actual experimental science at hand. Again, Darwinian evolution simply has no real-time empirical evidence whatsoever to support its grandiose claims that all life on earth arose via unguided, mindless, processes.

Darwin vs. Microbes (Where’s the substantiating evidence for Darwinian evolution?) https://docs.google.com/document/d/16umLl1dnEuGcRfGqErD_XzZXVbOxcAJmIRPaF7PBOVg/edit

bornagain77

LoL! @ Bob O'H- All you do is equivocate and bluff. Your comments are worth investing time on because it is easy to expose you as the poseur that you are. ET

ba77 @ 10 -

The main flaw in Bob’s paper is that, number one, they never evolved anything over and above the original wild type bacteria, and they, therefore, never really demonstrated that Darwinian evolution has the capacity within itself to create anything above and beyond what already exists in the wild-type bacteria.

Err, so the main flaw is that the paper was not about what you wanted it to be about. Not much of a flaw, really. EugeneS @ 11 - if you can't even be bothered to look at something before commenting on it, I don't think your comments are worth investing any more time on. Bob O'H

Bob I haven't even looked into that paper. Mine is a general statement that whatever "evolution can do it" proponents present as achievements of evolution, are results of carefully crafted and carefully controlled experimentation. "Carefully crafted" refers to making available at time 0 all the necessary components that are at the exactly right concentrations, purified to the industrial standards, at the exactly right temperature ranges, exactly right timing etc. In nature everything exists in mixtures. "Carefully controlled" means controlling the chemical synthesis by an intelligent experimenter, e.g. by removing or manipulating the intermediate reagents in order to achieve the end goal that is in the minds of the experimenters, which is bona fide Intelligent Design. Either of these two points, as any unbiased researcher would admit, defeats the purpose. Now, I pointed you to an earlier OP by GPuccio that deals with this and other issues. Amongst the other issues is the one that simple functions can really be achieved by evolution. BUT these functions are rather irrelevant to ID inference GP proposes, because they are not complex enough and consequently not identifiable as intelligently created. Second, often these simple functions are irrelevant because they are not naturally selectable. EugeneS

Bob O'H cites this following paper as (finally) providing experimental proof for Darwinian 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

The main flaw in Bob's paper is that, number one, they never evolved anything over and above the original wild type bacteria, and they, therefore, never really demonstrated that Darwinian evolution has the capacity within itself to create anything above and beyond what already exists in the wild-type bacteria. Moreover, my bet is that is they 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 eventually see small declines in fitness for the mutated bacteria when compared to the wild-type bacteria. But anyways,,, the second flaw in their paper is that the authors are apparently unaware that it is now known that there is a tremendous amount of 'genetic redundancy' that is 'Intelligently Designed" into cells that compensates for 'missing' elements in the genome. In fact, such inbuilt 'genetic redundancy' led Darwinists to, for years, severely underestimate what the minimal genome size for life should actually be. The following studies highlight the inherent fallacy in gene deletion/knockout experiments that have led many (Darwinian) scientists astray in the past as to underestimating what the minimal genome for life should actually be:

Minimal genome should be twice the size - 2006 Excerpt: “Previous attempts to work out the minimal genome have relied on deleting individual genes in order to infer which genes are essential for maintaining life,” said Professor Laurence Hurst from the Department of Biology and Biochemistry at the University of Bath. “This knock out approach misses the fact that there are alternative genetic routes, or pathways, to the production of the same cellular product. “When you knock out one gene, the genome can compensate by using an alternative gene. “But when you repeat the knock out experiment by deleting the alternative, the genome can revert to the original gene instead. “Using the knock-out approach you could infer that both genes are expendable from the genome because there appears to be no deleterious effect in both experiments. http://www.news-medical.net/news/2006/03/30/16976.aspx How Many Genes Do Cells Need? Maybe Almost All of Them - May 2018 Excerpt: By knocking out genes three at a time, scientists have painstakingly deduced the web of genetic interactions that keeps a cell alive. Researchers long ago identified essential genes that yeast cells can’t live without, but new work, which appears today in Science, shows that looking only at those gives a skewed picture of what makes cells tick: Many genes that are inessential on their own become crucial as others disappear. The result implies that the true minimum number of genes that yeast — and perhaps, by extension, other complex organisms — need to survive and thrive may be surprisingly large,,, “Perhaps what we’re sampling here,” Andrews said, “are some functional connections in the cell that we weren’t able to see before.” One set of new connections, for example, was between genes involved in transporting proteins and genes involved in DNA repair. On the surface, it’s difficult to see what would connect these two functions. And in fact, the researchers still don’t have a mechanistic explanation. But they are sure there is one. “Our immediate reaction was, ‘Well, that’s kind of random,’” Andrews said. “But we’ve learned over the course of doing this project that it’s not random. We just don’t understand how the cell is connected. https://www.quantamagazine.org/how-many-genes-do-cells-need-maybe-almost-all-of-them-20180419/

Genetic Redundancy is incompatible with Darwinian evolution:

A Darwinian Paradox Excerpt: the very existence of genetic buffering, and the functional redundancies required for it, presents a paradox in light of the Darwinian (or: selectionist) concept. On one hand, for genetic buffering to take place there is a necessity for redundancies of gene function, on the other hand such redundancies are clearly unstable in face of natural selection and are therefore unlikely to be found in evolved genomes. Still, over 90% of the genes studies of model organisms were observed to be redundant [Conant GC et al, 2004; Kobayashi K et al, 2003; Baba T et al, 2006]. http://archive.is/YxXhd

Oh well, so much for Bob's supposed experimental proof for Darwinian evolution. Like everything else in Darwinian evolution, Bob's supposed evidence for Darwinian evolution is 'smoke and mirrors' that does not bear up to scrutiny. Darwinists simply have no substantiating scientific evidence whatsoever to support their grandiose claims that all life on earth evolved via mindless undirected processes..

Darwin vs. Microbes (Where’s the substantiating evidence for Darwinian evolution?) https://docs.google.com/document/d/16umLl1dnEuGcRfGqErD_XzZXVbOxcAJmIRPaF7PBOVg/edit

bornagain77

Wow. Earth to Bob O'H- evolution by means of blind and mindless processes is total nonsense. The DI promotes the approach because it proves that people like you are full of that nonsense. ET

EugeneS - OK, so you're saying that the JTB paper that the OP is about is irrelevant to ID. You might want to tell the DI about this, as they are promoting this approach. Bob O'H

Bob O'H is confused. There isn't any evidence that blind and mindless processes produced E. coli. There isn't any evidence that blind and mindless processes are what produced the results in the paper Bob linked to. ET

Bob Thank you. People can't back up their claims even in a controlled lab environment. That is reality. With random libraries and no control you can demonstrate non complex functions at best. ID inference kicks in at or beyond 140 functional bits. Please see GP's original posts here of three years back where he dealt with this at length. In particular, he quotes Hayashi paper presenting phage infectivity landscape and discusses in detail why this paper is actually evidence of ID claims. The OP is on the Texas sharpshooter fallacy and why it doesn't apply to ID. EugeneS

EugeneS - In reality they aren't "highly likely globally optimized" this is 10% of all the random sequences tested. I gave you think link, so at least you can read the abstract. Bob O'H

Bob, Re 10%: in many cases protein functions observed in reality are highly likely globally optimized, which is really hard to achieve even in a lab by guided search. Nowhere near 10%. Would you be willing to drive a car on a motorway if you knew that it was just 10% of the industry reliability standard? EugeneS

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.

Whereas in reality (i.e. in an experiment that was done) a 10% pass mark is good enough. Or 60% if you're allowed 2 tries. Strange the authors didn't notice this. Bob O'H

Thanks, Polistra at 1. They seem to have stopped doing it - for now. But we can;t really know whether the posts were allowed to be visible. We would rather not have to start covering the need to reign in Big Tech half the time (it's not really our our mission) but we will if we must. News

Peer-reviewed, the stamp of official approval. It's harder for the outragers to bash a peer-reviewed paper. Facebook is doing weird and random stuff. Not just censorship. The way they disorganize comments now makes it impossible to use for 'news' purposes. Seems like they're trying to lose their customers in every possible way. polistra