15.5 hours.

Over two working days.

In this comment colewd says: “Let’s start with this overview.”

An “overview” that according to this tool contains 187153 words.

Where those words according to this tool will take over 15 hours to read.

15 hours for an “overview”. 15 hours.

If only there was some way to take a sprawling set of claims and refine them down into a core that could then be reviewed by others and feedback given until it is a reasonable size (typically 3,000 to 10,000 words on the average scientific paper) where all claims have been tested by other experts and errors removed.

It seems to be it’s a strategy. Never get pinned down on anything too specific and you never have to be wrong. Hence the sprawl.

colewd, do you seriously expect people to spend 15 hours reading an “overview”? How long is the main argument? A million or two words?

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90 thoughts on “15.5 hours.

  1. I’ll be honest, even though I ‘engaged’, I never even clicked the link. Just kinda guessed what was in it. It’s a massive time-saver.

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  2. Bill doesn’t weight arguments by quality of evidence. With ID-Creationist bullshit it’s all about quantity. If gpuccio says “this is too complex!!” a thousand times that counts as a thousand pieces of evidence for Bill’s disembodied mind as the Creator.

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  3. Neil Rickert,

    Let’s be fair. It was just a typo. When he said “overview”, he really meant “bullshit”.

    It is actually real science and a very good description of how a critical cellular mechanism works. It turns out the guys accusing the other guys of pseudo science were projecting all along.

    Allan unless you have a understanding of how the ubiquitin systems works you should read the article unless you have completely retired your mind from cellular biology.

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  4. colewd: It is actually real science and a very good description of how a critical cellular mechanism works.

    The bullshit part was gpuccio copying scientific descriptions from elsewhere then adding “This is too complex, it’s impossible to evolve, must be DESIGNED!!”.

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  5. Allan Miller: I’ll be honest

    Why?
    You hadn’t been honest?

    Allan Miller: even though I ‘engaged’, I never even clicked the link. Just kinda guessed what was in it. It’s a massive time-saver.

    Aha! And you’ve accused me of reading abstracts and scanning articles and you don’t even bother to click the links… I have suspected it all along…👍😉

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  6. colewd:
    Neil Rickert,

    Allan unless you have a understanding of how the ubiquitin systems works you should read the article unless you have completely retired your mind from cellular biology.

    I already know how ubiquitin works. Why would I need a blog post when I have a textbook? I also know how ‘gosh it’s complicated’ apologetics approaches such systems. The details of ubiquitin are actually irrelevant. Any system could be subject to the same approach. It’s just a question of looking erudite, bamboozling the audience with data then saying ‘therefore Design’. Sal does it in every post.

    That biology is complex is news to no-one.

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  7. J-Mac: Why?
    You hadn’t been honest?

    It’s a common idiomatic approach, like ‘to be fair’ or ‘frankly’ or ‘honestly’, which you’ve picked me up on before. They don’t mean that their opposite had hitherto been the case. Is English your first language? You seem rather blind to idiom.

    Aha! And you’ve accused me of reading abstracts and scanning articles and you don’t even bother to click the links…

    So you’re gonna tell me you’ve spent 15.5 hours on it. I already know a fair bit about ubiquitin. Why would I need a refresher?

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  8. colewd:
    Allan Miller,

    But don’t forget it was built by a series of selected random accidents

    Or Some Bloke. I don’t know where you think a trivialised expression of mechanism gets you.

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  9. colewd:
    Allan Miller,

    But don’t forget it was built by a series of selected random accidents

    Bill makes the argument from ignorance based personal incredulity for the 10,000th time.

    Then Bill wonders why everyone considers him such a disingenuous jerk.

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  10. Allan Miller,

    Or Some Bloke. I don’t know where you think a trivialised expression of mechanism gets you.

    My first observation is you had to label it so you don’t have a good counter argument. Next it is a check and alternative hypothesis to keep evolution honest. If the universe is designed we are going to see more of this same wall that hit us when we observed the transcription translation mechanism in biology.

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  11. colewd: Next it is a check and alternative hypothesis to keep evolution honest.

    Pity no one’s thought of a good way to keep ID-Creationists honest. Refuting their science-free stupidity with published scientific evidence doesn’t even slow down their lie-machine.

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  12. colewd:
    Allan Miller,

    My first observation is you had to label it so you don’t have a good counter argument.

    You didn’t present an argument, just a deliberately trivialised, and rather petulant, expression of mechanism. So I did the same, to illustrate the non-point you made.

    Next it is a check and alternative hypothesis to keep evolution honest.

    What keeps ‘Design’ honest?

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  13. colewd: My first observation is you had to label it so you don’t have a good counter argument.

    You’re the fool(I got that word-usage from phoodoo, take it up with him) making vague handwaves in the direction of how old people’s textbooks are, and then you complain when people don’t take you seriously.

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  14. colewd: My first observation is you had to label it so you don’t have a good counter argument.

    You keep coming up with this nonsensical excuse. No Bill, people really do some times label things out of frustration and boredom, not because they don’t have good responses. Perhaps they’re tired of wasting time giving good responses to nonsense, and call you (rightly) the tool you are. Is that a possibility? That they’re “labeling” you and your fatuous arguments (see, another label, omg that means nobody can say anything because they used a label) because they’ve grown tired of doing 5000-post-threads on your lack of understanding? Could that be it?

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  15. You keep coming up with this nonsensical excuse. No Bill, people really do some times label things out of frustration and boredom, not because they don’t have good responses. Perhaps they’re tired of wasting time giving good responses to nonsense, and call you (rightly) the tool you are. Is that a possibility? That they’re “labeling” you and your fatuous arguments (see, another label, omg that means nobody can say anything because they used a label) because they’ve grown tired of doing 5000-post-threads on your lack of understanding? Could that be it?

    This was a trivial point. You are arguing for Trumps #1 skill.

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  16. Allan Miller,

    What keeps ‘Design’ honest?

    It’s simply a default hypothesis to compare to. You are asking a question like what keeps random honest.

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  17. colewd: It’s simply a default hypothesis to compare to.

    Fail again Bill. “A disembodied mind used magic to POOF biological life” isn’t the default to evolution any more than “invisible pixies use magic to push matter around” is the default position for gravity.

    You never seem to miss a chance to demonstrate your science illiteracy.

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  18. colewd:
    Allan Miller,

    It’s simply a default hypothesis to compare to.You are asking a question like what keeps random honest.

    Somehow I am reminded of a sentence written (about schoolbook battles) by William Benetta: In all of their efforts, the creationists make abundant use of a simple tactic: They lie. They lie continually, they lie prodigiously, and they lie because they must.

    And that in turn is a perfect description of the difficulties faced by the gaggle of sycophants in Washington, trying to paint lipstick on Trump’s 18 lies a day. When your god lies continually, what else can you do?

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  19. colewd:
    Allan Miller,

    It’s simply a default hypothesis to compare to.

    Why is it the default hypothesis? Suppose some money disappeared. I insist God did it, because no evidence could be provided for an alternative explanation. Would that be ‘honest’?

    You are asking a question like what keeps random honest

    Nope. People advancing the Design hypothesis don’t get a free ride. It’s an intellectually feeble non-explanation, when baldly stated. Why do the planets move? God pushes them. How do elements form? God shoves them together. What causes gravitation? God. It’s the default explanation, don’cha know?

    Design actually has a huge problem, IMO. Even if provided with the molecular constituents of what you would regard as the minimal possible cell, I contend that these could not be assembled into that working configuration, because physics. So your ‘honest’ appeal is to an entity that can somehow transcend thermodynamic restrictions. That’s more ‘honest’ than accepting that gaps are an expected consequence of evolution itself, an explanation rooted in the real. Your ‘honesty’ also requires you to pretend the vast molecular evidence on common descent does not exist. Excuse me while I laugh my ass off.

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  20. colewd,

    It’s simply a default hypothesis to compare to.You are asking a question like what keeps random honest.

    So I picked a component of the ubiquitin system, the E3 ub-protein ligase. Ligases perform molecular ‘joining’ operations. Naturally I chose the pinnacle of Creation, the chimp, as my start point: H2QNL0. I ran a BLAST search and got 100% identity in human, gorilla, orang utan, macaque, gibbon, baboon, mangabey, night monkey, marmoset.

    I got 99.7% identity on sifaka (a primate), brown bear, cat, sea otter, bushbaby, then 99.1% on goat and pig …

    This happens with pretty much every gene I pick, however low-level its function (and you don’t get much lower-level than generalised ‘tagging’ of proteins).

    What’s going on here, on the ‘default’ Design paradigm? What functional explanation groups almost all primates on exactly the same sequence, but then ‘requires’ a different variant in the carnivores, etc etc – what non-descent cause essentially ‘recovers’ the Linnaean, morphological hierarchy on non-morphological genes?

    Be honest.

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  21. colewd: If the universe is designed we are going to see more of this same wall that hit us when we observed the transcription translation mechanism in biology.

    Who is “we” here? Name names.

    And you say “if” the universe is designed. Do you have some doubt then?

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  22. colewd: It is actually real science and a very good description of how a critical cellular mechanism works.

    Has it been reviewed by other experts in the field?
    Is this OP real science as well? Why not?

    colewd: It turns out the guys accusing the other guys of pseudo science were projecting all along.

    It turns out that anybody can make a blog post and call it science. That does not make it so.

    colewd: Allan unless you have a understanding of how the ubiquitin systems works you should read the article unless you have completely retired your mind from cellular biology.

    There are many claims made in the world and little time to evaluate them. If you want this ‘work’ to make the impact you seem to think it has in the actual scientific community then you will have to publish it.

    And yet gpuccio refuses to do such, refuses to submit his work in a venue where it can be critiqued formally by knowledgeable people.

    Could it be that Intelligent Design is merely a misunderstanding of how biology actually works?

    It certainly seems so, and it seems that gpuccio seems to know this, given his irrational reluctance to submit his work to a real journal.

    Recently I asked for evidence that ID papers are being rejected for ideology only. Nobody could provide any evidence for such.

    So if you believe that link is ‘real science’ then why not publish it yourself as a paper and submit it to a reputable journal? Then you can claim all the credit that gpuccio refuses to take! And ID replaces evolution!

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  23. Gpuccio’s post has, like all things ID, all the advantages of theft over honest toil. The strategy is a straightforward act of duplicity:

    1. description of a complex system that can be modeled as if it were using a code.
    2. insistence that codes cannot occur “naturally”
    3. Therefore, the existence of a code implies a designer (or: makes one a much more probable explanation)

    The first move, (1), involves presenting all the actual hard work — the real science — done by molecular biologists, or whomever’s credentials are being borrowed for this exercise.

    The next step, (2), usually goes by so fast that it’s easy to miss — yet it’s the decisive move. It involves a rapid equivocation between the concepts of code, language, and intelligence. Here the really decisive error lies in the assumption that (1) codes are languages and (2) languages arise through deliberate acts of individual creative intelligence.

    I say this because it is only these background assumptions that make the step from (2) to (3) appear intuitive.

    This argument also relies on omitting from consideration what we know about far-from-equilibrium thermodynamics and the use of complexity theory to show that genes in vivo are much more like the far-from-equilibrium thermodynamics of complex systems than they are like “codes” or “languages”.

    To reiterate a point I’ve made too many times to count: the serious rival to ID/creationism is not evolutionary theory but complexity theory.

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  24. Allan Miller,

    Why is it the default hypothesis? Suppose some money disappeared. I insist God did it, because no evidence could be provided for an alternative explanation. Would that be ‘honest’?

    We have a good explanation for money disappearing so I would not use the design hypothesis is this case.

    Nope. People advancing the Design hypothesis don’t get a free ride. It’s an intellectually feeble non-explanation, when baldly stated. Why do the planets move? God pushes them. How do elements form? God shoves them together. What causes gravitation? God. It’s the default explanation, don’cha know?

    Good point. It is certainly not interesting once it has a tested explanation available.

    That’s more ‘honest’ than accepting that gaps are an expected consequence of evolution itself, an explanation rooted in the real. Your ‘honesty’ also requires you to pretend the vast molecular evidence on common descent does not exist. Excuse me while I laugh my ass off.

    The gaps are no longer an accepted consequence once we observed the organized complexity of the cell.

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  25. Allan Miller,

    So I picked a component of the ubiquitin system, the E3 ub-protein ligase. Ligases perform molecular ‘joining’ operations. Naturally I chose the pinnacle of Creation, the chimp, as my start point: H2QNL0. I ran a BLAST search and got 100% identity in human, gorilla, orang utan, macaque, gibbon, baboon, mangabey, night monkey, marmoset.

    Spectacular thanks for aligning these. I am seeing more data like this as when you align mammal amino acid sequences with alpha actin 1 including humans rats mice etc. you get 100% alignment. While common descent is certainly an explanation it is at best a partial explanation as it can explain similarities but not differences. A question remains.

    -How did the ubiquitin or alpha actin sequence get into the global optimum we are observing given the almost infinite sequence space it lives in?

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  26. colewd: -How did the ubiquitin or alpha actin sequence get into the global optimum we are observing given the almost infinite sequence space it lives in?

    Hey Bill, how did you convince yourself that these sequences represent the global optimum?

    Who lied to you and told you that you know that? Where is your empirical evidence of that?

    I see you’re making the same blind assertion over on peacefulscience.

    Try to explain how you suddenly got that idea. What happened in your head to cause you to become convinced of that?

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  27. Kantian Naturalist,

    To reiterate a point I’ve made too many times to count: the serious rival to ID/creationism is not evolutionary theory but complexity theory.

    This is a very interesting point that you have made in the past as I remember. Who are the key people focused on this theory?

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  28. Rumraket,

    Hey Bill, how did you convince yourself that these sequences represent the global optimum?

    Good catch Rum :-). I got this idea from you. If in any group like mammals or primates if we see no alignment differences that is the most conserved position possible therefor it is a global maximum or optimum.

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  29. colewd: Good catch Rum :-). I got this idea from you. If in any group like mammals or primates if we see no alignment differences that is the most conserved position possible therefor it is a global maximum or optimum.

    No, you haven’t got it from me Bill, because I have never said any such thing. I’ve said we can explain a conserved sequence with it having got stuck on a LOCAL optimum. We do not need to think it represents the GLOBAL optimum.

    Do you understand the difference between LOCAL and GLOBAL?

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  30. Rumraket,

    Do you understand the difference between LOCAL and GLOBAL?

    I understand you borrowed a phantom phrase local optimum from some work on enzymes where this analogy was created. I took your word and changed it based on the fact that you cannot exceed 100% preservation. It is by definition a global optimum. There is no evidence for your claim and no reason to believe it is true for proteins that need to interact with other specific complex proteins.

    The important point is my use of global optimum is based on evidence your use of local optimum is not.

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  31. colewd: I understand you borrowed a phantom phrase local optimum from some work on enzymes where this analogy was created.

    Phantom phrase? Don’t be childish Bill. The concept of a local optimum is an established idea in both physics, computer science and engineering (relating to optimization problems and algorithms), and in evolutionary biology.

    So no Bill, that’s not something you understand, because that’s something you’ve just dreamt up.

    The concept also applies to understanding other things in biology than just enzymes, such as adaptive phenotypes, and while on the topic of sequence evolution, to regulatory elements such as transcription factor binding spots in DNA. As I also wrote a post showing over on peacefulscience just a few hours ago.

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  32. colewd:
    Kantian Naturalist,

    This is a very interesting point that you have made in the past as I remember.Who are the key people focused on this theory?

    Probably the most readable person in complexity theory is Stuart Kauffman. In particular I liked and would recommend A World Beyond Physics: The Emergence and Evolution of Life (2019), Humanity in a Creative Universe (2016), Reinventing the Sacred (2008), and At Home in the Universe (1996).

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  33. But hey, this is a good a place as any to copy-paste that post to here: Oh by the way, just to show this idea with local optima and many peaks in the fitness landscape of some sequence isn’t anything unusual, and to show that Bill Cole’s insinuation that it’s only for enzymes that there are other possible hills, here’s a paper where researchers completely explored the fitness landscape in the sequence space of a 10-nucleotide binding spot for a regulatory protein. This is the spot where a protein that regulates a downstream gene binds, so the function is specific binding between the DNA and protein molecule.

    Rowe W, Platt M, Wedge DC, Day PJ, Kell DB, Knowles J. Analysis of a complete DNA-protein affinity landscape. J R Soc Interface. 2010 Mar;7(44):397-408. DOI: 10.1098/rsif.2009.0193

    ABSTRACT
    Properties of biological fitness landscapes are of interest to a wide sector of the life sciences, from ecology to genetics to synthetic biology. For biomolecular fitness landscapes, the information we currently possess comes primarily from two sources: sparse samples obtained from directed evolution experiments; and more fine-grained but less authentic information from ‘ in silico ’ models (such as NK -landscapes). Here we present the entire protein-binding profile of all variants of a nucleic acid oligomer 10 bases in length, which we have obtained experimentally by a series of highly parallel on-chip assays. The resulting complete landscape of sequence-binding pairs, comprising more than one million binding measurements in duplicate, has been analysed statistically using a number of metrics commonly applied to synthetic landscapes. These metrics show that the landscape is rugged, with many local optima, and that this arises from a combination of experimental variation and the natural structural properties of the oligonucleotides.

    They keep the protein sequence constant, and vary instead the DNA sequences to see how the fitness landscape for the protein looks in response to different DNA sequences.

    What do they find? Well in the sequence space of that 10-mer stretch of DNA there are a total of 4^10 = 1.048.576 different possible combinations, which they all experimentally characterize and find:

    Because of the comprehensive nature of the 10-mer landscape we are not confined to making assumptions about its properties based purely on statistical measures from sampling. It is thus possible to enumerate each of the sequences and determine those that represent local optima. This can be accomplished using a ‘steepest ascent hill-climber’ (Kauffman & Levin 1987) which, starting from a sequence x , considers all the Hamming neighbours of x and moves to the fittest one, repeating this procedure until there is no neighbour fitter than the current sequence. By starting the hill-climber at every sequence, we can not only determine the number of local optima and their properties, but also the points in the landscape that are attracted to each optimum. These so-called ‘basins of attraction’ are useful in characterizing local optima. We are interested in how they will affect genetic algorithm performance and how likely they are to have arisen purely from noise.

    This hill-climber reveals 6805 local optima within the complete sequence landscape. Quantitative assessment of this figure relative to the noisy NK -landscapes is difficult to obtain. However, there is a smooth decline in the mean maximum basin sizes observed with increasing values of K (see electronic supplementary material for a summary of these data). Within the experimental landscape, the size of the basins of attraction varies considerably, from one associated sequence to nearly 30 000.

    Almost seven thousand peaks(aka local optima). And the hills(which they call ‘basins of attraction’) they sit on vary in size from literally one sequence constituting it’s own local “hill”, up to clusters of 30.000 sequences.

    The paper is well worth a read as they also describe how these hills are distributed in the space (hint: not uniformly), and what fraction of the space is covered by the hills representing the top 1% of all sequences:

    In the 10-mer landscape, the local optima are far from evenly distributed, with the top 1 per cent of local optima (68 sequences) containing 47 per cent of sequences from the landscape within their basins of attraction. (…) The diameter of the basins of attraction gives an indication of how the local optima are dispersed within the sequence landscape. We take the diameter as the Hamming distance from each local optimum to the most dissimilar sequence within the set of local optima. From table 3, it can be seen that the diameters for all local optima are maximally dissimilar (a Hamming distance of 10). When the set of local optima are reduced to the top 10 and 1 per cent in terms of binding affinity, they become progressively more localized. This localization of high-affinity optima can be visualized in the classical multidimensional scaling plot shown in figure 5 a . From the plot in figure 5 b it can be seen that these clustered sequences generally possess adenine as the first base at the 5′-end.

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  34. Rumraket, thanks for posting that. In my university department we have a very active group of experimental evolution researchers doing these kind of things. They will often make all possible single-base substitutions in a sequence and then when giving a talk on this, say that they have completely explored the sequence space. But that is completely exploring the nearby part of the space of sequences. The 2010 Rowe et al. paper you cite really did explore the whole space, at least for this 10-base stretch of protein-binding DNA.

    Alas, to explore the space thoroughly for 10 amino acids would require a 30-base stretch of DNA, which would have 4^{30} or 2^{60} possible nucleotide sequences, which is more than 10^{18}. Even if one looked only at different amino acid sequences for 10 positions, there would be 20^{10} or more than 10^{13} possibilities.

    ETA: calculation corrected.

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  35. Rumraket,

    Now let’s see the papers that apply to the proteins that gpuccio is using. You are trying to equate apples and oranges which you did when you made the claim that Axe’s estimates were 6 or more orders of magnitude off. To test a claim about a protein you actually need to use the protein that the hypothesis is based on.

    This is why I call your claim phantom use of local maximum or optimum.

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  36. colewd:
    I took your word and changed it based on the fact that you cannot exceed 100% preservation.

    That makes no sense. It does not explain why you changed my word just because the sequence is conserved.

    colewd:
    It is by definition a global optimum.

    No, the global optimum is defined as the best of all possible solutions. That’s how a global optimum is defined. You don’t establish that some sequence is a global as opposed to local optimum merely from the observation that it is conserved, since that observation is predicted from both concepts, that’s why the sequence doesn’t change.

    You can only establish that a sequence IS the global optimum by actually probing all of sequence space, or a representative fraction of it from which it is possible to approximate the overall topology.

    You can’t do that if all you have are conserved sequences. The very reason it is being conserved is that it is better than mutant versions of it, hence sampling is constantly restricted to the neighborhood of the sequence being conserved.

    colewd:
    There is no evidence for your claim and no reason to believe it is true for proteins that need to interact with other specific complex proteins.

    Yes there is evidence for my claim that alpha-actin sits on a local optimum. First of all the sequence being conserved is literally what a local optimum predicts. Second, mutant versions of it are known to exist at low frequencies in the human population as I showed in this post, and they are associated with various muscle-related diseases.

    Bill you’ve told this falsehood so many times now, and I have corrected you on it, it’s now time we start to consider the option that you are lying. You can’t just be so biased you keep forgetting about it. Some times as little as ten minutes pass between me reminding you of that evidence and you saying no evidence has been presented. You can’t forget it that fast unless you have some sort of neurological disorder like Alzheimer’s disease. Do you, Bill? If not, you’re lying.

    Stop being a liar, stop bearing false witness. The religion you believe in explicitly condemns lying. It is a sad state of affairs that I, an atheist, have to remind you, a Christian, of this:
    Exodus 20:16: Thou shalt not bear false witness against thy neighbour.

    Let us recall where Exodus 20:16 supposedly came from according to Christian scripture: God himself.

    Not men interpreting his words. God is supposed to have written those words into stone. In the biblical story, Moses didn’t chisel them down in the rocks, God did it himself. There is thus no possibility that they are in error unless people who passed them got it wrong. I don’t think you believe that they did. And here you are effectively pissing all over them.

    You keep saying there is no evidence, and yet I keep both explaining what that evidence is, and showing it to you. You are not abiding by the standards of your own faith.

    colewd:
    The important point is my use of global optimum is based on evidence your use of local optimum is not.

    For reasons already explained the mere observation of a conserved sequence is not capable of determining that we are seeing the global optimum, so you shouldn’t claim it is one as you would be claiming something you don’t actually know to be true. Even if it is the global optimum (which we do not have evidence that allows us to conclude), it would not be incorrect to call that a local optimum until such a time as that evidence is gathered, since even the global optimum would still also be the optimum in it’s local sequence-neighborhood.

    Now Bill, you have an opportunity to be a better person(and a better Christian) and stop lying about what has or has not been said, and about what there is evidence for.

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  37. Stuart is one of the most readable, and most interesting, people working in the somewhat-vague field of “complexity”. Perhaps because his original training is as an MD, and he has always been focused on biological “complexity” rather than the totally abstruse.

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  38. colewd: Now let’s see the papers that apply to the proteins that gpuccio is using.

    Now you’re contradicting yourself. You want the same experimental assessment of the proteins being discussed as the one I showed in that paper, but that means you are conceding that empirical evidence could overturn your extrapolation, so you are admitting you don’t actually know how many functional sequences there are in the sequence space of the protein in question.

    Also, no, I don’t have to bring a paper that shows such an experiment on the proteins you obsess about, since it is you who is claiming to know how many functional sequences there are by plugging in a number of sequences that meet the minimal threshold for function. And you’d need to actually know that so you can take -log2 of the fraction of functional sequences out of all possible sequences.

    Hence it is YOU who should be proving how many or few hills there are with empirical evidence. I have merely been saying that you cannot conclude, merely from observing that the sequence is being conserved, that there are no other functional sequence, as that observation can be explained simply by the sequence having been driven to some local optimum by selection. See the attached figure again.

    colewd:You are trying to equate apples and oranges

    No I am refuting a claim you made that the concept of multiple hills and peaks in the fitness landscape of some functional protein only applies to enzymes.

    colewd:To test a claim about a protein you actually need to use the protein that the hypothesis is based on.

    To refute your claim that the concept only applies to enzymes, I need only show an example of the concept being applied to a non-enzyme.

    So now we basically went through the same subject again for the tenth time, I showed all your assertions to be wrong or misguided for the tenth time, and here we are again back to square one. With you having forgotten all about it, and repeating the same LIES over and over again.

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  39. Joe Felsenstein,

    Alas, to explore the space thoroughly for 10 amino acids would require a 30-base stretch of DNA, which would have 4^{60} or 2^{120} possible nucleotide sequences, which is more than 10^{36}. Even if one looked only at different amino acid sequences for 10 positions, there would be 20^{10} or more than 10^{13} possibilities.

    This is why statistical methods of taking samples of functional sequences and aligning them is a reasonable method of getting an estimate as population sizes are not the critical factor in the accuracy of the estimate. Over time we will get better sampling which is the critical factor.

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  40. Joe Felsenstein: Rumraket, thanks for posting that. In my university department we have a very active group of experimental evolution researchers doing these kind of things. They will often make all possible single-base substitutions in a sequence and then when giving a talk on this, say that they have completely explored the sequence space. But that is completely exploring the nearby part of the space of sequences. The 2010 Rowe et al. paper you cite really did explore the whole space, at least for this 10-base stretch of protein-binding DNA.

    Alas, to explore the space thoroughly for 10 amino acids would require a 30-base stretch of DNA, which would have or possible nucleotide sequences, which is more than . Even if one looked only at different amino acid sequences for 10 positions, there would be or more than possibilities.

    Yes it is still only possible, in practice, to do these kinds of exhaustive explorations for very short sequences. For even small proteins in the 20-30 amino acid range, the problem becomes almost completely intractable.

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  41. colewd: This is why statistical methods of taking samples of functional sequences and aligning them is a reasonable method of getting an estimate as population sizes are not the critical factor in the accuracy of the estimate. Over time we will get better sampling which is the critical factor.

    Just for the benefit of anyone lurking in this thread, I’d like to point out that what Bill just wrote here is meaningless gibberish and a non-response. It’s cargo-cult science. There are some science-sounding words there, half-conceived as relevant to the subject, such as “taking samples of functional sequences and aligning them”.

    But it’s essentially gibberish. Don’t be fooled, Bill is not really responding in a sensible way as much as keeping up the pretense that he is.

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  42. Rumraket,

    Also, no, I don’t have to bring a paper that shows such an experiment on the proteins you obsess about, since it is you who is claiming to know how many functional sequences there are by plugging in a number of sequences that meet the minimal threshold for function. And you’d need to actually know that so you can take -log2 of the fraction of functional sequences out of all possible sequences.

    Mercer is pushing hypothesis at PS. If you talk about an apple and claim it applies to an orange you need to show the orange really behaves like you are claiming. This gets you to the first inning of trying to make your point.

    You’re claim that we cannot use statistical methods to estimate FI is based on the flawed idea that population size is a significant factor in estimation.

    Are apples and oranges sciency words Rum 🙂

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  43. BruceS: Complexity theory is good stuff, but I’m not clear on how it figures in contradicting ID.

    What I had in mind was the following: ID relies on the intuition that order can only come about through a top-down, mind-first organizing principle — and that “mechanistic” physical law cannot explain complexity. (Hence the frequent complaint by IDists that “emergence” is nonsense!)

    By contrast complexity theory explains how localized regions of matter and energy can move away from near-equilibrium conditions, and thereby shows how order can spontaneously emerge in a “bottom-up” way.

    In a way, Dennett was right to say (in Darwin’s Dangerous Idea) that naturalism became plausible only when we figured out how to disentangle the concept of order from the concept of design. But Dennett gives Darwin too much credit here — although Darwin did play a significant role here, the decisive breakthrough was more due to the founders of complexity theory such as Ilya Prigogine.

    Joe Felsenstein: Stuart is one of the most readable, and most interesting, people working in the somewhat-vague field of “complexity”. Perhaps because his original training is as an MD, and he has always been focused on biological “complexity” rather than the totally abstruse.

    Yeah, I like Kauffman for his readability specifically. Though presently I am reading Juarrero’s Dynamics in Action (1999) and she is much more clear in her analysis as to how exactly complexity theory and non-equilibrium thermodynamics involves rejecting assumptions that we have inherited from Newton (about how to think about causation) and from Hume (about how to think about explanation).

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  44. Kantian Naturalist: What I had in mind was the following: ID relies on the intuition that order can only come about through a top-down, mind-first organizing principle

    That makes sense to me. I was thinking of ID in terms of CSI and ASC and other information-based arguments.

    Though presently I am reading Juarrero’s Dynamics in Action (1999) and she is much more clear in her analysis as to how exactly complexity theory and non-equilibrium thermodynamics

    I enjoyed that book, although I think it gets somewhat speculative in the information arguments. But it’s speculation that makes intuitive sense to me!

    I am not sure of the relevance of Newtonian causation — causation philosophy has come a long ways since him.

    I do like her use of constraints emerging from non-linear dynamics (complexity) as an explanation of downward causation without invoking strong emergentism. Bechtel and co-author do something similar here:
    https://www.researchgate.net/publication/322875100_Rethinking_Causality_in_Biological_and_Neural_Mechanisms_Constraints_and_Control

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