Aphrodite’s head: Eight questions for Douglas Axe

Over at Evolution News, Dr. Douglas Axe argues that merely by using very simple math, we can be absolutely certain that life was designed: it’s an inescapable conclusion. To illustrate his case, he uses the example of a rugged block of marble being transformed by natural weather processes into a statue of a human being. Everyone would agree that this simply can’t happen. And our conclusion wouldn’t change, even if we (i) generously allowed lots and lots of time for the statue to form; (ii) let each body part have a (discrete or continuous) range of permitted forms, or shapes, instead of just one permitted shape; (iii) relaxed the requirement that all body parts have to form simultaneously or in sync, and allowed the different parts of the statue to form at their own different rates; and (iv) removed the requirement that the different parts have to each form independently of one another, and allowed the formation of one part of the statue to influence that of another part.

In his post, Axe rhetorically asks: if we’re so sure that a rugged block of marble could never be transformed by the weather into a human statue, then aren’t we equally entitled to conclude that “blind natural causes” could never have “converted primitive bacterial life into oaks and ostriches and orangutans”? In each case, argues Axe, the underlying logic is the same: when calculating the probability of a scenario which requires many unlikely things to happen, small fractions multiplied by the dozens always result in exceedingly small fractions, and an event which is fantastically improbable can safely be regarded as physically impossible.

In an attempt to persuade Dr. Axe that his logic is faulty on several grounds, I’d like to put eight questions to Dr. Axe, and I sincerely hope that he will be gracious enough to reply.

My first question relates to the size and age of the universe. As I understand it, Dr. Axe, you define “fantastically improbable” as follows: something which is so improbable that its realization can only be expected to occur in a universe which is much bigger (or much older) than our own. Indeed, on page 282 of your book, Undeniable, you further stipulate that “fantastically improbable” refers to any probability that falls below 1 in 10116, which you calculate to be the maximal number of atomic-scale physical events that could have occurred during the 14-billion-year history of the universe. You calculation requires a knowledge of the age of the universe (14 billion years), the amount of time it takes for light to traverse the width of an atom, and the number of atoms in the universe. So here’s my first question for Dr. Axe: how is the design intuition supposed to work for an ordinary layperson who knows none of these things? Such a person will have no idea whether to set the bar at one in a million, one in a billion, one in 10116 , or even one in (10116)116. I should also point out that the figure you use for the number of atoms in the universe refers only to the observable universe. Astronomers still don’t know whether the size of the universe as a whole is finite or infinite.  And it gets worse if we go back a few decades, in the history of astronomy. Until the 1960s, the Steady State Theory of the universe was a viable option, and many astronomers believed the universe to be infinitely old. How would you have argued for the design intuition back then? 

My second question relates to functional coherence. You make a big deal of this in your book, Undeniable, where you managed to distill the case for Intelligent Design into a single sentence: “Functional coherence makes accidental invention fantastically improbable and hence physically impossible” (p. 160), where functional coherence is defined as a hierarchical arrangement of parts contributing in a coordinated way to the production of a high-level function (p. 144). The problem with your statue illustration should now be apparent. A statue has no functions. It just sits there. Consequently, whatever grounds we may have for rejecting the supposition that ordinary meteorological processes could transform a block of marble into a statue, they obviously have nothing to do with the argument you develop in your book, relating to functional coherence and whether living things could possibly be the product of unguided natural processes. So my question is: will you concede that the marble block is a bad illustration for your argument relating to functional coherence?

My third question relates to the identity of the object undergoing transformation. In your statue illustration, you ask whether “a rugged outcrop of marble would have to be altered by weather in only a few reasonably probable respects in order to convert it into a sculpted masterpiece.” Obviously, the answer is no: the number of steps would be extremely large, and the steps involved would be fantastically improbable. You then compare this case with the evolutionary claim that “blind natural causes converted primitive bacterial life into oaks and ostriches and orangutans.” But there is an obvious difference in the second case: the primordial bacterium itself is not being changed into an orangutan. Its very distant embryonic descendant, living about four billion years later, is developing into an orangutan. Its ancestors 20 million years ago were not yet orangutans. Self-replication, along with rare copying mistakes (mutations), is required in order for evolution to work. So I’d like to ask: why do you think it’s valid to infer from the fact that A’s changing into B is a fantastically improbable event, that A’s distant descendants gradually mutating into B is also fantastically improbable?

My fourth question relates to chemistry. Let me return to your original example of a block of marble being transformed by weather events into a human statue. I think we can all agree that’s a fantastically improbable event. However, the probability is not zero. I can think of another event whose probability is much, much lower: the likelihood of weather processes transforming a block of diamond, of adamantine hardness, into a human statue. What’s the moral of the story? Chemistry matters a lot, when you’re calculating probabilities. But the average layperson, whom you suppose to be capable of drawing a design inference when it comes to living things, knows nothing about the chemistry of living things, beyond the simple fact that they contain atoms of carbon and a few other elements, arranged in interesting structures. An ordinary person would be unable to describe the chemical properties of the DNA double helix, for instance, even if their life depended on it. So my question to you is: why do you think that a valid design inference can be made, without knowing anything about their underlying chemistry?

My fifth question relates to thermodynamics. I’d like you to have a look at the head of Aphrodite, below (image courtesy of Eric Gaba), known as the Kaufmann head. It’s made of coarse-grained marble from Asia Minor, and it dates back to about 150 B.C.

You’ll notice that her face has worn away quite a bit, thanks to the natural weather processes of weathering and erosion. This is hardly surprising: indeed, one might see weathering and erosion as an everyday manifestation of the Second Law of Thermodynamics: in an isolated system, concentrated energy disperses over time. Living things possess an unusual ability to locally decrease entropy within their
highly organized bodies as they continually build and maintain them, while at the same time increasing the entropy of their surroundings by expending energy, some of which is converted into heat. In so doing, they also increase the total entropy of the universe. But the point I want to make here is that a living thing’s highly useful ability to locally decrease entropy is one which a block of marble lacks: its thermodynamic properties are very different. So my question to you is: why would you even attempt to draw an inference about the transformations which living things are capable of over time, based on your observations of what happens to blocks of marble? And why would you encourage others to do the same?

My sixth question relates to your probability calculations. In your post, you explain the reasoning you employ, in order to justify a design inference: “it takes only a modest list of modestly improbable requirements for success to be beyond the reach of chance.” You continue: “Once again, the reasoning here is that small fractions multiplied by the dozens always result in exceedingly small fractions.” Now, this kind of reasoning makes perfect sense, if we are talking about dozens of improbable independent events: all you need to do is multiply the probability of each event, in order to obtain the probability of the combination of events. But if the events are not independent, then you cannot proceed in this fashion. Putting it mathematically: let us consider two events, A and B. If these events are independent, then P(AB) is equal to P(A) times P(B), and if both individual probabilities are low, then we can infer that P(AB) will be very low: one in a million time one in a million equals one in a trillion, for instance. But if A and B are inter-dependent, then all we can say about P(AB) is that it is equal to P(A) times P(B|A), and the latter probability may not be low at all. Consequently, in an inter-dependent system comprising dozens of events, we should not simply multiply the small probability of each event in order to compute the combined probability of all the events occurring together. That would be unduly pessimistic. And yet in your post, you attempt to do just that, despite your earlier statement: “Do I assume each aspect [of the statue] is strictly independent of the others in its formation? No.” So I’d like to ask: if you’re willing to grant that the even the formation of one aspect of a statue may depend on the formation of other aspects, thereby invalidating the method of calculating the probability of the forming the whole statue by multiplying dozens of “small fractions,” then why do you apply this invalid methodology to the formation of living things?

My seventh question relates to the vast number of possible pathways leading to the formation of a particular kind of living thing (such as an orangutan) from a primordial ancestor, and the even vaster number of possible pathways leading to the formation of some kind of living thing from the primordial ancestor. The point I want to make here is a simple one: this or that evolutionary pathway leading to an orangutan may be vanishingly improbable, yet if we consider the vast ensemble of possible pathways leading to an orangutan, the probability of at least one of them being traversed may not be so improbable. And even if we were to agree (for argument’s sake) that the likelihood of an orangutan evolving from the primordial ancestor is vanishingly low, when we consider the potentially infinite variety of all possible life-forms, the likelihood of evolutionary processes hitting on one or more of these life-forms may turn out to be quite high. It is this likelihood which one would need to calculate, in order to discredit the notion that all life on earth is the product of unguided evolutionary processes. Calculating this likelihood, however, is bound to be a very tricky process, and I doubt whether there’s a scientist alive today who’d have even the remotest idea of how to perform such a calculation. So my question is: what makes you think that an untutored layperson, with no training in probability theory, is up to the task? And if the average layperson isn’t up to it, then why should they trust their intuition that organisms were designed?

My eighth and final question relates to algorithms. Scientific observation tells us that every living thing, without exception, is put together by some kind of biological algorithm: a sequence of steps leading to the formation of an individual of this or that species. The algorithm can thus be viewed as a kind of recipe. (Contrast this with your illustration of a statue being formed by blind meteorological processes, which bears little or no relevance to the way in which a living thing is generated: obviously, there’s no recipe in the wind and the rain; nor is there any in the block of marble.) In order for “blind natural processes” (as you call them) to transform a bacterial ancestor into an orangutan, the algorithm (or recipe) for making an ancient bacterial life-form needs to be modified, over the course of time, into an recipe for making an orangutan. Can that happen?

At first blush, it appears fantastically unlikely, for two reasons. First, one might argue that any significant alteration of a recipe would result in an unstable hodgepodge that’s “neither fish nor fowl” as the saying goes – in other words, a non-viable life-form. However, this intuition rests on a false equivalence between human recipes and biological recipes: while the former are composed of letters which need to be arranged into meaningful words, whose sequence of words has to conform to the rules of syntax, as well as making sense at the semantic level, so that it is able to express a meaningful proposition, the recipes found in living things aren’t put together in this fashion. Living things are made of molecules, not words. What bio-molecules have to do is fit together well and react in the appropriate way, under the appropriate circumstances. Living things don’t have to mean anything; they simply have to function. Consequently, the recipes which generate living things are capable of a high degree of modification, so long as the ensembles they produce are still able to function as organisms. (An additional reason why the recipes found in living things can withstand substantial modification is that the DNA found in living organisms contains a high degree of built-in redundancy.)

Second, it might be argued that since the number of steps required to transform a bacterial ancestor into an orangutan would be very large, the probability of nature successfully completing such a transformation would have to be fantastically low: something could easily go wrong along the way. But while the emergence of an orangutan would doubtless appear vanishingly improbable to a hypothetical observer from Alpha Centauri visiting Earth four billion years ago, it might not seem at all improbable, if the Alpha Centaurian also knew exactly what kinds of environmental changes would befall the Earth over the next four billion years. The probability of evolution traversing the path that leads to orangutans might then appear quite high, notwithstanding the billions of steps involved, given a suitably complete background knowledge of the transformations that the Earth itself would undergo during that period. In reality, however, such a computation will never be technically feasible: firstly, because we’d probably need a computer bigger than the cosmos to perform the calculation; and second, because we’ll never have the detailed knowledge of Earth’s geological history that would be required to do such a calculation. So my concluding question to you is: given that the probability of nature generating an orangutan from a bacterial ancestor over a four-billion-year time period is radically uncomputable, why should we trust any intuitive estimate of the probability which is based on nothing more than someone eyeballing a present-day bacterium and a present-day orangutan? 

Over to you, Dr. Axe. Cheers.

311 thoughts on “Aphrodite’s head: Eight questions for Douglas Axe

  1. Mung: You’re appealing to a frequentest interpretation of probability, in which can you don’t get to assume that we expect to see it x times in 4.5 billion years. I’d say your sample size is too small.

    Nope, it’s an extremely simple calculation using the Poisson distribution. Try it.

  2. Mung: You guys crack me up. If we see it alot it means it’s probable.

    How about “If we see it a lot it means it’s probably probable.”?
    You keep missing the point though. You’re the ones making arguments from improbability without showing anything in the way of supporting evidence for your bullshit probabilistic claims.

    What’s the probability of a miracle Mung? Are miracles miracles if they are extremely improbable and why?

  3. Mung: You guys crack me up. If we see it alot it means it’s probable. If we never see it, it is still probable. How does that logic work, exactly?

    Haven’t seen anyone making that argument. No idea what you’re talking about

  4. dazz: Are miracles miracles if they are extremely improbable and why?

    Yes. And because that’s the whole point of Darwinian evolutionary theory. To do away with the need to appeal to the miraculous.

  5. dazz: You keep missing the point though. You’re the ones making arguments from improbability without showing anything in the way of supporting evidence for your bullshit probabilistic claims.

    You keep missing the point. Your arguments from ignorance don’t make the probabilities wrong. You need to show your math or you are just handwaving and expecting people to believe you based on a complete lack of evidence.

    Why not just admit that your position is based on ignorance and blind belief?

  6. Mung: And because that’s the whole point of Darwinian evolutionary theory. To do away with the need to appeal to the miraculous.

    You’re psychotic. Check your xmas turkey or whatever you have for xmas eve there, someone might have dropped something in there.

  7. Mung: Your arguments from ignorance don’t make the probabilities wrong

    What probabilities?

    Mung: You need to show your math or you are just handwaving and expecting people to believe you based on a complete lack of evidence.

    OK since you seem completely incapable of googling it, I can totally spoon feed you the math. would that make you feel better?

  8. Mung: Rumraket: If the probabilities were a barrier, there would be no reason to have the kind of data we do. If de novo protein evolution was so improbable as to be practically impossible, why is there so much evidence that it happens?

    Mung: Post hoc, ergo propter hoc. Texas sharpshooter. etc.

    What are you trying to say here?

    Did you take into account all the proteins that did not evolve and their probabilities? I’m guessing that no, you didn’t.

    I don’t even understand what you’re asking me to do here. It looks like you’re asking a question like “what is the probability that you ended up being you, instead of some other person?”.

    Rumraket: I concede that I can not convince a person of that mindset.

    What, specifically, are you trying to convince Bill of?

    That his claim that there is a “combinatorial problem” is based on faulty reasoning. I try to show this by, mostly, using the socratic method. I ask Bill to explain how his conclusion follows, and he just piles irrelevant assertions on top.

    He states some factoid, for example that the size of sequence space is 20^L, then by this alone declares this shows a combinatorial problem.

    I ask him how that follows? He then says that must means there are all these “trials” needed. I ask him why he thinks that’s the case? He says because the protein is conserved. I ask him whether that isn’t at least equally compatible with the sequence having been pushed up some local optimum by selection? Then he says the very existence of the hill shows functional constraint. I ask him to explain how it shows that, and whether functional constraint shows it couldn’t have been pushed up that hill by selection, and he then ignored the question and instead tried to switch the burden of proof to me by asking for evidence of “substitutability”. I then gave examples of significantly more diverged sequences, and then Bill absurdly and hilariously declared that their dissimilarity is somehow evidence AGAINST them having evolved.

    He then pulled the reset switch and went back to just asserting his conclusion, that there’s a “huge combinatorial problem”. Despite my questioning having revealed his complete failure to show this.

    So Bill has effectively argued two contradictory cases. If the sequences are highly similar, then they can’t have evolved because of “limited substitutability”, and when the sequences are significantly more diverged, this shows they can’t have evolved because now evolving two such dissimilar sequences must require a lot of mutations, and so that can’t happen, or something.

  9. Mung: And Rumraket, just look at all the mountains. So the probability of Everest is actually quite high.
    Your use of it as an example of something of low probability is the Texas sharpshooter fallacy.

    Explain how.

  10. colewd: If the mechanism has to be deterministic, it can’t have been a mind with free will. Right?

    Minds can be both.

    Really? So we can have free will on materialism? Interesting.

    It looks like the spliceosome is required to splice in the lower regulated mg+ environment that exists in the eukaryotic cell nucleus. Performance may also be an issue as intron complexity grew. Bigger chicken and egg issue then I thought.

    How so?

  11. Mung: So you’ve actually seen purely natural processes bring about a sculpture that looks like the head of Aphrodite? Go on!

    I don’t see why we have to think something supernatural was involved in creating a sculpture. Does some supernatural force have to intervene to make sandpaper work or something?

    You guys crack me up. If we see it alot it means it’s probable. If we never see it, it is still probable. How does that logic work, exactly?

    I don’t know either, but I’ve yet to see anyone here actually argue that if we never see something it is still probable.

  12. Mung: And because that’s the whole point of Darwinian evolutionary theory. To do away with the need to appeal to the miraculous.

    What does “appeal to the miraculous” mean?

  13. colewd: So you guys have failed to defend your position and make the claim the mechanism is true because the structure is there.

    What does this even mean? “The mechanism is true because the structure is there”?

    The combinatorial explosion problem is telling you your theory is wrong.

    You have yet to show even a single logically valid argument to the effect that there is a “combinatorial explosion problem”. You have claimed there is, but no fact that you have referenced have done any work towards establishing that conclusion.

    It doesn’t follow from the fact that some sequence is conserved.
    It doesn’t follow from the fact that some sequences are diverged.
    It doesn’t follow from the fact that the total sequence space is 20^L.
    It follows from NOTHING you’ve said.

    You’re still just brainlessly declaring that there’s a “combinatorial problem” despite clearly not having even a single valid reason for thinking that.

    We cant even come up with a clean explanation of how blind and unguided processes created the secondary folds of one protein.

    By mutations and natural selection, doh!

    The kinds of data we have only makes sense on the hypothesis that proteins evolve. We have even cited references directly to the effect that this happens. Bill, the Bsc4 protein in yeast is a de novo evolved protein with secondary structure.

    All you guys have are the mathematical innovations of Jock and Entropy trying to redefine how we calculate a sequence.
    The RNA of this protein has introns that require the structure it is a small piece of (spliceosome) to remove so it can even start the secondary fold ouch :-).

    See, this is you again just stating an irrelevant factoid, and not actually explaining how this factoid entails or even implies your conclusion.

    Let me repeat,
    You have yet to show even a single logically valid argument to the effect that there is a “combinatorial explosion problem”. You have claimed there is, but no fact that you have referenced have done any work towards establishing that conclusion.

    It doesn’t follow from the fact that some sequence is conserved.
    It doesn’t follow from the fact that some sequences are diverged.
    It doesn’t follow from the fact that the total sequence space is 20^L.
    It follows from NOTHING you’ve said.

    Now that I think of this the 10^150 is looking way too conservative. Lets add another 3500 orders of magnitude to solve this chicken and egg problem If you think my estimate of 3500 orders of magnitude to solve the chicken and egg problem is too high

    I don’t even know what these numbers refer to any more. 3500 orders of magnitude? Of what?

    Are you VOMITING these numbers up?

    let me know how you think blind and unguided processes would be able to simultaneously create PRPF8 and the spliceosome

    But the evidence we have shows that this didn’t actually happen in the way you are demanding.
    PRPF8 predates the spliceosome, as group II self-splicing introns encode a homologous protein. It’s like 3 posts ago that I cited a reference for this, and you even acknowledged that when I did. Jesus fucking Christ Bill. Have you gone “reset” again now for the 2nd time in less than 24 hours?

  14. I’ve only just briefly looked in at this thread, so I apologise if what I say below has already been mentioned.

    One other complicating factor that is worth considering is that proteins are dynamic structures which are themselves within dynamic structures. For instance alpha helices are like complex springs so it is not just that they need to be the correct length to make up the tertiary structure. They need to have the correct tension and stiffness in the right places in order to allow the whole complex to move or be held in the required way. And these inner forces need to be coordinated with whatever the individual helices and sheets are attached to, either within or external to the whole complex. I don’t see how any probability calculations or estimates can be made without taking this feature into account. This adds further complexity to the tertiary structure.

    For those of you who celebrate Christmas, I hope you have a merry Christmas, and for those of you who don’t celebrate Christmas, I hope you have a merry 25th of December.

  15. CharlieM: I don’t see how any probability calculations or estimates can be made without taking this feature into account. This adds further complexity to the tertiary structure.

    To calculate the probability of what? I mean, if your goal is to drive the probability or something down, why stop there? How about “it also needs to fold on wednesday”? Or “It needs to be rainy in Tucson”?

  16. dazz: Here’s a little exercise. Let’s say we have evidence that a certain event has occurred 10 times during the whole existence of the universe. What’s the probability that we would see at least the same 10 occurrences of the event if we assume that it’s underlying probability is such that we should only expect to see it once every 4.5 billion years?

    Wow, can you imagine how improbable a light sensitive spot, that gets mutated to focus light even better must be?

    How many times has that happened in 14 billion years?

    Talk about rare!

  17. Rumraket,

    Group II introns are evolutionarily related to nuclear spliceosomal introns of eukaryotes (1, 11, 49). According to one scenario, group II introns entered eukaryotes with bacterial endosymbionts that gave rise to mitochondria and chloroplasts and invaded the nucleus, where they or their descendants proliferated before degenerating into spliceosomal introns and the spliceosome. The nuclear membrane has been hypothesized to have evolved in response to this group II intron invasion as a means of separating transcription from translation, thereby preventing translation of unspliced introns (50). A further consequence of the nuclear membrane was sequestration of the genome into a separate compartment, where Mg2+ is chelated by chromosomal DNA (51), possibly leading to lower free Mg2+ concentrations than in the cytoplasm. Indeed, such differential Mg2+ concentrations between the nucleus and cytoplasm may explain recent findings that an Ll.LtrB-ΔORF intron cannot be spliced by the LtrA protein in the yeast nucleus but can be spliced by the LtrA protein after export of precursor RNAs to the cytoplasm (52). Spliceosomal introns have evolved to function at lower Mg2+ concentrations in eukaryotes, perhaps reflecting their disintegration into snRNAs, which may facilitate conformational changes, and their increased reliance on protein cofactors, which can substitute for Mg2+ to promote RNA folding. However, the lower Mg2+ concentrations now constitute a natural barrier to further group II intron proliferation in eukaryotic nuclear genomes. The ability to select group II introns that function at lower Mg2+ concentrations may ultimately enhance their utility in gene targeting in higher organisms, although selections done directly in eukaryotes using libraries with mutations throughout the intron may be required t o achieve maximal retrohoming efficiency.

    Lets re establish the facts of the case.
    -PRPF8 is the largest protein in the spliceosome. It consists of 2500AA’s and is one of about 200 proteins that make up this structure
    -In order to produce PRPF8 you currently need the spliceosome structure to splice out its introns. This creates a chicken and egg challenge.
    -Type 2 introns (simpler structure then the spliceosome) can do splicing yet there is no evidence they can do this in a eukaryotic cell’s nucleus with the necessary speed and accuracy given the chemical make up of this structure
    -The number of ways to arrange PRPF8 is 20^2500
    -The protein is conserved over a billion years which shows limited substitutability among its amino acids
    -The probability of a secondary is 10^190 assuming a substitutability of 31% for every 6 amino acids and those structures forming being independent.

  18. colewd: Lets re establish the facts of the case.
    -PRPF8 is the largest protein in the spliceosome. It consists of 2500AA’s and is one of about 200 proteins that make up this structure
    -In order to produce PRPF8 you currently need the spliceosome structure to splice out its introns. This creates a chicken and egg challenge.

    Sure, you’re asking how splicing could take place before the spliceosome if introns inserted in the Prp8 protein coding gene of group II introns? This is actually not a bad question at all, but there’s a solution.

    One of two possibilities that can happen, is that the splicing elements in the nucleus never drops to 0, which is not at all unusual, as countless other RNAs and transcription factors (in essence, the transcriptional state of the cell) is passed on, just divided in half, during cell division. This is actually one form of epigenetic inheritance. So under that scenario, at no point was there a cell that had no active splicing factors(if there was, it died). This has to be the case even today if you think about it.

    Suppose a cell divides, and loses all of it’s actively expressed splicing proteins. How it is it now going to functionally express any gene if it first has to express it’s splicing apperatus, but those very genes are themselves invaded by introns that need to be spliced out? Well it obviously can’t, so will die.

    So either the solution is that the concentration of splicing elements in the nucleus never drops to 0, or that at least some splicing elements can be functionally expressed with introns in them. I’d be putting my money on the concentration of splicing elements never dropping to 0. This fits well with how we already know transcriptional states can be partially inherited.

    -Type 2 introns (simpler structure then the spliceosome) can do splicing yet there is no evidence they can do this in a eukaryotic cell’s nucleus with the necessary speed and accuracy given the chemical make up of this structure

    Group II self-splicing introns are actually significantly faster than the spliceosome, in part because they don’t require the assembly of the large spliceosomal complex. The evolutoin of the spliceosomal complex is in part an adaptation to the fact that so many genes were invaded by introns, requiring more diverse and targeted mechanisms of splicing. Even so, remember that the spliceosomal complex is actually quite inaccurate, and that probably every protein coding gene is alternatively spliced at some very low level, most of which would be junk splicing transcripts.

    -The number of ways to arrange PRPF8 is 20^2500
    -The protein is conserved over a billion years which shows limited substitutability among its amino acids

    And?

    Let’s go over this again:
    You have yet to show even a single logically valid argument to the effect that there is a “combinatorial explosion problem”. You have claimed there is, but no fact that you have referenced have done any work towards establishing that conclusion.

    It doesn’t follow from the fact that some sequence is conserved.
    It doesn’t follow from the fact that some sequences are diverged.
    It doesn’t follow from the fact that the total sequence space is 20^L.
    It follows from NOTHING you’ve said.

    -The probability of a secondary is 10^190 assuming a substitutability of 31% for every 6 amino acids and those structures forming being independent.

    I have no idea what this even means.

  19. Rumraket,

    It doesn’t follow from the fact that some sequence is conserved.
    It doesn’t follow from the fact that some sequences are diverged.
    It doesn’t follow from the fact that the total sequence space is 20^L.
    It follows from NOTHING you’ve said

    This is the assertion you keep repeating and I disagree with you. If the substitutability is 50% which is a high number if you look at the level of preservation, you have 2500bits of functional information. Asserting that this is not a problem for evolution is not at all credible to me.

    How can science show that substitutability is high enough that this structure can evolve given the size of the sequence space and the level of preservation.

  20. colewd: This is the assertion you keep repeating and I disagree with you. If the substitutability is 50% which is a high number if you look at the level of preservation, you have 2500bits of functional information. Asserting that this is not a problem for evolution is not at all credible to me.

    What is credible to you is not an argument, that’s a statement about your personal psychology.

    You’re claiming there is a combinatorial problem, but none of the facts you cite entail that conclusion. It doesn’t logically follow.

    How can science show that substitutability is high enough that this structure can evolve given the size of the sequence space and the level of preservation.

    By first of all understanding that the size of sequence space is irrelevant (it is the local connectedness of the space that is relevant), and that conservation of sequence can simply be a consequence of strong purifying selection maintaining a sequence that was driven up some local hill from somewhere nearby in sequence space. Attempts to get you to explain how you rule out such a scenario have met with failure as you just hit a “reset” switch and started saying the same stuff all over again.

    You think there’s a combinatorial problem, for irrelevant reasons(the size of sequence space and how conserved the sequence is at the level of some particular clade), and you want science to prove you wrong to your level of satisfaction. But once we give you evidence (less conserved homologous sequences, the fact that they exhibit nesting hiearchical structure, actual examples of de novo protein evolution that function despite lacking well-defined tertiary structures), you say that evidence somehow also proves there’s a combinatorial problem. Which you ALSO fail to articulate how can be the case.

    You cite conservation as a reason to think there’s a combinatorial problem, and attempts to explain to you why that doesn’t follow were met with even more irrelevant statements. But then we show more divergent sequences, and then you say the LACK of conservation is ALSO evidence against the sequence being evolvable. That is an irrational double standard, based essentially on moving the goalposts or special pleading.

    Ultimately your position that there’s a “combinatorial problem” isn’t based on reason or evidence at all. The way you try to argue here makes it look like it’s the conclusion you want to be true, and you simply interpret (as in declare, but don’t derive by logical reasoning) the facts to fit the conclusion. You never really argue that it follows.

    Attempt to get you to really lay out the reasoning that show this conclusion must follow was met with you trying to shift the burden of proof. As in, rather than you explaining what it is that supports the conclusion you keep saying must be true, after enough iterations of digging through irrelevant nonsense, you simply ran away from the claim and wanted me to disprove it before you had shown it to be true.

    Bill how do you know that the present sequence didn’t evolve from some sequence further down the hill? The red dots could be eukaryotic PRPF8, and the orange dots on the other hill could be the Prp8-homologue from group II self-splicing introns. These could, at least in principle, have derived from some common ancestral sequence further downhill, midway between them in a scenario ala “B” in my figure here below.

    You think that B can’t be the case, because… [insert reason from which it follows or is implied it can’t be the case]. You seem to be saying we have good reason for concluding that we are in situation A. Merely pointing to how big the total space is (how big is that flat surface), or how tightly the sequences on either hill are packed, does not suffice to show what the interconnectedness, or global topology of the space is actually like. I don’t see how it could.

  21. Rumraket,

    Well put.
    It is sad to see colewd unwittingly loop back to positions that he has admitted are wrong, such as his “50% substitutability” which leads to the conculsion that there are 10,000,000,000,000 times more ATP binding 80-mers (10^93) than there are 80mers that can fold (10^80).
    Ineducable.

  22. dazz: To calculate the probability of what? I mean, if your goal is to drive the probability or something down, why stop there? How about “it also needs to fold on wednesday”? Or “It needs to be rainy in Tucson”?

    My goal is to think realistically about protein function. Do you not agree that for protein complexes to play their part in organisms then the properties of the material they are composed of is of absolute vital importance?

    As an example here are two questions you might consider:
    1. What have the days of the week or the weather got to do with the function of the bacterial flagellar hook?
    2.What have the material properties of the hook protein got to do with the function of the bacterial flagellar hook?

    I think that it is obvious the hook would fail as a universal joint if it were too floppy or too rigid. Do you disagree?

  23. CharlieM,

    Probabilities, Charlie, I was referring to those probability calculations that you were hinting in your previous post. I asked you a very straightforward question, what are you calculating the probability of and why are those functional constraints relevant to that probabilistic model? Billy loves to assume equiprobability of all sequences, so his calculation ends up modeling a stupid tornado-in-a-junkyard scenario that no one believes in. Can you do a little better? I mean the bar is pretty damn low

  24. Mung: It depends, doesn’t it. Oh, and are they independent events?

    You tell me. You are the one that thinks you can calculate the probability of protein evolution. You want me to tell you how to do it? Just have some regard to biological reality, is all I advise.

    That’s a non-sequitur. You frankly don’t know whether there are probabilistic barriers or not, because you have never done the calculations. You’re simply choosing to believe what you want to believe.

    Get knotted; you’re not having that! If someone tells me they have calculated the probability of me visiting Baltimore is 1 in 1^150, and I say that’s bollocks, I don’t have to calculate what the probability actually is.

    Your calculation is bollocks therefore probabilities are unimportant? Yeah, you need a reason to hold that position. Or just agree it’s irrational.

    So I accept any calculation that anyone makes? ‘Cos, y’know, probabilities are important? Here’s my rational reason: calculating the probability of a peptide of a modern length arising by random pick of each residue is bollocks. Because what mechanism makes proteins in that way? What about duplication and transposition, or selection and constraint? Why expect people to accept a calculation when it appears to have been made by a biological illiterate?

    Well, I think it is your notion that evolutionary theory is at heart probabilistic but that you can’t be bothered to do show the actual probabilities involved. For good reason I might add.

    That biological evolution is probabilistic does not mean that proteins are assembled by random pick from the set of 20 acids.

    Me: I’m just explaining why the simplistic independent approach is full of shit, is all.
    Mung: It’s better than what your side has come up with. Your position is that there are no independent events at all in evolution?

    No, not at all. But proteins aren’t assembled by random pick from a 20-letter alphabet.

    And you do realise that the entirety of evolutionary theory comes from ‘my side’? I’m slightly open-mouthed that you think a naive random pick of primary structure is somehow better than that.

    What if we don’t know whether two events are independent? We just throw up our hands in disgust?

    You don’t over-egg your conclusions and decide you have completely destroyed evolutionary theory by some dubious and oft-refuted numbers game, is what you (don’t) do. It’s obvious – and he even admits it – that Bill is making up the numbers. But somehow you’re casting your lot with him. Which is odd, because you actually think (if I understand you correctly) the space is navigable, and needs no tinkering.

  25. Allan Miller: Which is odd, because you actually think (if I understand you correctly) the space is navigable, and needs no tinkering.

    I don’t think Mung knows what he believes or doesn’t about evolution, let alone why

  26. Mung,

    Here’s a patterning repeat that reliably generates alpha helical turns:

    PNPPNNP.

    P is polar, N is non-polar. As an exercise for the student, calculate how often this motif will appear in a fully random set of picks from the canonical set of 20 amino acids. You’ll need to find out which are the Polar and Nonpolar acids, and which are ‘helix-killers’. It’s not quite the same as the frequency with which HTHHTTH appears in runs of coin tosses, but it’s not a million miles off …. if you got 1 in 20^7, you’ve made a mistake.

    I don’t think the probability of this sequence is a barrier to the evolution of alpha helixes.

    Whaddya reckon? Am I just believing what I want to believe?

  27. Allan Miller:
    Mung,

    Here’s a patterning repeat that reliably generates alpha helical turns:

    PNPPNNP.

    P is polar, N is non-polar. As an exercise for the student, calculate how often this motif will appear in a fully random set of picks from the canonical set of 20 amino acids. You’ll need to find out which are the Polar and Nonpolar acids, and which are ‘helix-killers’. It’s not quite the same as the frequency with which HTHHTTH appears in runs of coin tosses, but it’s not a million miles off …. if you got 1 in 20^7, you’ve made a mistake.

    I don’t think the probability of this sequence is a barrier to the evolution of alpha helixes.

    Whaddya reckon? Am I just believing what I want to believe?

    I get ~0.83% of the time

    So roughly one in one hundred and twenty 21 nucleotide-long stretches.

  28. Rumraket,

    You’re claiming there is a combinatorial problem, but none of the facts you cite entail that conclusion. It doesn’t logically follow.

    Got it. This is your conclusion. I don’t think you are taking the facts into account but that is my opinion. We essentially agree on the facts of the case and come to a different conclusion. The facts that cause me to conclude that the hypothesis of evolution causing the transition from prokaryotic cells to eukaryotic cells is false are the following.

    -The sequence space is very large of the new proteins we are observing (PRPF8) and there is strong evidence against a substitutability (preservation) that would allow random change to navigate through it looking just at the largest protein of one the cells new features. For this to be true the substitutability would have to be far greater then 50%. There is currently no evidence that the substitutability is this high or even close to this high.

    -There is a chicken and egg problem given the evidence tells us the structure the protein is a part of requires the structure to even process the secondary fold of PRPF8.

    -The existence of type 2 introns is a possible explanation for how the chicken and egg problem can be solved but at this point they are only speculation as far as their ability to operate inside the nucleus of a eukaryotic cell. The chemical make up of the nucleus may be problematic for their adequate functionality. I also believe solving this would do little to support your conclusion given the other facts.

    -The protein we are talking about is only one protein of many new proteins that we are observing in the eukaryotic cell.

    -There are few observable intermediates that show a path from the prokaryotic cell to the eukaryotic cell.

    These are the facts that lead me to conclude that the eukaryotic cell is a separate origin event.

  29. colewd: These are the facts that lead me to conclude that the eukaryotic cell is a separate origin event.

    Yes, the origin of the eukaryotes was a separate origin event that originated from prokaroyotes. 🙂

  30. colewd:
    So you guys have failed to defend your position and make the claim the mechanism is true because the structure is there.

    What? I never made such a claim. What are you talking about?

    colewd:
    The combinatorial explosion problem is telling you your theory is wrong.

    Nope. Nothing in evolutionary theory tells me that evolution works by putting together 2500 aa-long random sequences and then testing them for black-and-white functions. So, your “combinatorial explosion” only informs me that the 2500 aa-long protein didn’t evolve that way. But I already knew that.

    colewd:
    We cant even come up with a clean explanation of how blind and unguided processes created the secondary folds of one protein.

    I did that already a billion times here. It’s very simple: the physical-chemical properties of amino-acid combinations make them prone to take such structural forms as alpha-helices, beta-strands, loops, turns. Naturally, even before considering the effects of selection, a 2500 aa-long sequence will contain combinations that form all of those kinds of structures. This is so simple that it was predicted before any 3D protein structure was solved.

    colewd:
    All you guys have are the mathematical innovations of Jock and Entropy trying to redefine how we calculate a sequence.

    These are not mathematical innovations, this is knowledge about the physical-chemical properties of amino-acids. This is as simple as knowing that coins have two sides. A row of 2500 coins will be composed of a combination of heads and tails. What’s so hard about it? What so mathematically innovative?

    colewd:
    The RNA of this protein has introns that require the structure it is a small piece of (spliceosome) to remove so it can even start the secondary fold ouch :-).

    What the heck are you talking about? A protein produced from an unspliced RNA would still acquire secondary structures.

    colewd:
    Now that I think of this the 10^150 is looking way too conservative.

    it keeps looking ignorant to me, rather than conservative.

    colewd:
    Lets add another 3500 orders of magnitude to solve this chicken and egg problem

    What chicken and egg problem? There’s plenty of homologs to your 2500 aa-long protein that don’t have introns, and plenty that have self-splicing introns. I don’t see any problem even if most of them had spliceosome-dependent homologs.

    colewd:
    If you think my estimate of 3500 orders of magnitude to solve the chicken and egg problem is too high let me know how you think blind and unguided processes would be able to simultaneously create PRPF8 and the spliceosome creating the ability to splice out the introns we are observing and create the secondary fold.

    You’re very confused Bill. There’s no chicken-egg problem, as I explained above. The secondary structures we’ve been discussing are a natural outcome of the properties of the amino-acids in the protein. Introns are in the RNA, not in the proteins, and their splicing does not “create” protein secondary structures.

    colewd:
    Maybe Axe’s thinking is slightly ahead of you guys.

    Axe is a nauseating IDiot who should know better and be ashamed of himself.

  31. At this stage I think we’re just going around in circles. We have each stated our arguments and counter arguments and we are consigned to just repeat ourselves now it seems. I don’t have any need to continue this discussion. I think we have all said enough for anyone to be able to decide for themselves.

  32. Rumraket:
    At this stage I think we’re just going around in circles. We have each stated our arguments and counter arguments and we are consigned to just repeat ourselves now it seems. I don’t have any need to continue this discussion. I think we have all said enough for anyone to be able to decide for themselves.

    So you are posting to say you have nothing further to say?

    Jock is going to be pissed!

  33. Mung: Um. No. Wherever did you get that idea?

    From the fact that you state that Hoyle-style combinatorial probabilities are better than what ‘our side’ has come up with. Your comments on these matters seem invariably more critical of the ‘evolutionists’ and correspondingly supportive of their opponents. If you think the opposite, you keep that firmly under your hat.

  34. Alan Fox:
    Allan Miller,

    Easy to know what ID proponents are against. But what are they for?

    Anything an evolution skeptic may say, seems to cover it. Charlie’s vague woo; the combinatorial argument; both divine tinkering and the design of the space to obviate the need for divine tinkering; the Argument From Pointless Semantics; front loading; the ineffectiveness of evolutionary computation … all fit into that big tent, and nary a contrary peep is heard.

  35. Entropy,

    What? I never made such a claim. What are you talking about?

    That is true. You get a pass on this one 🙂

    only informs me that the 2500 aa-long protein didn’t evolve that way.

    The problem is with 2500 AAs and only limited substitutability time and resources won’t help you as the number of possible of ways to arrange it are too long.

    What the heck are you talking about? A protein produced from an unspliced RNA would still acquire secondary structures.

    Have you looked at the large repeat counts in introns?

    You’re very confused Bill. There’s no chicken-egg problem, as I explained above. The secondary structures we’ve been discussing are a natural outcome of the properties of the amino-acids in the protein. Introns are in the RNA, not in the proteins, and their splicing does not “create” protein secondary structures.

    Are you making the claim that the secondary structures are independent of sequence?

    Axe is a nauseating IDiot who should know better and be ashamed of himself.

    I have met Doug and exchange emails with him. He is a salt of the earth guy in my opinion. Do you know him?

  36. Rumraket,

    At this stage I think we’re just going around in circles. We have each stated our arguments and counter arguments and we are consigned to just repeat ourselves now it seems. I don’t have any need to continue this discussion. I think we have all said enough for anyone to be able to decide for themselves.

    A man of reason 🙂 Happy New Year Rum.

  37. colewd:
    The problem is with 2500 AAs and only limited substitutability time and resources won’t help you as the number of possible of ways to arrange it are too long.

    Didn’t you just tell me that some of their homologs had very little similarity? If so, then where’s that “limited substitutability”? Also, as others keep telling you, if the protein has changed less within the few eukarya whose sequences have been explored it means that the protein has been under somewhat strong negative selection. That doesn’t mean it was like that for its whole evolutionary history, as proven by those very-divergent homologs in bacteria and archaea (and perhaps other homologs in eukarya).

    colewd:
    Have you looked at the large repeat counts in introns?

    Do you think those would have any effect on a protein’s secondary structure? If so, how?

    colewd:
    Are you making the claim that the secondary structures are independent of sequence?

    Hell no. I’m pointing you to the well established fact that the amino-acid physical-chemical properties have nothing to do with whether there was introns or not in the RNA that was translated into such a protein. I’m telling you that the RNA and the protein are not the same thing.

  38. Entropy,

    .Didn’t you just tell me that some of their homologs had very little similarity? If so, then where’s that “limited substitutability”? Also, as others keep telling you, if the protein has changed less within the few eukarya whose sequences have been explored it means that the protein has been under somewhat strong negative selection. That doesn’t mean it was like that for its whole evolutionary history, as proven by those very-divergent homologs in bacteria and archaea (and perhaps other homologs in eukarya).

    I understand this argument. How does this get your substitutability to under 50%?

    Can repeated AA’s fold into an alpha chain or beta sheet?

    Hell no.

    Thats end the year on this. Happy New Year E 🙂

  39. colewd:
    I understand this argument.How does this get your substitutability to under 50%?

    By the fact that many of those homologs share much less than 50% identity with the eukaryotic proteins.

    colewd:
    Can repeated AA’s fold into an alpha chain or beta sheet?

    Yes, they can (hell, yes!).

    I don’t see what this has to do with the RNA and the protein being different things though.

    colewd:
    Thats end the year on this. Happy New Year E

    Happy new year to you too Bill.

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