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A reply to Professor Moran

Professor Moran has graciously replied to my recent post, “Will this do, Professor Moran?” (18 December 2011) in which I attempted to flesh out the argument that irreducible complexity requires an Intelligent Designer. I would like to thank him for taking the trouble to write a detailed rebuttal of my argument.

Since Professor Moran is a respected biochemist, I won’t be contesting his claim that the citric acid cycle evolved in a Darwinian fashion. What I’ll attempt to show is that it fails as a counter-example to my argument.

“Unlikely” is not the same thing as “impossible”

Before I address Professor Moran’s scientific arguments, I’d like to draw his attention to one brief but important passage in my post:

Note: The argument here is not absolutely ironclad; it is a probabilistic one…

I also wrote that “intelligent design is the best explanation for the generation of irreducibly complex systems.” However, I didn’t claim that it was the only possible explanation.

So I was astonished when I read the following passage in Professor Moran’s post:

It’s quite easy to think of examples that correspond to the steps that Torley says are impossible.

“Impossible” is not a word I used in my argument. (I did use the term “cannot,” but only in relation to states of affairs that were impossible by definition – e.g. a system with a large number of parts cannot have only a very small number of parts.) The phrase I used, over and over again in my argument, was “very unlikely.” Professor Moran is putting words into my mouth.

I’d also like to mention that I accept common descent. What I do not accept is the adequacy of any unguided mechanism (e.g. NDE) in accounting for the origin and development of life. I’m quite sure that Darwinian mechanisms played a role; I just don’t think they’re the stars of the show.

Which version of irreducible complexity am I talking about?

Towards the end of his post, Professor Moran expresses understandable frustration at the fact that Intelligent Design proponents don’t have a single, common definition of “irreducible complexity.”

Now Professor Moran is a biochemist, so I’ll answer him with a question: what’s an acid? He knows perfectly well that there’s more than one definition of that chemical term, just as there’s more than one definition of the biological term “species.” Multiple definitions for a scientific term are fine, so long as everyone is clear about which definition is being used. At the outset of my article on irreducible complexity, I used a definition which I quoted from a 2004 paper by Professor William Dembski.

Professor Michael Behe now uses a different definition from the one he originally formulated in Darwin’s Black Box: The Biochemical Challenge to Evolution (The Free Press: New York) in 1996, where he wrote:

By irreducibly complex I mean a single system which is composed of several well-matched, interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning. (Behe 1996, 39)

This is pretty close to Dembski’s definition:

A functional system is irreducibly complex if it contains a multipart subsystem (i.e., a set of two or more interrelated parts) that cannot be simplified without destroying the system’s basic function.

In a 2000 paper entitled, In Defense of the Irreducibility of the Blood Clotting Cascade:
Response to Russell Doolittle, Ken Miller and Keith Robison
, Behe proposed replacing his old definition of irreducible complexity with an evolutionary definition:

An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway.

While Professor Behe’s new definition is more mathematically rigorous than his old one, it is less intuitive. From a layperson’s perspective, it’s nice having a definition which you can picture easily. Behe’s original definition came with a handy visual illustration: the mousetrap. This is something which you can see won’t work if one of its parts goes missing – that is, unless someone cleverly tinkers with the remaining parts. (Yes, one can imagine a freak occurrence which might render the remaining parts functional, but once again, that would be “very unlikely.”) Another reason why I chose not to use Behe’s new definition is that it’s an historical definition. Unfortunately, many biochemical systems don’t wear their history on their sleeves, so to speak – but they do display their functionality in a way that everyone can see.

Professor Moran’s “foot in the door”

Now let’s go back to Behe’s 1996 definition. Notice that he spoke of “several well-matched, interacting parts that contribute to the basic function” (italics mine). Professor Dembski didn’t use these exact words in his 2004 definition; he used the somewhat more ambiguous term “inter-related.” This definitional ambiguity was Professor Moran’s “foot in the door.”

In his post, Professor Moran argued that the citric acid cycle would satisfy this definition of irreducible complexity: it has multiple parts (enzymes); these parts are inter-related, insofar as they constitute a chemical cycle; and finally, if you remove any of the parts, you break the cycle, so the system’s basic function is detroyed. And yet the citric acid cycle clearly evolved from two other pathways that originally had different functions. Game, set and match?

Not quite. If you look at my post and Professor Dembski’s article, Irreducible Complexity Revisited (version 2.0; revised 2/23/2004), you’ll see that we both used the term “configuration” to describe the arrangement of the parts. Take these two rhetorical questions which Dembski poses, when describing the “daunting probabilistic hurdles” that a Darwinian mechanism for assembling an irreducibly complex system must face:

(5) Interface Compatibility. Are the parts that are being recruited for inclusion in an evolving system mutually compatible in the sense of meshing or interfacing tightly so that, once suitably positioned, the parts work together to form a functioning system? …

(7) Configuration. Even with all the right parts slated to be assembled in the right order, will they be arranged in the right way to form a functioning system? (2004, pp. 30-31)

What Professor Dembski had in mind was not a set of separate components, each of which perform a task in some fixed temporal sequence, but rather, a structure composed of spatially contiguous, inter-locking components – such as the parts of a bacterial flagellum. This becomes apparent when he describes the difficulties attending hurdle number (5) – interface compatibility – when building a bacterial flagellum by a gradual Darwinian process:

For the Darwinian mechanism to evolve a system, it must redeploy parts previously targeted for other systems. But that’s not all. It also needs to ensure that those redeployed parts mesh or interface properly. (2004, p. 35)

Dembski goes on to highlight the difficulty: “The products of Darwinian evolution are, after all, … systems formed by sticking together items previously assigned to different uses” (2004, p. 35, italics mine).

Likewise, in step (iv)(a) of my own argument – the step which Professor Moran attacks – I explicitly used the term “configuration”:

However, it’s very unlikely that a system with function G, which gains one new part, while keeping the existing parts in nearly the same configuration as they were before, should suddenly be able to perform a totally new function F, especially if the number of parts in the system is large. (Emphasis mine – VJT.)

So, is the citric acid cycle irreducibly complex? If not, what is?

It should be clear by now that the citric acid cycle isn’t the sort of thing that Professor Dembski or I would want to describe as “irreducibly complex.” The enzymes in the cycle make up a pathway – i.e. an ordered sequence of reactions. The enzymes in the cycle aren’t all stuck together in some giant superstructure, so there is no multi-part configuration.

For my part, I’m prepared to go further and say that the blood clotting cascade isn’t the sort of thing I’d want to call “irreducibly complex” according to my definition. That doesn’t mean I necessarily think it evolved through a Darwinian process; it just means that according to the definition of “irreducibly complex” which I’m using, the question of whether it originated in that way is impossible for me to answer. Is that a problem? No. Remember: the aim of my argument was simply to develop a case for intelligent design, using a definition of “irreducible complexity” which applies to at least some of the systems which ID proponents would identify as irreducibly complex. I’m happy to focus on the bacterial flagellum, for argument’s sake.

The bacterial flagellum: draw me some pictures, please!

And that was what step (iv)(a) of my argument was about. Co-option is the standard neo-Darwinian explanation for the evolution of the bacterial flagellum, but when you’re dealing with something that has 30 parts, and the nearest functional sub-unit is a piece that has 10 parts, then I’d say you still have a lot of explaining to do. (That’s why the TTSS story doesn’t impress me: it’s a very long way from 10 to 30.)

You could suppose the existence of some “magic pathway,” where the successive addition of each new part somehow generates a new biological function, but then you’ve got to confront the configuration question: when I add a new part, do I substantially retain the old configuration of parts, or do I reshuffle the parts I already have? The idea that 30 succcessive biological functions could appear by the successive addition of parts to an existing configuration without any re-shuffling beggars belief, and the idea that dramatic reshuffling of the configuration could generate this successive appearance of functions as the structure gets bigger and bigger also appears ludicrous: it’s too much of a miracle.

Yes, you could imagine two or more smaller functional structures evolving in parallel and then coming together to make a bigger 30-part system. But the more sub-units you invoke, the harder it is to envisage them all coming together and producing something with a new function of its own. It’s much more likely that the sub-units wouldn’t mesh properly.

So I’d like to ask Professor Moran: how do you envisage the bacterial flagellum evolving? I’m not asking for lots of details here – just a conceptual scenario will be fine. They say a picture is worth a thousand words. Personally, I’d be happy with two or three simple pictures, because I really can’t picture any good way of building an irreducibly complex structure with 30 parts, without making a lot of “iffy” assumptions.

Darwinists can’t keep up with the science

One way in which a layperson like myself can tell when someone’s losing a scientific argument is when the number of new facts they can’t explain keeps growing faster than their ability to generate hypotheses to explain old facts. Looking at what has been happening in the field of research relating to the bacterial flagellum, this is precisely what seems to be happening. Professor Michael Behe’s 2007 book, The Edge of Evolution, has a whole Appendix devoted to what scientists now know about how the flagellum is built, and the system of controls that regulate its construction. Behe writes:

Complex, functional structures such as the cilium and flagellum are just the beginning. They demand intricate machinery and control programs to build them. Without those support systems. the final structure wouldn’t be possible. The bacterial flagellum contains several dozen protein parts. The cilium, which has so far resisted investigation of its DNA control program, has several hundred. There is every reason to think that the control of its construction will have to be much more intricate than that of the flagellum. (2007, p. 100)

In a diagram on page 99, Behe adds:

Genes for the construction of the bacterial flagellum are activated in a precisely timed fashion. Those needed for the construction of the bottom of the molecular machine are switched on first, followed in order by those needed for more distant parts.

Wait a minute. There’s a timing sequence? That really creates problems for evolutionary scenarios where you have lots of little sub-units coming together to make a flagellum, doesn’t it? How did the timing for the activation of the genes get re-regulated, so that the whole thing would develop in the right sequence, from bottom to top? I’m not saying it’s impossible. All I’m saying is: if I were a Darwinian, I’d be pouring myself a brandy. Your headache isn’t getting better; it’s getting worse.

Back to the citric acid cycle

I declared at the beginning of this post that I wouldn’t be contesting Professor Moran’s claim that the citric acid cycle evolved in a Darwinian fashion. But that doesn’t mean that I think the components of the system evolved in a stepwise fashion. I’m talking about enzymes here. I couldn’t help noticing that one of these enzymes is called citrate synthase. Here’s what Wikipedia says about it:

Citrate synthase’s 437 amino acid residues are organized into two main subunits, each consisting of 20 alpha-helices. These alpha helices compose approximately 75% of citrate synthase’s tertiary structure, while the remaining residues mainly compose irregular extensions of the structure, save a single beta-sheet of 13 residues. Between these two subunits, a single cleft exists containing the active site.

437 amino acids? We’re really talking about configuration problems here, if we try to imagine a step-wise scenario for its origin. I’ll let readers have a look at the beast, and judge for themselves:

Those who are familiar with the work of Dr. Douglas Axe will recognize the problem I’m talking about. Only a tiny fraction of amino acid sequences are in any way functional. The odds against proteins such as citrate synthase forming in this way are astronomical.

I’m sure that Professor Moran will insist that there are other more likely explanations for the origins of proteins. What about RNA, for instance? OK, fine. I have just one question. Can you point out an alternative scenario, and show me some calculations (back-of-the-envelope will do) indicating that your scenario is more likely to generate a functional protein than the nightmare scenario of building up an amino acid chain step by step? If you can’t quantify, then you’re not doing science. Well, what are you doing? Theorizing. Mmm. That sounds like religion to me. Don’t you think?

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82 Responses to A reply to Professor Moran

  1. Goodness gracious, VJ, there’s no need to abandon the blood-clotting cascade as not being IC. The reason that Behe doesn’t accept metabolic pathways as IC has nothing to do with a temporal arrangement of reactions. It has to do with the fact that the proteins do not interact with each other. Instead, each protein (or enzyme) interacts with a substrate. Such a system could evolve one protein at a time, with the last substrate being the first one that was used by the organism, with additional substrates being available that can be turned into the last one, once the necessary protein is available, also. Try reading Behe’s chapter on it.

  2. And forget about Dembski.

  3. Yes, if you use what needs to be explained in the first place to do the explaining then the claim of IC could appear to disappear.

    Also if you don’t understand the concept it is easier to erect and refute a strawman.

    And why don’t “they” seem to understand that by demonstrating that a 3-part configuration can arise via stochastic processes that does NOT mean a 40-part configuration can arise via stochastic processes. It’s the other way around- once it is demonstrated that a 40-part configuration can arise via stochastic processes that takes care of everything of equal or fewer number of parts in the configuration.

  4. Vincent,
    If Irreducible complexity is not about impossibilities, only improbabilities, it loses its any substance, and becomes just another argument from ignorance.

  5. Behe’s original concept, obvious from the term he gave it, was intended as a way to rule out the evolutionary development of an irreducibly complex system.

  6. Improbable simply means you don’t understand the mechanism.

    There has never been a time in the history of science when supernatural intervention was the useful hypothesis.

    But it has been popular. Even Newton indulged.

  7. Wow. Just, wow. So, blood-clotting isn’t IC, even though Behe says it is, and the TCA cycle isn’t IC, even though Behe has claimed certain metabolic pathways as IC on other occasions.

    And, to top it off, vjtorley is asking questions about the flagellum that were asked and answered years ago, as if no answers exist.

    C’mon, ID folks, I’m not going to do your work for you this time. If you guys are serious about doing science, you will correct vjtorley’s abyssmally poor research in this thread.

    Please tell him:

    How many flagellum proteins are actually universally required?

    How many of those flagellum proteins have homologs to other proteins within the flagellum?

    How many of those flagellum proteins have homologs to nonflagellar systems?

    Of those proteins with nonflagellar homologs, how many of them are (a) functionally isolated from other flagellar proteins, i.e. they would have to be coopted into the flagellum one-at-a-time, versus (b) functionally connected to other flagellar homologs, i.e. they could be coopted as a preexisting complex of several nonflagellar proteins which already interact with each other before becoming part of the flagellum?

    This is flagellum 101 stuff guys, I’ve put it all free online. If you don’t clean up your own house and do the relevant literature research before opening your big mouth about some topic you know virtually nothing about, you have zero chance of ever getting to the status of serious science.

  8. “Improbable simply means you don’t understand the mechanism.”

    And so you would then agree that the highly improbable odds underlying the probabilistic nature of evolution means that…

    “There has never been a time in the history of science when supernatural intervention was the useful hypothesis.”

    Sure it has, there have been various studies done on the efficacy of prayer and other such notions. What has never been useful are hypotheses that are untestable or unfalsifiable. Both crosses are borne by the angry siblings, ID and Evolution.

  9. 437 amino acids? We’re really talking about configuration problems here, if we try to imagine a step-wise scenario for its origin.

    You may be getting ahead of yourself considering you’ve just stated:

    I couldn’t help noticing that one of these enzymes is called citrate synthase. Here’s what Wikipedia says about it

    We’re talking about a protein that’s new to you and your knowledge begins and ends with Wikipedia. Should you really be speculating about its origins and evolution?

    You seem impressed by its length at 437 amino acids. Sometimes its not the size but how you use it: how many of these residues are essential to the enzyme’s function and how many could be substituted to a different amino acid without disabling its function?

  10. Also, how can anyone dare to raise a question about how citrate synthase without even bothering to do a BLAST search or literature search to see if there are any related proteins with different functions?

    To even have something worth reading in a journal, any evolutionary biologist would, at a minimum, have to download all related sequences, align them, and run several different phylogeny packages on them, and then compare the phylogenetic trees that each package found to see where citrate synthase fits in the phylogeny under different statistical methods (usually they don’t differ much). Often this gives you HUGE hints about the origins of a system. If one hasn’t done this, one really shouldn’t talk about how the origin of the system is implausible, undocumented, etc.

  11. Nick,

    Can accumulations of random mutations even account for ONE of the required flagellum proteins? I would love to see that.

    But anyway homology is one thing. Taking 30-40 different proteins of differing quantities and configuring in such a way as to be useful is something entirely different.

    Could be coopted? Via the mechanism of “it just happened”? How do we test any of your claims that A) random mutations can create the required proteins and B) once created the right amounts and propoer configuration would just emerge?

    Or do you still just not give a damn about science?

  12. Nick,

    You still have to explain those other alledgedly related proteins with different functions.

    But then again, as I said you HAVE to start with that which requires an explanation in the first place.

    And that is why we don’t take you seriously…

  13. Pathetic- If you don’t like the design inference just start producing evidence that stochastic processes can design irreducibly complex configurations.

    Otherwise you are just whining from ignorance…

  14. But anyway homology is one thing.

    But you guys can’t even get the basics of the homology facts about the flagellum correct — vjtorley doesn’t in his post, and none of you have corrected them, even though they are well-known to people who have bothered to look into it. There’s no point in discussing anything else until you guys get that right and identify the errors in vjtorley’s statements about the number of required flagellum parts and their homologies.

    Your let’s-distract-from-vjtorley’s-utter-ignorance-about-flagellum-homologies argument is also wrong, e.g. it assumes that the evolution of a binding site is hard, when actually it is pretty easy.

    Re: someone else’s comment — you don’t get to say “hey, evolutionists, the flagellum is a great argument against evolution!” and then when people point out all the ways your argument falls apart, switch to “oh well, actually I meant the flagellum doesn’t matter at all, what I really meant is that you haven’t explained anything unless you explain the origin of life itself while you’re at it.” It’s called moving the goalposts and it’s a pointless, insipid tactic and a tacit acknowledgement of defeat on the original argument.

  15. Joe,

    Very simple yet totally valid point.

    It’s not so much ‘the parts’ that make up the bacterial flagellum and whether or not they are homologous to other ‘parts’ within similar systems that is the question here, but how these systems assembled themselves to carry out their ‘specified functions’ in the first place.

    Saying something isn’t IC because it shares ‘parts’ with other systems doesn’t answer this.

  16. Anyway, I think it is useful to make a distinction between a PROCESS ans a SYSTEM. The flagelum is an IC functional system.
    Citric acyd cycle, like blood-clotting cascade, are processes. I think there are more that enough reasons to assert than neither a IC system nor a process of the like of the blood-cloting cascade can emerge just by chance. But I am not sure that the theoretical approach to show it should be the same. That is why, probably, Dr Behe adapted his definition of IC to the case of the B-C cascade

  17. Nick,

    Most of the time homolgy, ie common descent, is ASSUMED due to sequence similarity. However sequence similarity can be due to convergence and/ or a common design.

    Also you still think ID is anti-evolution, meaning that you don’t know a damn thing about ID.

    So there isn’t any point discussing anything with you seeing that A) You do NOT understand ID and B) You cannot suport your claim that the bacterial flagellum arose via an accumulation of random mutations.

    I bet you can’t even produce a testable hypothesis for that.

    Pathetic…

  18. NickMatzke:

    Re: someone else’s comment — you don’t get to say “hey, evolutionists, the flagellum is a great argument against evolution!” and then when people point out all the ways your argument falls apart…

    Yet no one has ever shown how the flagellum argument falls apart. All YOU have ever done is point out there are some similarities between flagella proteins and other proteins.

    You 1) have NEVER provded a testable hypothesis for the premise that flagella can arise via an accumulation of random mutations nor 2) any testable way that the proteins can be configured correctly via stochastic processes.

    IOW Nick all you are is a legend in your own mind.

    But anyway Nick that you avoided the meat of my post pretty much demonstrates that you have nothing.

  19. I agree that we should distinguish between systems and processes. I also think that it is absolutely essential to talk about formal function following Abel. “Chemistry” can be spontaneous as Prigogine et al argue. That is fine by me. However, function cannot because function means purpose and purpose means choice contingency. That is why evolutionists resist to the last in front of evidence of semiosis in nature.

  20. Petrushka,

    “There has never been a time in the history of science when supernatural intervention was the useful hypothesis.”

    This controversy is deeply rooted in history of scientific thought. I did not expect you not to know this. A thesis and an anti-thesis as usual. Don’t underestimate the theistic impulse in science as it gives metaphysical motivation to science, without which science will be castrated. Partly, we are seeing this happening today.

  21. Correction to the OP-

    The T3SS contains about 30 proteins, 10 of which are similar to (could be homologous) flagella proteins.

    And THAT is what the evolution from one to the other problematic- you have quite a bit of subtracting and adding that needs to be done.

  22. Nick,

    Evolution and evolvability are fine by ID conceptually. What is argued is:

    (i) how to get to functionality in the first place;
    (ii) what formal functionality and meaning are and how they came about in living systems;
    (iii) the extent to which biosystems are evolvable.

    It is true that living systems are complex, possibly even redundantly complex which allows for evolution as such to occur (which in fact is nothing more than rearrangement of the already existing function). ‘The mechanics’ of modern bioresearch or the validity thereof are not disputed. It is only the interpretations of the results that are.

    Irrespective of all misunderstandings on both sides, serious grounds for ID argumentation do exist.

  23. Yes, that’s true. But rule out “practically” or “operationally” i.e. based on empirical evidence. Events of prohibitively small odds do not occur in practice no matter how you allow them to happen, sequentially or all at once. I think 14 billion years is too short a period for anything like we see in biosystems (formal function and semiosis) to pop up by fluke or necessity without intelligent heuristic guidance. That is the Achilles’ heel of materialism.

  24. Something that must be kept in mind is that, if proponents of the creative power of the Darwinian mechanism are correct, every aspect of every biological system in every living thing that has ever existed — from functional proteins, to the flagellum, to the human mind — must be approachable in a step-by-tiny-step fashion through the accumulation of random errors. This should strike reasonable people as belief in something that can only be described as a miracle.

  25. No miracles required when you have vast eons of time.

    The equation is:

    Mother Nature + Father Time + things happening = all we observe

    A scientist explains it here

  26. Hi Nick,

    Thanks for your posts. A couple of quick points:

    1. I’m quite aware that homologs exist for many of the proteins in the flagellum, and that some proteins in the flagellum are homologous to others within the flagellum. That doesn’t prove much, except common descent. But I’m not interested in counting homologs. What really interests me is: assuming some sort of duplication process gave rise to these variants, what functions did they originally have when they were added to the precursor of the flagellum? How many intermediate-stage functions were there along the evolutionary pathway leading from a very small system to the modern flagellum, with its function of producing cell movement? (Let’s take the smallest modern one – that’ll do.) Additionally, roughly how many separate sub-units came together, and how many times, before we arrived at the modern minimal bacterial flagellum? Also, how many instances of co-option occurred along the way? As I said above, I don’t think co-option is impossible; I just think that the configurational problems of adding a new component that configures with the rest of the system become increasingly difficult as the number of components gets larger and larger. Maybe I’m wrong about this. I’m not a chemist.

    2. Looking at your 2006 article at http://www.pandasthumb.org/arc.....evolu.html , I see I should have said that 23 proteins are absolutely indispensable to the flagellum rather than 30. Mea culpa.

    3. You wrote: “Of those proteins with nonflagellar homologs, how many of them are (a) functionally isolated from other flagellar proteins, i.e. they would have to be coopted into the flagellum one-at-a-time, versus (b) functionally connected to other flagellar homologs, i.e. they could be coopted as a preexisting complex of several nonflagellar proteins which already interact with each other before becoming part of the flagellum?”

    Well, I had a look for that one online, and here’s what I got back from Google:

    No results found for Nick Matzke “functionally isolated from other flagellar proteins”.

    No results found for Nick Matzke “functionally connected to other flagellar homologs”.

    OK. If you’ve got the answers to these questions, would you care to enlighten us?

    4. Finally, you might want to address the arguments put forward in Jonathan M’s online article, Michael Behe Hasn’t Been Refuted on the Flagellum . Jonathan M makes a far better case than I do, and he does it much more eloquently, as he has a scientific research background.

    Cheers, Nick. Over to you.

  27. Paulmc and Nick,

    The point of my raising the number 437 is that it’s big. Douglas Axe claims to have shown that the assembly of even a functional 200-aa protein is such an astronomically improbable event that one could not expect it to occur anywhere in the observable cosmos, at any stage in its long 13.7 billion year history. 437 is a lot bigger than 200. That was my point. If you think Axe’s work is badly flawed, please explain why.

    There may well be related proteins with different functions. Indeed, I’m sure there are. But if the stepping stones that would take us from one protein to another are too far apart, then obviously stepwise evolution won’t work. In which case you’ll need to come up with another scenario, and demonstrate that it will at least work better than the old one.

    Look, there’s one thing I do know about science: no numbers, no science. Quantification is fundamental. I’m not asking you to show me how we got from simple organic compounds to a cell. Just show me how we got from amino acids to proteins. Or at least, show me some numeric calculations suggesting that protein synthesis not at all improbable, given a billion years (I’m feeling generous today). I’ll set the bar very low: anything above 10^-120 will do me fine. If you can’t do that for one of the simplest steps in the evolution of life, then Heaven help us all: we haven’t even scratched the surface yet, if that’s how little scientists know.

  28. Hi lastyearon,

    Thank you for your post. In a nutshell; if the improbability of an irreducibly complex structure arising can be quantified, and shown to fall below a certain threshold, such that the event in question would not be expected to happen even once in the history of the observable universe, then it is reasonable to infer that an intelligent cause produced such a highly specified system.

    Of course, my post was about irreducibly complex systems in general. To infer an intelligent designer, you need to look at a particular system and calculate the probabilities, so ascertain whether it falls below Professor Dembski’s universal probability bound.

  29. Hi Bilbo I,

    Thank you for your post. I no longer possess a copy of Darwin’s Black Box, although I had one some years ago. Not having one on hand, I wasn’t sure precisely how Professor Behe distinguished the blood-clotting cascade from metabolic pathways, so I thought it safer to put the B-C cascade to one side. It was not my intention to abandon the cascade as not being irreducibly complex; I simply chose to focus on a subset of irreducibly complex systems.

    Felipe,

    I think your distinction between a process and a system is an excellent one. Thanks.

  30. Did everyone from UD take early Holidays? Just curious, there hasn’t been to many articles posted…

  31. The point of my raising the number 437 is that it’s big. Douglas Axe claims to have shown that the assembly of even a functional 200-aa protein is such an astronomically improbable event that one could not expect it to occur anywhere in the observable cosmos

    That claim would be more convincing if you had some theory of what makes a sequence functional. Or a theory of why a particular length is necessary, or a theory predicting the effects of code changes.

    From what I’ve seen, the fabled “dFSCI” is not a metric that can tell you how close you are to functionality. It’s a step function. One point mutation and your 437 AAs are all rubbish.

    436 correct elements and you have no way of knowing that you are close. So how does the designer figure this out? Don’t you at least have to demonstrate proof of concept?

  32. One point mutation and your 437 AAs are all rubbish.

    436 correct elements and you have no way of knowing that you are close.

    Aren’t you arguing for the wrong side? That sounds almost like an argument for irreducible complexity.

    From what I’ve seen, the fabled “dFSCI” is not a metric that can tell you how close you are to functionality.

    Who has ever proposed using it as a metric for that?

  33. Why is it an argument for irreducible complexity? It’s an argument that evolution can navigate a connected functional space simply by trying all the one step variations from a given functional point.

    If you can demonstrate a shortcut that does not involve cut and try, feel free. Show me that design is possible without cut and try. Show me a theory of design.

    dFSCI is proposed as a metric, which in ordinary usage means it has incremental values along a continuum. But gpuccio’s measurement cannot be made on non-functional sequences. So the metric produces only true or false, not a point on a continuum.

  34. So how does the designer figure this out?

    Intelligent designers have more methods at their disposal than attempting random combinations of elements and hoping for function. That’s an especially useless plan if you’re looking for a specific function.

    An intelligent designer imagines screws that are inserted with screwdrivers. He does not arrange random configurations of metal and suddenly say, “Look! This four-pronged configuration is useful for both impaling food and twirling noodles. I wasn’t looking for that, but having stumbled upon it, how convenient. I can’t wait until another random configuration of elements and processes produces noodles.” And then, millions of attempts later, after attempting all sorts of random additional ingredients such as mustard, sand, and horse excrement and finding them less than desirable, the designer stumbles upon a paste made from boiled tomatoes which incrementally improves on the unadorned noodles. At last!

    Can you see how useless such an approach would be for designing something as simple as screws and screwdrivers, which have no purpose whatsoever except as part of a separately envisioned design?

    You assert, against all evidence and common sense, that designers must act by random variation and selection, and then place the burden on others to explain how that might work.

    Intelligence is not so limited. I think this has been said over and over – that’s what makes it “intelligent.”

  35. An intelligent designer imagines screws that are inserted with screwdrivers. He does not arrange random configurations of metal and suddenly say, “Look! This four-pronged configuration is useful for both impaling food and twirling noodles.

    Fine. Prove it. Demonstrate that what you claim is possible with coding sequences. But even the gurus of the ID movement say there is no shortcut.

    Yes, I do put the burden of demonstrating that design is possible on those that claim it is. You are making a claim that has no basis in theory or in practice.

    You claim the existence of an unobserved entity that just happens to have the magic abilities you want and need it to have.

    When Darwin wrote Origin, he spent the first third of the book demonstrating the power of variation and selection. He did not fantasize about this. He demonstrated it.

  36. Petrushka,

    That argument has gotten quite stale. Every day we use technology designed using technology designed using technology that wasn’t even imaginable 100 years ago.

    If you’re prepared to seriously argue that A) something is impossible, and B) the only counterargument is to show how exactly how to do it, then please alert the rest of the world, as they are busy trying to figure out how to do things that they don’t know how to do at present, and the poor lost souls have no idea that by definition, that makes it impossible.

    Is any complex physical process more consistent than the folding of proteins? To argue that something consistent is also unpredictable is irrational.

    And, as usual, you assert a rule of logic that only applies when you want it to. I don’t see you stating that the evolution of complex systems is impossible because no one has demonstrated exactly how it might happen. How are we to take this rule that you’ve invented seriously when you implicitly contradict it?

  37. You claim the argument is stale because you have no counterargument, and you wish it would go away.

    The evolution side of the argument has invested the last 150 years and the work of thousands of researchers digging int other details of how evolution works, how fast it occurs, and whether there are intermediate sequences linking new functions to old sequences.

    Is any complex physical process more consistent than the folding of proteins?

    What do you mean by consistent? The same sequence may produce the same fold reliably, but that tells you next to nothing about what would happen if you made one change to the sequence.

    There are ways of calculating folds, but they run into the problem of big numbers. Chemistry is simply many orders of magnitude faster. Which is why the designer uses evolution.

  38. P:

    Kindly look around you, and go talk to a designer.

    When you look around, start with this thread. Were the long strings here created by trial and error? Obviously not.

    Similarly, the strings in a computer objective code are not the result of trial and error.

    Now, go look at how proteins are made in the living cell, observing the algorithmic, stepwise, phase by phase process. Ask yourself on the empirically warranted source of algorithms and the machines that physically implement them.

    Then ask yourself again — this has been repeatedly pointed out, just you seem to want to drum out your talking points over and over, utterly unresponsive to cogent reply — why should it even enter your mind to think that a known impotent process is to be preferred to the known effective one.

    Intelligent design routinely produces systems like we are seeing. The combinatorial explosion overwhelms any blind process as a credible source.

    GEM of TKI

  39. why should it even enter your mind to think that a known impotent process is to be preferred to the known effective one.

    That’s actually the question I’m asking.

    Evolution is used by the pharmaceutical industry to develop biologically active molecules because it’s the fastest and cheapest known method. No one has been able to design useful coding strings from scratch, so the alternative to evolution is nonexistent.

    Yes, it’s directed evolution, but all industrial methods are refined versions of natural processes. It’s important to note that protein design starts with variations of known sequences. Even in that basic regard it is just incremental change.

    Directed evolution may be the fastest way to achieve a specific target, but populations don’t have specific targets. They have varying individuals, some of which leave more offspring than others.

  40. Hi Nick,

    Good to see ya’. You stated: “…Behe has claimed certain metabolic pathways as IC on other occasions.

    Where exactly has Behe made such a claim?

  41. KRock: “Did everyone from UD take early Holidays? Just curious, there hasn’t been to many articles posted…

    Perhaps they should take holidays more often. BTW, KRock, are you also known as Rock?

  42. You do understand that I am out on a limb on this.

    Several people have argued that technology will prove me wrong.

    I’m aware of this possibility.

    I have two responses. The first is that there are things which appear to be unpredictable for good reasons that will not succumb to technological advance. Because calculations are dependent on unmeasurably small differences in initial conditions. I think organic chemistry and the attributes of complex molecules fall in this category.

    There is also the fact that protein folding is simply a very difficult calculation. It gets geometrically more difficult with increments in complexity.

    The second response is that it is always up to those who claim the sufficiency of a process to demonstrate the sufficiency. ID lacks both evidence for a designer and the theory of design that might be employed by a designer.

    Evolution obviously has gaps, but studying them is the work of evolutionary biologists. That’s what they do: extend the knowledge of how things work.

  43. Bilbo I:

    “Perhaps they should take holidays more often”.

    I actually enjoy most of what is posted at UD, it’s a breath of fresh air unlike the Darwin’istic ideology that plagues our society. You can’t even use a “public restroom” these days with out being informed of how Neo- Darwinism has somehow influenced your decision to do so.

    No… I’m not the same person as the Rock! KRock is a nickname the guys I work with gave me and judging by some of the other nicknames given to people I work with, I did pretty well, I guess… Lol..

  44. Petrushka,

    This has been the linchpin of your logic for hundreds of posts, despite having been refuted from more than one angle.

    You have seized upon the accurate observation that no one has figured out how to functionally fold proteins and upon that you base the claim that it is impossible.

    Meanwhile no one attempts to explain how the proteins used to assemble a sea sponge evolved or can even demonstrate that the supposed pathways even exist to make it possible at all. But in this case you do a full 180 and suddenly the “how” isn’t so important. Your rigorous skepticism is nowhere to be found.

    Upon this faulty foundation you routinely reassert that ‘evolution is the only process known to be capable of such things,’ which is inexplicable as no such thing is known at all. It’s as if you think that if you repeat it enough, others will grow weary of pointing out that it isn’t remotely true, and then it will be.

  45. The second response is that it is always up to those who claim the sufficiency of a process to demonstrate the sufficiency.

    I’m beginning to suspect that in some perverse way you are amused by the irony of such statements, and that it is deliberate. That’s fine. I appreciate that type of humor, and it makes sense of something that would otherwise make none.

  46. Hi KRock,

    I’ve been working on a couple of long posts. That’s why I’ve been away for a while. You should see another post in the next couple of days. Merry Christmas, by the way.

  47. Have another look at the table in the Panda’s Thumb blogpost, and at the referenced article therein, and your questions will be answered. I’m not going to re-write the answers again and again for people unwilling to do minimal amounts of research.

  48. Hi Bilbo! Here:

    http://pandasthumb.org/archive.....oopti.html

    So have Dembski and Luskin. There goes the metabolic-pathways-don’t-qualify defense. Whoops!

  49. Meanwhile no one attempts to explain how the proteins used to assemble a sea sponge evolved or can even demonstrate that the supposed pathways even exist to make it possible at all. But in this case you do a full 180 and suddenly the “how” isn’t so important. Your rigorous skepticism is nowhere to be found.

    It’s true that I am more skeptical of imaginary friends than I am of observable processes.

  50. It’s true that I am more skeptical of imaginary friends than I am of observable processes.

    Oh really? I find that hard to believe. What about the physically observable dynamics within systems?

    You say: ‘It’s not a semiotic system?’

    Then by all means, answer the question: If in one instance we have something that is a symbol, and in another we have something that just acts like a symbol, then surely you can look at the physical evidence and point to the distinction between the two.

    Instead, you’ve chosen to simply ignore it. You are living inside a delusion where you willfully apply one standard of evidence for the things you like, and another for the things you don’t. The observable artifacts of a beginning to this universe seem to give you no pause, even though we have absolutely no experience with ‘universes coming into being’ and therefore absolutely no reference beyond what the evidence itself is telling us. Yet. In order for you to simply acknowledge the material artifact of a semiotic system in protein synthesis, you stomp your feet and demand to know a designer’s hair color and shoe size. You want to know where he came from, while at the same time, you completely ignore the fact that you don’t know where anything else came from either (and that doesn’t make you question background radiation). You reserve that particular standard as a tool for the things you dislike, because for you, it’s not about the evidence. It’s about being able to manipulate your standards of evidence in order to please yourself. You don’t have the integrated standards of a materialist who can acknowledge what the material is telling you.

    There is one thing we can know for sure; you won’t be pointing out any distinctions in the physical evidence between protein synthesis and any other semiotic system.

  51. Petrushka,

    It’s true that I am more skeptical of imaginary friends than I am of observable processes.

    I observed that you apply your logic precisely when it suits you, and in response you have retreated to the safe corner of rhetoric. Better not to respond at all, in which case I would generously assume that you were busy.

  52. You say: ‘It’s not a semiotic system?’

    I’ve tried to engage you on this half a dozen times and been ignored.

    I want to know if you are referring to the origin of life.

  53. The semiotic argument claims that the transfer of recorded information during protein synthesis demonstrates a semiotic state, as evidenced by a coherent review of the physical objects and dynamics observed within the system.

  54. Hi Nick. I haven’t read Dembski’s and Luskin’s stuff, but Behe had already replied to Miller’s example of the Lac Operon Gene here (five years before Dover, and after we, including you, had already discussed it at length at ARN):

    http://www.discovery.org/a/441

    I think it is a mistake to site this example as an admission by Behe that metabolic pathways are IC. The lac operon example qualifies as an example of IC, because the product — lactose — actually causes the lac operon to activate. Thus the substrate isn’t just a passive player, but an active one. So yes, for any metabolic pathway where a substrate activates further genes to be turned on, it’s probably an IC system. This is not the same as admitting that all metabolic pathways are IC. Try thinking through what Behe says a little more carefully, Nick.

  55. Hi Nick,

    Referring to your last link it appears that you are a pathetic imp. Let’s see why:

    Minnich, who had previously read the paper, explained that to evolve this pathway required the modification of maybe 2 or 3 preexisting enzymes. There was really nothing new here, and certainly nothing approaching an irreducibly complex biomolecular machine. Minnich called this microevolution.

    2 or 3 EXISTING enzymes. That means you have to account for those enzymes and guess what? It is only talking about 2 or 3 components. And no IDists says that is beyond stochastic processes. Behe’s mousetrap contains 5.

    Try again…

  56. Nick,

    You might be interested to know that the links to the article you mentioned only give the abstract. Fortunately, I’ve managed to locate the article at another Web address – http://home.planet.nl/~gkortho.....Matzke.pdf – and I shall have a look at it over the next few days.

    In your table, your function column doesn’t indicate whether the function in question is only in relation to the working of the flagellum, or whether it’s independent of the existence of the flagellum (i.e. modular). Your homologies column lists homologues, but doesn’t say where they are found. Call me dense if you like, but it took a while for the penny to drop, and for me to realize that homologues starting with Flg, Flh or Fli were flagellar, while the others were not. Finally, listing a protein as “FlgBCFG” gives the layperson the misleading impression that it’s just a single big protein with an ugly long name.

    May I also suggest that you or one of your friends set up a Web page, aimed at Joe Q. Citizen, where you can get your points across more effectively to the masses. Some free marketing tips:

    (1) avoid jargon and long scientific names like sigma factor, N-methylase, Caulobacter and Gram-positive bacteria – it just makes people’s eyes glaze over;
    (2) use as many pictures as possible;
    (3) use progress bars to illustrate what scientists have accomplished to date and what remains to be done (e.g. a progress bar showing what percentage of the 23 essential proteins had known homologs in 2003, in 2006 and 2011);
    (4) have an FAQ’s page with answers to the top 20 or 30 objections you get from ID proponents, as well as place where people can submit questions of their own;
    (5) have a little quiz at the end, where people can test what they’ve learned about the bacterial flagellum;
    (6) keep your language at about the level that a 12-year-old could comfortably read. Why? Because when you’re absorbing an unfamiliar scientific concept (as co-option is to a lot of people), that’s enough strain on your brain, without having to plow through difficult terminology and/or convoluted syntax as well;
    (7) for all the scientific papers you cite, attach an additional link to a plain-language summary of the paper’s contents, which a layperson could readily understand.

    Like it or not, science is largely about PR.

  57. I would agree that it would be helpful to simplify these things for the layman, but I don’t think you can simplify things in an argument. You either have to follow at the expert level or stay out of the way of those who are at the expert level.

    This is not too different from the situation in quantum theory, where it takes several years of graduate study even to qualify to ask intelligent questions.

  58. Petrushka,

    You wrote:

    I would agree that it would be helpful to simplify these things for the layman, but I don’t think you can simplify things in an argument. You either have to follow at the expert level or stay out of the way of those who are at the expert level.

    This is not too different from the situation in quantum theory, where it takes several years of graduate study even to qualify to ask intelligent questions.

    Let’s say this is true, that really you need years of graduate school to understand the underlying principles of
    this subject. Then I’ve got a problem, because, the internet is full of people calling other people stupid, as well as newspaper columnists, who are not necessarily science writers, calling politicians stupid, the moment they express doubts about evolution.

    (I’ve seen
    some suggesting a litmus test should applied to anyone who doesn’t accept evolution to state that such people should be ruled out of any consideration for science degrees, political office, etc)

    But, based on this premise there are really very few people who understand
    the details, and all others are dependent
    on them for their knowledge. It’s unlikely
    the average person commenter on the internet, clubbing someone else over the head,
    for not understanding evolution, could really know
    what he’s talking about.

    Further, if there are people, like Behe, who disagree
    with them, that would make it even harder for
    the average person to reach a valid conclusion, because
    they are now forced to select from a group
    of people who are highly trained in an area where
    they are not trained. And therefore, their skepticism
    might be even more justified.

    It’s also difficult to deal with those who
    seem to proclaim that this stuff should obvious to anyone,
    because, they’re contradicting themselves if the detaiils
    are really so esoteric.

    Thanks

  59. Hi Bilbo. Various responses:

    (a) If metabolic pathways can be IC, you guys shouldn’t be going around saying that metabolic pathways aren’t IC and that Larry Moran is dumb for thinking they are. Whaddya wanna bet that the TCA/Krebs cycle is substrate-regulated?

    (b) If what makes a metabolic pathway IC the fact that “a substrate activates further genes to be turned on”, well then, most metabolic pathways ARE IC after all, and therefore see (a).

    (b2) Point (b) would mean that the difference between an IC metabolic pathway and a non-IC metabolic pathway would be that the former is a substrate-activated metabolic pathway, whereas the latter is a constituitively-activated metabolic pathway. “Constituitive” means that the genes for the pathway are always “on”. Such pathways are not the most common sort — it’s kind of wasteful of resources to leave genes on when they are not being used. But they work just fine, they are observed in the wild (particularly in recently-evolved metabolic pathways), and they can be easily produced in lab mutation experiments.

    (b3) So it turns out that the question of whether or not the evolution of IC is plausible apparently boils down to the question of whether or not a constituitive metabolic pathway can evolve into a substrate-regulated metabolic pathway. Are you really going to argue that this is wildly implausible? That point mutations can never increase or decrease the binding of a promoter or repressor in the presence of a substrate?

    (c) If what makes the lac operon IC is that it has multiple required parts, well then,

    (c1) actually the “interacting” and “well-matched” parts of the definition are not crucial, are forgotten about when inconvenient by ID proponents, and are only arbitrarily dragged back into discussion by ID proponents to dodge fatal counterexamples they can answer in no other way.

    (c2) all metabolic pathways having more than one enzyme are IC, and unfortunately for you we have several examples of such metabolic pathways evolving in bacteria in the last few decades.

    So, basically, the IC guys are still stuck at total bankruptcy once you dig into their position. The IC argument is only appealing in a short popularized argument. Once you get into details and the literature, it falls apart. As it did in court.

  60. Hey VJ,

    Is it customary at UD to allow people to refer to commenters as “pathetic imps”, as Joe has done to Nick?

  61. Hi Joe,

    LOL, as they say.

    (0) I wasn’t discussing Minnich’s comments in this UD thread, but since you brought it up, it is relevant to whether or not metabolic pathways can evolve.

    (a) The lac operon has only 3 genes, yet Behe and Bilbo here say it is IC. Oops!

    (b) Please show me the part of some authority’s definition of IC that says “four or more parts required”. You can’t. The words are always “multiple parts” or “several parts”.

    (c) And, anyway, Minnich was wrong about what Johnson & Spain said about the evolutionary origins of the 2,4-DNT degradation pathway. Here are the papers, introduced into evidence in the Kitzmiller case:

    Origins of the 2,4-Dinitrotoluene Pathway

    Glenn R. Johnson, Rakesh K. Jain† and Jim C. Spain*

    + Author Affiliations

    Air Force Research Laboratory, U.S. Air Force, Tyndall Air Force Base, Florida 32403

    doi: 10.1128/?JB.184.15.4219-4232.2002 J. Bacteriol. August 2002 vol. 184 no. 15 4219-4232

    The degradation of synthetic compounds requires bacteria to recruit and adapt enzymes from pathways for naturally occurring compounds. Previous work defined the steps in 2,4-dinitrotoluene (2,4-DNT) metabolism through the ring fission reaction. The results presented here characterize subsequent steps in the pathway that yield the central metabolic intermediates pyruvate and propionyl coenzyme A (CoA). The genes encoding the degradative pathway were identified within a 27-kb region of DNA cloned from Burkholderia cepacia R34, a strain that grows using 2,4-DNT as a sole carbon, energy, and nitrogen source. Genes for the lower pathway in 2,4-DNT degradation were found downstream from dntD, the gene encoding the extradiol ring fission enzyme of the pathway. The region includes genes encoding a CoA-dependent methylmalonate semialdehyde dehydrogenase (dntE), a putative NADH-dependent dehydrogenase (ORF13), and a bifunctional isomerase/hydrolase (dntG). Results from analysis of the gene sequence, reverse transcriptase PCR, and enzyme assays indicated that dntD dntE ORF13 dntG composes an operon that encodes the lower pathway. Additional genes that were uncovered encode the 2,4-DNT dioxygenase (dntAaAbAcAd), methylnitrocatechol monooxygenase (dntB), a putative LysR-type transcriptional (ORF12) regulator, an intradiol ring cleavage enzyme (ORF3), a maleylacetate reductase (ORF10), a complete ABC transport complex (ORF5 to ORF8), a putative methyl-accepting chemoreceptor protein (ORF11), and remnants from two transposable elements. Some of the additional gene products might play as-yet-undefined roles in 2,4-DNT degradation; others appear to remain from recruitment of the neighboring genes. The presence of the transposon remnants and vestigial genes suggests that the pathway for 2,4-DNT degradation evolved relatively recently because the extraneous elements have not been eliminated from the region.

    Applied Microbiology and Biotechnology
    Volume 62, Numbers 2-3, 110-123, DOI: 10.1007/s00253-003-1341-4

    Mini-Review

    Evolution of catabolic pathways for synthetic compounds: bacterial pathways for degradation of 2,4-dinitrotoluene and nitrobenzene

    G. R. Johnson and J. C. Spain (2003)

    Abstract

    The pathways for 2,4-dinitrotoluene (2,4-DNT) and nitrobenzene offer fine illustrations of how the ability to assimilate new carbon sources evolves in bacteria. Studies of the degradation pathways provide insight about two principal strategies for overcoming the metabolic block imposed by nitro- substituents on aromatic compounds. The 2,4-DNT pathway uses novel oxygenases for oxidative denitration and subsequent ring-fission. The nitrobenzene pathway links facile reduction of the nitro- substituent, a novel mutase enzyme, and a conserved operon encoding aminophenol degradation for mineralization of nitrobenzene. Molecular genetic analysis with comparative biochemistry reveals how the pathways were assembled in response to the recent appearance of the two synthetic chemicals in the biosphere.

    In the 2003 paper, Figure 1, the 2,4-DNT degradation pathway is diagrammed. The genes involved are:

    dntAaAbAcAd
    dntB
    dntQ
    dntO
    dntG
    dntG
    dntE

    That’s, um, 7 genes/proteins at least, except that dntAaAbAcAd is actually 4 Open Reading Frames, of different sizes, so it is probably a multiprotein complex. This makes 11 genes/proteins. The genes are derived from chunks of 3 ancestral pathways (dntAaAbAcAd from the Naphthalene Dioxygenase pathway, dntB from the Chlorophenol monooxygenase/Polyketide hydroxylase pathway, and the rest from the Amino acid transport and metabolism system.

    Figure 1 was put on the screen, in color, at the trial, and the article was provided to him months before at his deposition and during discovery, but Minnich seems to not have paid much attention.

    (d) If ID advocates admit that stochastic processes can put together a 2- or 3-protein system, what exactly is it that keeps stochastic processes from adding a fourth protein to a 3-protein system? Or from sticking together two 2-component systems?

    The failure to seriously and substantively answer these questions raised in the Kitzmiller case — as opposed to dodging them with creative and inconsistent redefinition of terms and goalpost-moving — is why ID has gone into such a slump post-Dover.

  62. Nick: “So it turns out that the question of whether or not the evolution of IC is plausible apparently boils down to the question of whether or not a constituitive metabolic pathway can evolve into a substrate-regulated metabolic pathway.

    Yeah, I think that’s the question.

    Are you really going to argue that this is wildly implausible?

    No. I’m just an armchair philosopher. I’ll let others argue it.

    That point mutations can never increase or decrease the binding of a promoter or repressor in the presence of a substrate?

    Wouldn’t we first need a promoter or repressor?

  63. Hi Joe,

    You remind me a lot of a poster I knew and banned from my posts at TT on a regular basis. Why don’t you leave the insulting comments to our critics, such as Larry Moran?

  64. What’s that, vjtorley? You declared the downfall of a major, mainstream scientific theory based on a system, the bacterial flagellum, which you barely understand, and without bothering to get informed about even the basics of the facts necessary for even discussing the question of its evolution?

    And further, basically everyone here enthusiastically supported what you said, despite the above?

    All your suggestions for popularization are nice, but (a) that’s a huge amount of work and I’ve already done more than my part (have you even read my 2003 essay yet?), (b) I’m not convinced it would actually teach anyone anything — navigating through that degree of detail, translated into imprecise popular language, would quite possibly be harder than just learning the damn science in the old-fashioned way — working hard and learning it (much easier these days with wikipedia and google scholar), and (c) no one is paying me to do it. Occasional comments on blogposts are pretty much entertainment for me (I’m weird), but all of that would be actual work better spent writing scientific articles.

    Finally, you say:

    Like it or not, science is largely about PR.

    No, it’s not. The fact that you think so and no ID people disagreed is an example of one of the huge problems with the ID movement, and with pseudoscience generally.

  65. Then Behe shouldn’t have said that the reason IC systems couldn’t evolve was that a partial system was “by definition nonfunctional” and thus couldn’t have been preserved by selection.

  66. Of course, another ~10 of the flagellar proteins are homologous to each other (the axial proteins of the rod/hook/filament), and another ~8 or so aren’t universally required, but who’s counting? Oh, that’s right, me. Why don’t you guys ever try getting the counts right?

  67. Wouldn’t we first need a promoter or repressor?

    Handy that the regulatory sequences that are in front of genes can get copied and transposed, isn’t it?

  68. Nick,

    Nice to see that you are still confused.

    The # of part requirements is laid out by Behe himself:

    In fact, my argument for intelligent design is open to direct experimental rebuttal. Here is a thought experiment that makes the point clear. In Darwin’s Black Box (Behe 1996) I claimed that the bacterial flagellum was irreducibly complex and so required deliberate intelligent design. The flip side of this claim is that the flagellum can’t be produced by natural selection acting on random mutation, or any other unintelligent process. To falsify such a claim, a scientist could go into the laboratory, place a bacterial species lacking a flagellum under some selective pressure (for mobility, say), grow it for ten thousand generations, and see if a flagellum–or any equally complex system–was produced. If that happened, my claims would be neatly disproven.(1)

    So what that means, and my 9-year old understands this, is to refute all of IC you just demonstrate that the IC structure/ system with the greatest IC core can arise via stochastic processes. And that leads us to the origin of living organisms as that is the greatest IC value.

    (d) If ID advocates admit that stochastic processes can put together a 2- or 3-protein system, what exactly is it that keeps stochastic processes from adding a fourth protein to a 3-protein system? Or from sticking together two 2-component systems?

    What ALLOWS for it Nick? Science requires POSITIVE evidence, Nick. You need to demonstrate that stochastic processes can produce more than two new protein-to-protein binding sites if you want to have large protein complexes and according to the evidence as exposed by Behe, that is beyond the power of stochastic processes.

    And what slump are you talking about? ID is stronger than ever and supported by more data.

    But then again you still think that ID is anti-evolution…

  69. Hi Bilbo I,

    Yes I heard that you are very tempermental.

    Oh well, take care.

  70. Nick,

    1- That isn’t what Behe said.

    2- ID is not anti-evolution

  71. Yes Nick, but your position can’t even account for one protein. And that is a problem, don’t ya think?

  72. It sells tickets Bilbo I…

  73. Hmm, more polite at UD than here:
    http://intelligentreasoning.bl.....cking.html

  74. hi nick

    what about this paper…

    here is an research that prove how much of the protein length need for its minimal function-

    http://www.ncbi.nlm.nih.gov/pm…..PMC211289/

    in this case is the flagellin protein.

    its minimal length need 310 amino acid. no less.

    the sequance space for 310 aa is minimum 2^310!

    the protein cannt evolve from a simpler protein because its the minimum and the researcher get a invalid protein after they cut out near 190 amino acid

  75. Have you read what I say about you, Nick?

  76. More for matzke on the number of components:

    Irreducible Complexity:

    IC- A system performing a given basic function is irreducibly complex if it includes a set of well-matched, mutually interacting, non-arbitrarily individuated parts such that each part in the set is indispensable to maintaining the system’s basic, and therefore original, function. The set of these indispensable parts is known as the irreducible core of the system. Page 285 NFL

    Numerous and Diverse Parts If the irreducible core of an IC system consists of one or only a few parts, there may be no insuperable obstacle to the Darwinian mechanism explaining how that system arose in one fell swoop. But as the number of indispensable well-fitted, mutually interacting,, non-arbitrarily individuated parts increases in number & diversity, there is no possibility of the Darwinian mechanism achieving that system in one fell swoop. Page 287

    Minimal Complexity and Function Given an IC system with numerous & diverse parts in its core, the Darwinian mechanism must produce it gradually. But if the system needs to operate at a certain minimal level of function before it can be of any use to the organism & if to achieve that level of function it requires a certain minimal level of complexity already possessed by the irreducible core, the Darwinian mechanism has no functional intermediates to exploit. Page 287

  77. Your Behe quote says nothing about the number of parts required to qualify as IC.

    And, if you’ve already accepted that evolution can combine a 2-part system and a 1-part system to make a 3-part system, which you apparently have, then it’s a very fair question to ask why 3-parts to 4-parts is supposed to be such a huge barrier to evolution. Your prior concession puts the burden of proof on you to explain why going just a tiny bit further than what you concede is impossible.

    And, anyway, the 2,4-DNT degradation pathway is either 7 parts, or 11, depending on how you count.

    And what slump are you talking about? ID is stronger than ever and supported by more data.

    Well, let’s see, in this very thread we’ve seen:

    - that ID folks have confidently declared both that metabolic pathways *are* IC and *are not* IC,

    - we’ve had ID defenders conclude that evolving a several-part IC system is no big deal and that the Real Official Barrier to Evolution (TM) is at some ill-specified higher level, and we’ve had no answer to the challenge about why 3-part systems are perfectly evolvable and 4-part systems are not

    - we’ve had published, peer-reviewed literature demonstrating the evolution in recent times of a system with 7 (or 11) required parts, with no better rebuttal now in 2011 than existed in Dover in 2005 (and the ID guy in Dover conceded that evolution did succeed in explaining the system, although he appears to not have read the paper).

    This is the ID movement’s favorite argument, and this is the best you’ve got? Ergo, slump.

    Have you read what I say about you, Nick?

    Yep, I even saved it, which is good since you apparently have taken down the post. Maybe you were embarrassed about dropping the F-bomb on Bilbo and I…

  78. Nick,

    Two parts can count as IC- one part can. What Behe said was to refute IC you need to use the greatest IC. Obvioulsy that went over your head. No surprise there.

    You still need POSITIVE evidenec Nick and you cannot produce it.

    Also I see you are still confused and think ID is anti-evolution. Apparently you cannot learn.

    And Nick I have written several posts about you (on my blog).

    we’ve had published, peer-reviewed literature demonstrating the evolution in recent times of a system with 7 (or 11) required parts…

    Let’s see it then. But you still think that ID is anti-evolution which pretty much exposes your bias and agenda.

  79. Hello again Nick,

    I was just re-reading your PT article. Did you see that Dembski said :

    For certain enzymes (which are themselves highly complicated molecular structures) and metabolic pathways (i.e., systems of enzymes where one enzyme passes off its product to the next, as in a production line), simplification leads not to different functions but to the complete absence of all function. (bold added)

    That means not all enzymes and metabolic pathways.

    Also the rapid evolution of the “degradation pathway for a toxic compound 2,4-DNT” could very well be evidence for Dr Spetner’s “built-in responses to environmental cues”, a known design mechanism.

    As I have tried and tried to tell you but you won’t have any of it-> you are starting with that which needs to be explained in the first place.

  80. I was just re-reading your PT article. Did you see that Dembski said :

    For certain enzymes (which are themselves highly complicated molecular structures) and metabolic pathways (i.e., systems of enzymes where one enzyme passes off its product to the next, as in a production line), simplification leads not to different functions but to the complete absence of all function. (bold added)

    I’m familiar with the Dembski quote, and, ugh, what a mess. It again disproves the “metabolic pathways aren’t IC” defense, which people tried earlier in this thread. “Complete absence of all function” is almost meaningless, since probably any enzyme or collection of enzymes would be found to do *something* if tested against every conceivable substrate (an essentially infinite list of molecules and macromolecules). On the other hand, virtually any pathway, including ones already Officially Declared to Be IC, like the lac operon, converts substrates from A to B to C etc., and even if you knock out the A->B step. Thus the pathway still converts B->C, which is useful if you have any B, but you might not if A->B is the only source.

    The whole logic is backwards anyway. Breaking a modern system does not simulate evolution in reverse or serve as any kind of reasonable test of whether or not the ancestral system would have been functional. It’s like cutting off someone’s head and declaring that evolution is impossible because humans couldn’t have lived without heads and then gradually evolved them.

    Also the rapid evolution of the “degradation pathway for a toxic compound 2,4-DNT” could very well be evidence for Dr Spetner’s “built-in responses to environmental cues”, a known design mechanism.

    No it’s not, this is just “wow, that sure looks like evolution so I will desperately conjure out of thin air a way to make evolution seem like design”. If you would only read the articles I cited, you would find that the DNT pathway genes still retain parts of their ancestral pathways, i.e. junk left over from the ancestral chromosome chunks that recombined to produce the pathway. This isn’t some slick preprogrammed adaptation, it’s stuck together in slapdash fashion.

  81. Nick,

    Thank you for continuing to prove taht you do not understand what ID claims and you have no intention of learning about it.

    Intelligent Design is NOT anti-evolution

    (If there is a next Court case I am going to make sure the ID side hammers that home. How do you sleep at night knowing that you are still promoting darwin’s long exposed strawman?)

    And you are still starting with the very thing your position has to explain in the first place.

  82. Another Matzke strawman:

    If you would only read the articles I cited, you would find that the DNT pathway genes still retain parts of their ancestral pathways, i.e. junk left over from the ancestral chromosome chunks that recombined to produce the pathway. This isn’t some slick preprogrammed adaptation, it’s stuck together in slapdash fashion.

    The problem is, Nick, you don’t appear to know anything about designing yet you think you can tell when something is poorly designed.

    Notice I never said anything about being “some slick preprogrammed adaptation”- geez you just have to erect strawman after strawman and then tear them down so you can feel some sense of accomplishment.

    Dr Spetner’s “built-in responses to environmental cues” doesn’t have to be “some slick preprogrammed adaptation”. All it is is a GA that would help the organism find a solution. And finding a solution does not entail wiping out all past components and systems.

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