Friday, October 22, 2010

"Impossible" Molecular Machines

Someone named vjtorley just posted a list of things that would falsify his faith in Intelligent Design Creationism [The 10^(-120) challenge, or: The fairies at the bottom of the garden].

Normally this wouldn't be very interesting because the IDiots almost always set up impossible criteria reflecting their fundamental misunderstanding of evolution. This posting is no exception but I was intrigued by one of the items on the list.
2. An empirical or mathematical demonstration that the probability of the emergence of any of the irreducibly complex structures listed on this page, as a result of non-foresighted processes (“random mutations plus natural selection”) is greater than 10^(-120).
The link under "this page" is to an article by Casey Luskin from last June [Molecular Machines in the Cell]. He lists a whole bunch of molecular machines and claims that these structures pose a real problem for science.

Here's the list. Judge for yourselves whether they make you believe in God.
Molecular machines are highly complex and in many cases we are just beginning to understand their inner workings. As a result, while we know that many complex molecular machines exist, to date only a few have been studied sufficiently by biologists so that they have directly tested for irreducible complexity through genetic knockout experiments or mutational sensitivity tests. What follows is a non-exhaustive list briefly describing 40 molecular machines identified in the scientific literature. The first section will cover molecular machines that scientists have argued show irreducible complexity. The second section will discuss molecular machines that may be irreducibly complex, but have not been studied in enough detail yet by biochemists to make a conclusive argument.


I Molecular Machines that Scientists Have Argued Show Irreducible Complexity

1. Bacterial Flagellum
2. Eukaryotic Cilium
3. Aminoacyl-tRNA Synthetases (aaRS)
4. Blood clotting cascade
5. Ribosome
6. Antibodies and the Adaptive Immune System

II. Additional Molecular Machines

7. Spliceosome
8. F0F1 ATP Synthase
9. Bacteriorhdopsin
10. Myosin
11. Kinesin Motor
12. Tim/Tom Systems
13. Calcium Pump
14. Cytochrome C Oxidase
15. Proteosome
16. Cohesin
17. Condensin
18. ClpX
19. Immunological Synapse
20. Glideosome
21. Kex2
22. Hsp70
23. Hsp60
24. Protein Kinase C
25. SecYEG PreProtein Translocation Channel
26. Hemoglobin
27. T4 DNA Packaging Motor
28. Smc5/Smc6
29. Cytplasmic Dynein
30. Mitotic Spindle Machine
31. DNA Polymerase
32. RNA Polymerase
33. Kinetochore
34. MRX Complex
35. Apoptosome / Caspase
36. Type III Secretory System
37. Type II Secretion Apparatus
38. Helicase/Topoisomerase Machine
39. RNA degradasome
40. Photosynthetic system


39 comments :

  1. 5. Ribosome

    Ribosome? The 'smoking gun' evidence which crowns the case for the RNA World theory? Bwa ha ha!

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  2. Wow...

    It looks like Luskin just purchased a cell bio book, opened it up to the glossary, and wrote down everything, claiming it is all 'evidence' for ID.

    I like the fact that lists single molecules as 'machines'. Such folk actually seem to think that calling something a machine means it was made.

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  3. Now that I think about it, have any of these people actually 'proved' that the probability is LESS THAN 10^(-120)?

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  4. Sigh!

    If evolution is directed toward a particular goal, then these probabilities make it look like magic.

    If evolution is not directed, but is merely opportunistic, then these improbabilities don't mean a thing. With an evolutionary process that depends on combinations, anything that results will seem highly improbable.

    This is just the old creationist argument based on mistaken assumptions that evolution has a specific goal.

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  5. It's a silly list. The most crucial machine of all is not on the list and has yet to be found: a catalytic-RNA RNA-dependent RNA polymerase. Once you have that, everything else is easy. (I'm thinking particularly of the ribosome, where all the catalysis is done by RNA).

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  6. The funny thing that Luskin doesn't get is that some of his "machines" are relatives of the other systems he lists. Sometimes they are even basically functioning subsets. In one or two cases I think they are even pretty much the same system given different names in different organisms, different subfields, etc.

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  7. Had the great misfortune of witnessing some moronic deceitful scumbag – I mean, creationist – putting the final nails on the coffin of evolution today. Said nails involved showing stolen (unreferenced) clips of ATP synthase (check), kinesin (that's a new one for me) and RNA polymerase. I'm just sitting there thinking "they're not even prokaryotic there!" Apparently there was some point about energy or something, but because I'm just a dumb biologist, I failed to grasp it. Oh well.

    However, what sealed the deal for me was that fish float when they die. See, fossils are said to be formed when fish die and sink to the bottom, etc. There's even this textbook picture showing that. Obviously, the only possible way that can ever happen. Well, what paleontologists were too damn stupid to see was that upon death, fish FLOAT, as anyone with an aquarium would know! [cue: laughter. Those silly rock nerds, AHAHAHA!]

    In all seriousness, I have not seen such an outright deceitful, filthy, disgusting speaker ever. It was disturbing how one could miss the point of EVERY SINGLE SIMPLE CONCEPT EVEN A FIRST YEAR WOULD KNOW. The only way you can be so wrong is by intentionally lying. And preying on the poor education of the vulnerable masses. Disagree with me on whatever worldview or theory you want, but the predatory con artist aspect I find infuriating and absolutely intolerable. *vomits* /rant

    So yeah. I'm gonna go cuddle with a stack of evolution papers for the next few days as I try to convince my brain cells not to arrange a mutiny for my cruelty to them. Be back later...

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  8. The definition of irreducibly complex includes any system that consists of more than one component and that requires each component in place for the system to work.
    That means that a system of two parts, such as a protein and its binding partner is irreducibly complex. Indeed every single biological molecule that functions as part of some biochemical process that requires it binding or interacting with another molecule can be called irreducibly complex.
    Therefore every ligand receptor pair is irreducibly complex. Every interacting protein pair is irreducibly complex. Indeed even every double stranded DNA molecule is irreducibly complex - since you need the partner strand - a seperate molecule, for it to function.
    I think it is up to the ID proponents to defend the definition of irreducible complexity when faced with these simple examples rather than for us to try to explain all the elements of a hugely complex pathway (that is, after all, simply an accumulation of such simpler examples).

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  9. If a creationist ever asks for evidence of evolution happening right in front of them, all we need do is point out that only a few short years ago, they were arguing that giraffe's necks were long because God stretched them, and bananas were proof of creation because we could hold them in our hand and they were biodegradable (note: this is not a joke: http://hubpages.com/hub/the-atheists-nightmare).

    Those ideas have been wiped out, and are no longer effective, so instead of looking for home-spun, every day examples, they've had to evolve and adapt to discussion of proteins and structures that most people have never heard of. 'Hey,' the argument goes, 'do you know what a bacterial flagellum is? No? It's proof of God, that's what!'.

    "Sir, {a+b^n} over {n}=x, hence God exists—reply!"

    They've run out of animals, they've run out of bacteria, now they're on the proteins. Mark my words, in ten years, they'll be citing Higgs Bosons as evidence of irreducible complexity.

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  10. I like this bit of vjtorley's drivel:

    I wrote that my faith in Intelligent Design was falsifiable

    (my bold, the IDiot's italics).

    I don't think one is supposed to have faith in ID, because, doncha kno, ID is scientific! Or so they tell me...? Perhaps the creationist faith is not strong in this one? Did his lord not help him choose intelligently designed words?

    Of course, it's the usually creationist scumbaggery; he whimpers that he'd change his mind if he is shown the evidence, but the reality is that he'd (a) stick his fingers in his ears and go "la la la can't hear you", and (b) shift the goalposts somewhere else.

    IDiots are such liars. Too dishonest to call themselves creationists.

    Should one respond to that sort of gobshite hypocrite? Nah, let him get a proper education. And he can crow about how the rational world won't waste time addressing his delusions, so his delusions must be Twoo!!

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  11. I love how "Molecular Machines that Scientists Have Argued Show Irreducible Complexity" explicitly require one to be completely ignorant about said 'machine'.

    We learn about the evolution of the immune system in school. It was covered in undergrad immunology. The basics are so old, theyre in the damn textbook.

    And then we get to the nasty fact that 90% of the B-cells you make die. What an omnipotent, glorious designer who says "Meh. One out of ten. Good enough."

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  12. No proponent of intelligent design should argue that a Darwinian origin of the TTSS is implausible, for the simple reason that the TTSS is seen as having evolved from the bacterial motility system in the intelligent design proposition. Several papers have supported a model where the TTSS originates from the bacterial flagellum (although I believe that NickM would disagree with that view?) . Hence, the TTSS almost assuredly evolved via Darwinian processes in the intelligent design framework.
    It is really very simple to falsify intelligent design from the standpoint of biochemistry. If one could find an in vivo example of evolution of a protein-based system that requires a fairly large number of amino acid residues working simultaneously in order to maintain that function, then intelligent design will have been effectively falsified (a la Dr. Sean Pitman).

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  13. nwrickert, the argument from the sampling problem is not an argument that stems from an ignorance of evolutionary processes. While it is entirely true that there is no real goal in evolutionary processes, it is also true that the odds of a novel protein function evolving decreases exponentially the more amino acid residues that are required to maintain that function.

    It is my conviction that because of this exponential nature behind protein structure evolution we find many in vivo examples of novel protein functions evolving that require only one amino acid substitution [to name a few: see Kedzie et al. 1998, Cartelle et al. 2004, Safi et al. 2008], less in vivo examples of novel protein functions evolving that require two specific amino acid substitutions [for example, see Genda et al. 2007], and even less in vivo examples of novel protein functions evolving that require three amino acid substitutions, and so on.

    References:
    Cartelle Monica, del Mar Tomas Maria, Molina Francisca, Moure Rita, Villanueva Rosa, Bou German. High-Level Resistance to Ceftazidime Conferred by a Novel Enzyme, CTX-M-32, Derived from CTX-M-1 through a Single Asp240-Gly Substitution. Antimicrob Agents Chemother. 48(6): 2308–2313 (2004).

    Genda Yoshikatsu, Kanda Ayami, Hamada Hiroyuki, Sato Kyoko, Ohnishi Jun, Tsuda Shinya. Two Amino Acid Substitutions in the Coat Protein of Pepper mild mottle virus Are Responsible for Overcoming the L4 Gene-Mediated Resistance in Capsicum spp. Phytopathology, 97(7): 787-793 (2007).

    Kedzie Karen M., Donello John E., Krauss Heather A., Regan John W, Gil Daniel W. A Single Amino-Acid Substitution in the EP2Prostaglandin Receptor Confers Responsiveness to Prostacyclin Analogs. Molecular Pharmacology, 54(3):584-590 (1998).

    Safi Alexias, Wallace Kelley A., and Rusche Laura N. Evolution of New Function through a Single Amino Acid Change in the Yeast Repressor Sum1p. Mol Cell Biol, 28(8): 2567–2578 (2008).

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  14. Sigmund is right in that all biological functions are irreducibly complex, and in that respect Behe (1996) is wrong in saying that IC systems cannot plausibly evolve via Darwinian processes. What is true is that biological systems that have high levels of IC are less and less likely to evolve the more IC they are.

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  15. If evolution is not directed, but is merely opportunistic, then these improbabilities don't mean a thing. With an evolutionary process that depends on combinations, anything that results will seem highly improbable.

    Exactly. Using the same "math," we can show Casey Luskin doesn't exist, and the same for vjtorley.

    After all, what are the odds that out of a few billion people in the world, Mr. and Mrs. Luskin would meet, marry, and have a bouncing baby boy (reduce the scant probability by half right there), Casey? Multiply together the chances that the exact members of each and every couple in Luskin's and vjtorley's lineages, of all the people existing on Earth at the time, met and procreated through thousands of generations of genetically modern humans to arrive at these two people, and you must surely obtain a number far smaller than 1x10^-120.

    Thus these two don't actually exist, so we don't need to bother with their tripe.

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  16. Livingstone said: "What is true is that biological systems that have high levels of IC are less and less likely to evolve the more IC they are."
    In other words the more complex a system is then the more unlikely it is to evolve.
    I don't think that is a problematic statement from an evolutionary standpoint - its rather obvious, isn't it? The problem for the ID proponents is that it is relatively easy to demonstrate the evolution of simpler examples of "IC" (such as a gene duplication event that leads to an alternative isoform or splceform of a gene that interacts with the product of the remaining ancestral gene). Once we have demonstrate that simple "IC" can evolve then there is no fundamental reason why highly complex "IC" cannot evolve - after all its just an accumulation of smaller "IC" events.

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  17. Oh, and also -

    Do Luskin and vjtorley claim that lotteries are committing fraud whenever they announce winners?

    As Sean B. Carroll points out, the odds of a particular ticket winning the lottery may be billions to one, but winners are announced every week, and the same sort of math is involved in calculations regarding evolution. See Chapter 2 of The Making of the Fittest.

    For an additional example and discussion of the importance of genetic drift/neutral evolutionary pathways, see Joe Thornton's comments regarding Behe's misinterpretation of his research results at Carl Zimmer's blog here: http://blogs.discovermagazine.com/loom/2009/10/15/the-blind-locksmith-continued-an-update-from-joe-thornton/)

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  18. Jud:
    Your analogy of the lottery announcing winners (analogy a la Dr. Carroll) is hardly reflective of biological reality. Rather than attempt to draw vaguely relevant analogies we should rest our arguments upon what we actually observe in the real world of life. And what we do observe is this: that the more and more specifically arranged amino acids a novel protein function requires in order to maintain that function, then the less and less likely it is that that function will evolve in vivo. This is an observable fact, and hence your argument has little relevance to the evolution of highly specified protein-based systems.
    Moreover, if your argument really was applicable to biological reality than there would be no such thing as the sampling problem [see for example: Maynard, Smith J. Natural selection and the concept of a protein space. Nature 225 563–564 (1970)].

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  19. Regarding Sigmund's statement that,
    "The problem for the ID proponents is that it is relatively easy to demonstrate the evolution of simpler examples of 'IC'...Once we have demonstrate that simple 'IC' can evolve then there is no fundamental reason why highly complex 'IC' cannot evolve - after all its just an accumulation of smaller 'IC' events."

    This brings us back to the exponential nature that is manifested in the evolution of novel protein functions. It is entirely true that we see simple IC protein functions evolving -- such as a novel function that requires two specified amino acid residues -- but it is also an empirical observation that the more specifically arranged amino acid residues a novel function requires than the more implausible the evolution of such a system becomes. Complex IC is indeed just an accumulation of smaller IC events however it is an exponential accumulation, and hence it is rather unrealistic to expect Darwinian evolution to be able to produce high levels of IC. If one accepts the observation of an exponential nature behind protein function evolution, then what may I ask, is the implication for a protein function that requires several hundred specifically arranged amino acid residues?

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  20. After all, what are the odds that out of a few billion people in the world, Mr. and Mrs. Luskin would meet, marry, and have a bouncing baby boy (reduce the scant probability by half right there), Casey?

    The odds are [1/(10^120)], that's why although Casey is complex, he is not specified and definitely not intelligent!

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  21. " If one accepts the observation of an exponential nature behind protein function evolution"
    Exponential increases in complexity meaning a single change is followed by two simultaneous changes which is followed by four simultaneous changes, and so on?
    I most certainly don't accept that and neither does the scoentific community. Perhaps I've misunderstood what you mean by "exponential" - can you be more specific, give a few real life examples where the increase of complexity has not been linear but has in fact been exponential.

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  22. "the IDiots almost always set up impossible criteria reflecting their fundamental misunderstanding of evolution."

    OK lets accept as true this sentence with the built-in invective terminology. So we have thousands of ID supporters with advanced degrees in science, engineering, and including M.D.'s with a "fundamental misunderstanding of evolution."

    This indicates a situation in which there is no hope for secondary students to have a "fundamental" understanding of evolution, except maybe for a few geniuses. So this means that all of this instruction in our high schools is a total waste, and a source of terrible frustration for the majority of students. Oh wait a minute, I forgot. Maybe the real reason for this instruction is not so they have a better time finding a job, but rather to subtly attack their irrational beliefs.

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  23. Sigmund:
    "Perhaps I've misunderstood what you mean by "exponential" - can you be more specific, give a few real life examples where the increase of complexity has not been linear but has in fact been exponential."

    Excellent question. I would also be curious as to how this exponential increase is measured, and if there are any citations for this being done.

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  24. "Exponential increases in complexity meaning a single change is followed by two simultaneous changes which is followed by four simultaneous changes, and so on?"

    I think I haven't been sufficiently clear on this point. By the phrase "exponential nature behind protein structure evolution" I mean that the odds of a novel protein function that requires only one specific amino acid substitution at a particular position in a protein chain evolving are quite large; the odds however of a novel protein function evolving that requires more and more amino acid substitutions (working in concert) decrease exponentially. This, I might add, is in fact an empirical observation in biology, and for this reason we see many novel protein functions evolving in vivo that require only one amino acid substitution, fewer cases of novel protein functions evolving that require two specified amino acid substitutions, and so on.

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  25. "Excellent question. I would also be curious as to how this exponential increase is measured, and if there are any citations for this being done."

    I do not believe I ever mentioned exponential "increase", and for further elucidation of what I meant when I said "exponential nature" see my reply to Sigmund. A

    Regarding a citation, I refer both yourself and Sigmund to White, Nicholas J. Antimalarial drug resistance. J. Clin. Invest, 113(8):1084–1092 (2004).

    The per-parasite probability of P. falciparum evolving resistance to atovaquone is ~10^12, and atovoquone resistance is the result of a single amino acid substitution (intriguingly, higher mutation rates are recorded in the lab). Moreover, the per-parasite probability of P. falciparum evolving resistance to chloroquine is ~10^20, and two specific amino acid substitutions are required for said resistance to evolve. Here we see that there is obviously much more of an exponential nature behind protein function evolution and not a linear nature manifested in the evolution of novel protein functions.

    Also, to belabor the obvious, I quote the paper I cited:
    "...if the per-parasite probabilities of developing resistance to drug A and drug B are both 1 in 10^12, then a simultaneously resistant mutant will arise spontaneously every 1 in 10^24 parasites."

    I.e. there is an exponential decrease of odds of evolution of a novel protein function, rather than a linear one; if it was a linear one, then the per-parasite odds of simultaneously evolving resistance to drug A and drug B would be (obviously) 2.0 x 10^12, and not 10^24.

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  26. So, you are saying that the odds of evolving a resistance to a specific drug is the same as the odds of evolving any new protein?

    I have no problem with the evolution of a specific protein to deal with a specific drug being quite unlikely and difficult, I do have a problem with attempts to equate this with evolution in general as a means of arguing against it.

    If you are not doing this, then never mind. But if you are not doing this, I have to wonder what your point it?

    I am still waiting to see if any anti-evolution types have actually actually 'proved' that the probability is LESS THAN 10^(-120) (in ref. to the main post).

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  27. By the way, Livingstone - what is 'darwinism'? You say you are a critic of it.

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  28. "So, you are saying that the odds of evolving a resistance to a specific drug is the same as the odds of evolving any new protein?"

    Not per se', since the odds of evolving resistance to a specific drug depend on the drug deployed. I am merely saying that the odds of a novel protein function evolving decreases exponentially the more and more specific amino acid residues that novel function requires, in order to maintain that function.
    For example, the odds of a novel protein function evolving that requires only one amino acid substitution are greater than the odds of a novel protein function evolving that requires two specifically arranged amino acid residues.
    Thus, the evolution of novel protein functions are not a problem in the Darwinian synthesis if those novel functions only depend on a few specified amino acids. However, if a protein function requires several dozen very specifically arranged amino acid residues working in concert in order to function, then this does present a problem to the Darwinian synthesis.

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  29. "By the way, Livingstone - what is 'darwinism'? You say you are a critic of it."

    By Darwinism I mean the notion that everything we observe in the biological world are purely the result of stochastic processes, and I am critical of that notion.

    On a different topic, I might add that intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system. This is because there have been no more than 10^39 bacterial cells in the history of life on earth.

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  30. Livingstone Morford writes:

    Your analogy of the lottery announcing winners (analogy a la Dr. Carroll) is hardly reflective of biological reality.

    Yeah, 'cause after all, what the heck does Sean B. Carroll know about the mathematics relevant to evolution?

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  31. Livingstone, my previous reply was sardonic, so I thought I would provide a serious response to your objection.

    Because you seem to be having trouble with the concept, I'll try to simplify the parallel between lottery probabilities and evolutionary probabilities.

    They don't announce every week that you've won the lottery, do they (more's the pity)? The odds against a particular individual winning the lottery, let alone once a week, are astronomical. But the odds against someone winning the lottery are quite small - it's more usual to have a week with a lottery winner than without. So there is a huge difference between the odds of a particular individual succeeding, and at least one of a group succeeding.

    Same thing with evolution. It's completely backwards and mathematically incorrect to look back at an evolutionary step, or a series of them, and calculate the probability of that exact outcome or sequence of outcomes - that exact "evolutionary lottery winner" - just as it is incorrect to look back at a particular Powerball winner, ask how likely it is that this particular person would win, and take the answer as the odds of having a Powerball winner at all. (You can tell it's mathematically incorrect, because if it was correct as a matter of mathematical probability, no one would win the Powerball for millions or billions of years.)

    The correct procedure is to view things prospectively and consider the probability that some mutation(s), beneficial, neutral, or even slightly deleterious in nature, will occur from generation to generation and accumulate over time. That probability, of course, is a near-certainty, just as it is more likely than not that someone will win the lottery this week.

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  32. Livingstone:

    "Not per se', since the odds of evolving resistance to a specific drug depend on the drug deployed."

    Um, right, which is exactly what I wrote. Very astute. What if resistence does not depend on an altered amino acid sequence at all, but instead merely the increased expression of a protein already being produced?


    "I am merely saying that the odds of a novel protein function evolving decreases exponentially the more and more specific amino acid residues that novel function requires, in order to maintain that function."

    And if a novel protein function doesn't require that much change?
    Well, I guess your whole ideology falls apart, eh?

    "For example, the odds of a novel protein function evolving that requires only one amino acid substitution are greater than the odds of a novel protein function evolving that requires two specifically arranged amino acid residues. "

    And what if a novel protein function does not actually "require" ANY specific amino acid change?

    "However, if a protein function requires several dozen very specifically arranged amino acid residues working in concert in order to function, then this does present a problem to the Darwinian synthesis."


    Providing, of course, anyone actually indicated, implied, or actually thought that evolution operated that way - by requiring some specific outcome before the fact.

    For all your verbosity, you seem monumentally underinformed as to what evolution actually entails.

    .............
    By the way, Livingstone - what is 'darwinism'? You say you are a critic of it.


    "By Darwinism I mean the notion that everything we observe in the biological world are purely the result of stochastic processes, and I am critical of that notion."


    So, you are critical of the strawman that you erected. Classic.


    "On a different topic, I might add that intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system."

    Really? So if one were to concoct a formula showing that the odds of Livingstone existing are less than that number, we must conclude that you werre not born?

    "This is because there have been no more than 10^39 bacterial cells in the history of life on earth."

    Counted them, did you?

    And how, pray tell, do you suppose an Intelligent Design advocate might go about showing this in a way that does not entail erecting strawmen, using idiosyncratic definitions, using terms and concepts in unorthodox ways, and relying on unwarranted and unjustified assumptions and unexplained values?

    Thanks.

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  33. Jud:
    Your analogy still suffers from the inability of that analogy to be reconciled with biological reality. The question boils down to this: do you or do you not accept the reality that the more and more specifically arranged amino acid residues a protein function requires than the less and less likely it is for that protein function to evolve? While your argument stands on an analogy, my argument rests upon the peer-reviewed literature.

    Assume that there is a total of 1 million lottery tickets (I don’t know much about how lotteries work so if I make a glaring error regarding the lottery then that’s the reason), and 1 million people each with 1 lottery ticket. The odds of a particular person winning is 10^-6. However, the odds of someone winning is 1. Hence, there will be a winner every week.

    How does this pertain to the realm of biochemical evolution? It doesn’t. The difference between the analogy of the lottery and molecular evolution is that in evolution we are dealing with ratios which are far more different than the ratios involved in the lottery example. In the lottery analogy, the ratio of lottery tickets to “contestants” is 1:1, and hence the odds of someone winning is 1. However, in molecular evolution the ratio of say, functional amino acid sequences to nonfunctional amino acid sequences is much greater, i.e. there are far more potential nonfunctional amino acid sequences than potential functional amino acid sequences [see Radford 2000; Tracewell and Arnold 2009]. This is where your analogy falls apart.

    References:

    Radford Sheena E. Protein folding: progress made and promises ahead. Trends in Biochemical Sciences, 25, 12: 611-618 (2000).

    Tracewell CA, Arnold FH. Directed enzyme evolution: climbing fitness peaks one amino acid at a time. Curr Opin Chem Biol. 2009;13:3–9.

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  34. "What if resistence does not depend on an altered amino acid sequence at all, but instead merely the increased expression of a protein already being produced?"

    This has absolutely no relevance to my argument from the empirical observation that there is an exponential nature behind novel protein function evolution.

    “And if a novel protein function doesn't require that much change?
    Well, I guess your whole ideology falls apart, eh?”

    Apparently you didn’t read much of what I posted above; apparently you didn’t even see me citing some three peer-reviewed papers referring to the evolution of novel protein functions that do not require that much change; otherwise you wouldn’t be making such an irrelevant argument. If a novel protein function requires only a few specifically arranged amino acid residues, then such a function is more likely to evolve than a function that requires a large number of specifically arranged amino acid residues.

    “And what if a novel protein function does not actually ‘require’ ANY specific amino acid change?”

    Unless you are referring to a protein that would bind to a receptor or something pertaining to that effect, in which case a change in the receptor could prompt a change in protein function, then your argument is irrelevant for the simple reason that for a novel protein function to evolve then more or less specified amino acid changes are required. I suggest you look into the thermodynamic hypothesis before bringing this argument to the table.

    “Providing, of course, anyone actually indicated, implied, or actually thought that evolution operated that way - by requiring some specific outcome before the fact.”

    It is an empirical observation of the biological world that we see many novel protein functions evolving that require only one specifically arranged amino acid residue, less novel protein functions evolving that require two, even less that require three, and so on. The argument you advance above cannot be reconciled with the empirical observations we see in protein function evolution.

    “So, you are critical of the strawman that you erected. Classic.”

    Stochastic processes are defined as those processes that have a random variable. Does Darwinism have a random variable? Yes it does; namely, random mutation, not to mention genetic drift and the like. I am entirely aware that Darwinian processes are not entirely random. As such, I do not believe your charge that I am making a strawman holds.

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  35. “Really? So if one were to concoct a formula showing that the odds of Livingstone existing are less than that number, we must conclude that you werre not born?”

    See my response to Professor Larry Moran at my blog BioTalk.

    “Counted them, did you?”

    Regarding the number 10^39, I refer you to Whitman W.B, Coleman D.C, Wiebe W.J. Prokaryotes: the unseen majority Proc. Natl Acad. Sci. 95(12): 6578-6583 (1998).

    “And how, pray tell, do you suppose an Intelligent Design advocate might go about showing this in a way that does not entail erecting strawmen, using idiosyncratic definitions, using terms and concepts in unorthodox ways, and relying on unwarranted and unjustified assumptions and unexplained values?”

    In order to demonstrate the implausibility of a Darwinian origin of a particular biochemical system, the specificity of that biochemical system would have to be determined through various methods: directed enzyme mutagenesis being one of the major methods, with sequence alignments (to determine sequence conservation) being another method, albeit a less powerful one.

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  36. I would just like to comment that the malaria drug resistance scenario outlined by Livingston Monford is completely retarded. And I say this in the nicest way possible... The scenario as set forth does not coincide with any "real world scenario" that would arise. Speaking on observed human use of anti-biotics and anti-viral drugs, it is rare that a treatment group adheres 100% to any treatment regiment. Meaning that one person in the group not taking both medications, as outlined, would be infected with Malaria resistant to one of the drugs in question. The survivors of this group of Malaria would grow and replicate with the new resistance protein for the first drug and then be exposed to the second drug. This second drug would kill all the bacteria with the drug resistance to Drug 1, but would not kill any bacteria with any mutations offering resistance to Drug 2. Thus, these last stragglers would have the protein for Drug 1 resistance and now Drug 2 resistance. This group would grow and replicate with both proteins offering resistance against both drugs. I say this because the scenario you lay out is not a real world scenario. Bacteria are not going to need to make multiple protein changes in one generation. The bacteria may kill ONE host or all hosts that are using the drugs treatment 100% of the time. But in the real world, hosts do not act rationally or as expected 100% of the time. Also, now that I think about it, no antibiotic is 100% affective in any host, so even the retarded scenario you envision is moot.

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  37. “The scenario as set forth does not coincide with any "real world scenario" that would arise.”

    The scenario I outlined (I assume you are referring to my blog posts) is not meant to mirror a “real world scenario” down to the minor details.

    “Speaking on observed human use of anti-biotics and anti-viral drugs, it is rare that a treatment group adheres 100% to any treatment regiment.”

    True, but irrelevant to the topic at hand. You go on to argue that “Bacteria are not going to need to make multiple protein changes in one generation.”

    Not meaning to be a bio-pedant exactly, but malaria is not bacteria. At any rate, the problem with your argument is that you are “missing the point.” My point was to demonstrate that the rationale behind my reasoning is in line with the peer-reviewed literature. That said, it might interest you to know that malaria researchers are well aware of the problems with polyvalent drug treatments – the problems you outlined. Thus, we see that White (2004) says,
    “ As there is a cumulative total of less than 1020 malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years — provided the drugs always confronted the parasites in combination.” [emphasis mine]

    References:

    White, Nicholas J. Antimalarial drug resistance. J. Clin. Invest, 113(8):1084–1092 (2004).

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  38. For those interested in macro-machines, here's a fresh look at Behe's mousetrap and its hitorical predecessors (real ones, not figments of just-so stories).

    See:
    "Exploring Mouse Trap History"
    Evolution: Education and Outreach
    DOI: 10.1007/s12052-011-0315-8

    http://www.springerlink.com/content/k6pv4mn47t65154x/

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