Behe's Irreducible Complexity Is Refuted

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Overall, Behe's argument that irreducibly complex (IC) systems can not evolve is refuted by this one example.

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Nope, doesn't even touch Behe's argument since the ossicles don't form an IC system. If someone is going to refute Behe, they need to stick to systems that meet Behe's criteria.

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Yes it does. Remove one part and the whole system (hearing in this case) stops working.

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The function of the ossicles is hearing? Really? That's news to me.If someone is going to claim that a given system meets Behe's definition of IC, one of the first things he/she must do is identify the function of the proposed system. So, what is it? (And no, it's not hearing: the ossicles alone do not produce hearing).PS: I don't know why people don't stick to the systems Behe mentioned in his book: supposedly, he's been refuted on them.[This message has been edited by DNAunion, 03-08-2004]

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No, they do not but they are part of an IC system which does. If one of them is removed or damaged the hearing is affected or gone.

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We need to talk about one system at a time. I didn't read all the posts in this thread, but it was my impression that it was the ossicles that were claimed to be an IC system, not the complete hearing system. So I guess before we agree on the function of the system, we must first agree on what the system is.So everyone, what is the actual system under consideration?

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It is througly disengenuous to suggest that because more is needed that the ossicles are not necessary for hearing.

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But I didn't say that. I said the function of the ossicles themselves is not hearing, and that is correct.

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You seem to think that this doesn't meet the supplied definition that Behe supplied. How does it not in some detail please?

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The burden of proof is upon those who claim it is IC. Now, for them to assert that system X is IC, they must be able to identify the function of the system...they also need to be able to identify the system under consideration.[This message has been edited by DNAunion, 03-08-2004]

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The middle ear ossicles are part of the IC hearing system.

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So your "Refutation" of Behe is that a PART of an (alleged) IC system can evolve? How does that refute Behe?

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Are you saying, actually saying, that you don't know what the ossicles do?

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No, I'm not saying that...I know what they do: I want those making the claims to state it themselves, clearly and unambiguously, so there's no moving the goal posts later.But first, is it the ossicles or is it the complete hearing system that's under discussion?[This message has been edited by DNAunion, 03-08-2004]

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loudmouth: And actin alone does not produce flagellar motion.

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I’m curiouswhere did you hear that actin is involved in flagellar motion? Was it Kenneth Miller? He’s made the claim that actin is a major component of cilia, being involved in ciliary motion. But to the best of my knowledge, it doesn’t.Here’s some of my personal notes on this

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Kenneth Miller: biologists have known for years that each of the major components of the cilium, including proteins tubulin, dynein, and actin have distinct functions elsewhere in the cell that are unrelated to ciliary motion. (bold added, Ken Miller from http://www.millerandlevine.com/km/evol/design1/article.html
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and

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Kenneth Miller: But the individual parts of the cilium, including tubulin, the motor protein dynein, and the contractile protein actin are fully-functional elsewhere in the cell. (bold added, Ken Miller from http://www.millerandlevine.com/km/evol/design1/article.html
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DNAunion: Miller twice mentions the protein actin and calls it a major component of a cilium. But Behe doesn’t even mention actin when discussing the cilium, so why is Miller bringing that protein into the discussion as if it were one that Behe considered to be a required part?Actually, it’s worse for Miller than that: actin is not a major component of cilia. You see, Behe is not the only scientist who doesn’t mention actin when discussing cilia. Over the last couple of days I have read dozens of pages about cilia and microtubules from two molecular cell biology texts and nowhere do I recall any mention of actin (in microfilaments, yes; microtubules, no. in motility by muscular contraction, yes; motility by cilia, no). But before claiming Miller to actually be wrong, I wanted to make double sure, so I spent several hours carefully rereading every sentence of the pertinent sections of both molecular cell biology texts. Here are the topics I reread in full.The World of the Cell: Third Edition: Wayne M. Becker, Jane B. Reece, and Martin F. Poenie, Benjamin/Cummings Publishing Co., 1996
Chapter 20: Cytoskeletal Structure and Function
---Introduction (p644)
---Structural Elements of the Cytoskeleton (p644-645)
---Microtubules (p648-659)
------Introduction
------Structure and Polarity of Microtubules
------The Genetics of Microtubules
------Microtubule Assembly in Vitro
------The Dynamic Instability Model of Microtubule Assembly
------Drug Sensitivities of Microtubule Assembly
------Microtubule Organization, Function, and Regulation in the Cell
------Organization and Maintenance of Cell Shape
------The Role of Dynamic Instability and Capping Proteins in Microtubule Organization
------Regulation of Microtubules by Microtubule-Associated ProteinsChapter 21: Cellular Movement: Motility and Contractility
---Introduction (p675)
---Systems of Motility (p675)
---The Molecular Basis of Motility (p675-676)
---Intracellular Microtubule-Based Movement: Dynein and Kinesin (p678-680)
------Cytoplasmic Microtubules, Motor MAPs, and Axonal Transport
------Motor MAPs and the Transport of Intracellular Vesicles
---Microtubule-Based Motility: The Motile Appendages of Eukaryotic Cells (p702-706)
------Cilia and Flagella
------The Structure of Motile Appendages
------The Sliding-Microtubule Model for Motile Appendages
---The Bacterial Flagellum (p706-709)
------Nature’s Wheel: Locomotion by Rotation
------Flagellar Rotation and ChemotaxisMolecular Cell Biology: Fourth Edition: Harvey Lodish, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell, W. H. Freeman and Co., 2000
Chapter 19: Cell Motility and Shape II: Microtubules and Intermediate Filaments
---Introduction (p795-796)
---Microtubule Structures (p796-802)
------Introduction
------Heterodimeric Tubulin Subunits Compose the Wall of a Microtubule
------Microtubules Form a Diverse Array of Both Permanent and Transient Structures
------Microtubules Assemble from Organizing Centers
------Most Microtubules Have a Constant Orientation Relative to MTOCs
------The [gamma]-Tubulin Ring Complex Nucleates Polymerization of Tubulin Subunits
---Microtubule Dynamics and Associated Proteins (p802-809)
------Introduction
------Microtubule Assembly and Disassembly Occur Preferentially at the (+) End
------Dynamic Instability Is an Intrinsic Property of Microtubules
------Colchicine and Other Drugs Disrupt Microtubule Dynamics
------Assembly MAPs Cross-Link Microtubules to One Another and Other Structures
------Bound MAPs Alter Microtubules Dynamics
---Kinesin, Dynein, and Intracellular Transport (p809-817)
------Introduction
------Fast Axonal Transport Occurs along Microtubules
------Microtubules Provide Tracks for the Movement of Pigment Granules
------Intracellular Membrane Vesicles Travel along Microtubules
------Kinesin Is a (+) End-Directed Microtubule Motor Protein
------Each Member of the Kinesin Family Transports a Specific Cargo
------Dynein Is a (-) End-Directed Motor Protein
------Dynein-Associated MBPs Tether Cargo to Microtubules
------Multiple Motor Proteins Are Associated with Membrane Vesicles
---Cilia and Flagella: Structure and Movement (p817-823)
------Introduction
------All Eukaryotic Cilia and Flagella Contain Bundles of Doublet Microtubules
------Ciliary and Flagellar Beating Are Produced by Controlled Sliding of Outer Doublet Microtubules
------Dynein Arms Generate the Sliding Forces in Axonemes
------Axonemal Dyneins Are Multiheaded Motor Proteins
------Conversion of Microtubule Sliding into Axonemal Bending Depends on Inner-Arm Dyneins
------Proteins Associated with Radial Spokes May Control Flagellar Beat
------Axonemal Microtubules Are Dynamic and StableAll that material on the structure, function, dynamics, and assembly of microtubules; all that stuff on cilia, flagella, axonemes, axonemal dynein, etc.; and yet nothing about actin (at least not in relation to anything of relevance. There were several very brief mentions of actin, such as in one of the introductions where microfilaments, which are made of actin, were briefly contrasted to microtubules, which are not. But the few off-hand mentions were completely irrelevant to the matter at hand: nothing that would rescue Miller).Therefore I feel quite confident in proclaiming Miller to be wrong: it is quite clear that actin is in fact not a major component of cilia. Chalk up another biological boo-boo for Miller.

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NosyNed: The ossicles act as a transmission device between the motion of the eardrum and the oval window of the inner ear. They can both amplify the sound and, if it is too loud, attenuate it.

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That's more than one...which of those would you call the function of the ossicles?Apparently everyone is focussing on force transmission and not amplification since the claims that I have seen here involve deafness and not a mere reduction in hearing.So do we all agree that the function of the ossicles is the transmission of force from the tympanic membrane to the oval window?

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The hearing system is a complex enough system that it has some reasonably distinct subsystems.

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Wouldn't that make the overall hearing system an integrated system of systems? Note the Behe explicitly rejects such as being IC.

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If an overall system has some subsystem that is IC then the overall system is also IC is it not?

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No. Accessory parts can be added to an IC system and in such a case, it would not be the whole system that would be IC, but just the IC core.

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If that is true we can consider the whole hearing system as the system under consideration.

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Does everyone agree that it is the entire hearing system - and not jsut the ossicles - that is the system under consideration?Since there' still some basics to clear up, I'll stop here.

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My method, of using fossilized IC systems, gets around this problem. Since we can trace the morphological changes in these systems (middle ear, in this case), we should be able to judge whether these systems come about slowly over millions of years or in one fell swoop.

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But by switching to gross anatomy you are demoting your counter down to an argument from analogy.

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loudmouth: As his conclusion, Behe claims that these systems can not come about unless every piece evolved at the same time. He ignores the possibility of scaffolding and co-option of function

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Behe does not ignore the possibility of co-option: he considers it and rejects it. From my personal notes...DNAunion: From my many discussions of ID on the net, I knew that it was page 39 where Behe defines IC so that was a good place to start my search for examples of his mentioning the idea of exaptation. I needed to only skim a couple dozen pages to find a couple of examples.This first one is long — most of it is not pertinent to the point, but some may find the context as interesting as the few sentences that support my position.

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Michael Behe: So let us attempt to evolve a bicycle into a motorcycle by the gradual accumulation of mutations. Suppose that a factory produced bicycles, but that occasionally there was a mistake in manufacture. Let us further suppose that if the mistake led to an improvement in the bicycle, then the friends and neighbors of the lucky buyer would demand similar bikes, and the factory would retool to make the mutation a permanent feature. So, like biological mutations, successful mechanical mutations would reproduce and spread. If we are to keep our analogy relevant to biology, however, each change can only be a slight modification, duplication, or rearrangement of a preexisting component, and the change must improve the function of the bicycle. So if the factory mistakenly increased the size of a nut or decreased the diameter of a bolt, or added an extra wheel onto the front axle of left off the rear tire, or put a pedal on the handlebars or added extra spokes, and if any of these slight changes improved the bike ride, then the improvement would immediately be noticed by the buying public and the mutated bikes would, in true Darwinian fashion, dominate the market.

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Given these conditions, can we evolve a bicycle into a motorcycle? We can move in the right direction by making the seat more comfortable in small steps, the wheels bigger, and even (assuming our customers prefer the biker look) imitating the overall shape in various ways. But a motorcycle depends on a source of fuel, and a bicycle has nothing that can be slightly modified to become a gasoline tank. And what part of the bicycle could be duplicated to begin building a motor? Even if a lucky accident brought a lawnmower engine from a neighboring factory into the bicycle factory, the motor would have to be mounted on the bike and be connected in the right way to the drive chain. How could this be done step-by-step from bicycle parts? A factory that made bicycles simply could not produce a motorcycle by natural selection acting on variation — by numerous, successive, slight modifications — and in fact there is no example in history of a complex change in a product occurring in this manner.

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A bicycle thus may be a conceptual precursor to a motorcycle, but it is not a physical one. Darwinian evolution requires physical precursors. (Michael J. Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p44-45)

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Michael Behe:
AN INDIRECT ROUTE
Some evolutionary biologists — like Richard Dawkins — have fertile imaginations. Given a starting point, they almost always can spin a story to get to any biological structure you wish. The talent can be valuable, but it is a two-edged sword. Although they might think of possible evolutionary routes other people overlook, they also tend to ignore details and roadblocks that would trip up their scenarios. Science, however, cannot ultimately ignore relevant details, and at the molecular level all the details become critical. If a molecule nut or bolt is missing, then the whole system can crash. Because the cilium is irreducibly complex, no direct, gradual route leads to its production. So an evolutionary story for the cilium must envision a circuitous route, perhaps adapting parts that were originally used for other purposes. Let’s try, then, to imagine a plausible indirect route to a cilium using pre-existing parts of the cell.

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To begin, microtubules occur in many cells and are usually used as mere structural supports, like girders, to prop up cell shape. Furthermore, motor proteins also are involved in other cell functions, such as transporting cargo from one end of the cell to another. The motor proteins are known to travel along microtubules, using them as little highways to get from one point to another. An indirect evolutionary argument might suggest that at some point several microtubules stuck together, maybe to reinforce some particular cell shape. After that, a motor protein that normally traveled on microtubules might have accidentally acquired the ability to push two neighboring microtubules, causing a slight bending motion that somehow helped the organism survive. Further small improvements gradually produces the cilium we find in modern cells.

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Intriguing as this scenario may sound, though, critical details are overlooked. The question we must ask of this indirect scenario is one for which many evolutionary biologists have little patience: but how exactly?

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For example, suppose you wanted to make a mousetrap. In your garage you might have a piece of wood from an old Popsicle stick (for the platform), a spring from an old wind-up clock, a piece of metal (for the hammer) in the form of a crowbar, a darning needle for the holding bar, and a bottle cap that you fancy to use as a catch. But these pieces couldn’t form a functioning mousetrap without extensive modification, and while the modification was going on, they would be unable to work as a mousetrap. Their previous functions make them ill-suited for virtually any new role as part of a complex system.

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In the case of the cilium, there are analogous problems. The mutated protein that accidentally stuck to microtubules would block their function as highways for transport. A protein that indiscriminately bound microtubules together would disrupt the cell’s shape — just as a building’s shape would be disrupted by an erroneously place cable that accidentally pulled together girders supporting the building. A linker that strengthened microtubule bundles for structural supports would tend to make them inflexible, unlike the flexible linker nexin. An unregulated motor protein, freshly binding to microtubules, would push apart microtubules that should be close together. The incipient cilium would not be at the cell surface. If it were not at the cell surface, then internal beating could disrupt the cell; but even if it were at the cell surface, the number of motor proteins would probably not be enough to move the cilium. And even if the cilium moved, an awkward stroke would not necessarily move the cell. And if the cell did move, it would be an unregulated motion using energy and not corresponding to any need of the cell. A hundred other difficulties would have to be overcome before an incipient cilium would be an improvement for the cell. (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p65-67)

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Michael Behe: Perhaps, though, we are overlooking something. Perhaps one of the parts of a mousetrap was used for some purpose other than trapping mice, and so were the other parts. At some point several parts that were being used for other purposes suddenly came together to produce a functioning trap. And perhaps the components of the intracellular transport system were originally performing other tasks in the cell, then switched to their present role. Could that happen?

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An exhaustive consideration of all possible roles for a particular component can’t be done. We can, however, consider a few likely roles for some of the components of the transport system. Doing so shows it is extremely unlikely that components used for other purposes fortuitously adapted to new roles in a complex system. (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p111)

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Michael Behe: In Chapter 2 I noted thatone couldn’t take specialized parts of other complex systems (such as the spring from a grandfather clock) and use them directly as specialized parts of a second irreducibly complex system (like a mousetrap) unless the parts were first extensively modified. Analogous parts playing other roles in other systems cannot relieve the irreducible complexity of a new system; the focus simply shifts from making the components to modifying them. In either case, there is no new function unless an intelligent agent guides the setup. In this chapter we see that construction of a transport system faces the same problem: the system can’t be put together piecemeal from either new or secondhand parts. (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p112-113)

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Michael Behe: We are led inexorably to the conclusion that even this greatly simplified clonal selection could not have come about in gradual steps.

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Even at this simplified level, then, all three ingredients had to evolve simultaneously. Each of these three items — the fixed antibody, the messenger protein, and the loose antibodies — had to be produced by a separate historical event, perhaps by a coordinated series of mutations changing preexisting proteins that were doing other chores into components of the antibody system. Darwin’s small steps have become a series of wildly unlikely leaps. (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p126)

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Richard Dawkins: As for the evolutionary precursors of the system, both hydrogen peroxide and quinones are used for other purposes in body chemistry. The bombadier beetle’s ancestors simply pressed into different service chemicals that already happened to be around. That’s how evolution works.

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Michael Behe: Although Dawkins gets the better of the exchange [with Francis Hitching], neither he nor the creationists make their case. Dawkin’s explanation for the evolution of the system rests on the fact that the system’s elements happened to be around. Thus evolution is possible. But Dawkins has not explained how hydrogen peroxide and quinones came to be secreted together at very high concentration into one compartment that is connected through a sphinctered tube to a second compartment that contains enzymes necessary for the rapid reaction of the chemicals. (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p34)

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Thanks Mammuthusthat’s one reason I continue to post at these kinds of forumsI’m always learning something new!However, I don’t think these quotes you provided totally clear Miller (or counter me): his claim, made in the context of countering Behe, was that actin was a MAJOR COMPONENT of cilia (which I stressed twice).

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DNAunion: [Miller’s] made the claim that actin is a major component of cilia, being involved in ciliary motion. But to the best of my knowledge, it doesn’t.

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Here’s some of my personal notes on this

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Kenneth Miller: biologists have known for years that each of the major components of the cilium, including proteins tubulin, dynein, and actin have distinct functions elsewhere in the cell that are unrelated to ciliary motion. (bold added, Ken Miller from http://www.millerandlevine.com/km/evol/design1/article.html)
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and

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Kenneth Miller: But the individual parts of the cilium, including tubulin, the motor protein dynein, and the contractile protein actin are fully-functional elsewhere in the cell. (bold added, Ken Miller from http://www.millerandlevine.com/km/evol/design1/article.html)
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DNAunion: Miller twice mentions the protein actin and calls it a major component of a cilium. But Behe doesn’t even mention actin when discussing the cilium, so why is Miller bringing that protein into the discussion as if it were one that Behe considered to be a required part?

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Note the CONTEXT the statements were made in. Miller is acting as if actin were one of the major components of the cilium that Behe listed, but it is not.Now, look at the first sentence of your first quote

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Inner dynein arms in cilia and flagella contain actin as a subunit; however, the function of this actin is totally unknown.

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Since ciliary motion is understood well enough without having to reference actin, and, the function of actin is totally unknown here, then actin shouldn’t be considered a major component of the cilium in the current context.Furthermore, your quote states

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Six of the seven Chlamydomonas inner-arm dynein species separated by anion-exchange chromatography contain actin

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Only 6 out of 7. So according to the authors’ statement, 1 out of 7 didn’t require actin to function, so actin is not a required part of a cilium. If it’s not a required part, it isn’t a major component in the present context.As far as the second quote you posted, it basically boils down to

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This [novel form of actin which may structurally and functionally differe from other eukaryotic actins] was present not only in the flagella, flagellar pocket, nucleus and the kinetoplast but it was also localized on the nuclear, vacuolar and cytoplasmic face of the plasma membranes.

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That’s it: this novel form of actin was present in flagella. It doesn’t state anything about it’s being a major component of the flagellum.Finally, I should point out that Behe mentions in his book that there are something like 40 different proteins associated with cilia/flagella, even though he — like the college cell biology texts I referenced — only mention several (which is why I qualified my statements several times — I realized that actin could be one of the other 30+ proteins: the question was, was actin a MAJOR COMPONENT of the cilium in the context of countering Behe...it appears the answer is still no).

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loudmouth: The system is the middle ear ossicles.

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Well now we have disagreement among the anti-Behe crowd. NosyNed says the system under consideration is the whole hearing system, but you are limiting it to just the middle ear ossicles.Again, before any claims about what is and isn't IC can be made and supported/rejected we must agree on what the system is. Only makes sense, doesn't it?

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Behe himself does not rule out macroscopic IC systems, therefore macroscopic IC systems can be used as direct evidence.

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Behe does rule out macroscopic biological systems from being IC.

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NosyNed: What is being shown is that a system which meets Behe's definition of IC can and did evolve.

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No. What is being CLAIMED is that a system which SUPPOSEDLY meets Behe's definition of IC can and did evolve.

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DNAunion: The burden of proof is upon those who claim it is IC. Now, for them to assert that system X is IC, they must be able to identify the function of the system...they also need to be able to identify the system under consideration.

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loudmouth: Burden of proof has been met.

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No, it hasn't been. There's more to demonstrating that a system is IC according to Behe than just identifying the system (which still hasn't been nailed down by the anti-Behe crowd) and identifying its function (which also has not been nailed down - even you listed multiple functions for the ossicles).[This message has been edited by DNAunion, 03-09-2004]

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loudmouth: The sole function of the entire middle ear system is sound wave transfer.

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But you also said:

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loudmouth: Yes, there function is the transfer, amplification, and attenuation of sound vibrations. This is the function we will focus on.

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So what exactly are you claiming to be the function of the middle ear?

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DNAunion: So your "Refutation" of Behe is that a PART of an (alleged) IC system can evolve? How does that refute Behe?

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loudmouth: The sole function of the entire middle ear system is sound wave transfer. The parts of the mammalian middle ear are the malleus, stapes, and incus. This refutes Behe because this IC system was gradually formed via evolutionary mechanisms over millions of years.

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No, it doesn't refute Behe unless you can show that the system is actually IC according to Behe. Your simply stating over and over that it's IC doesn't make it IC.