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Author | Topic: Behe's Irreducible Complexity Is Refuted | |||||||||||||||||||||||||||
Loudmouth Inactive Member |
quote: The middle ear ossicles are part of the IC hearing system. They transfer sound waves from the outer tympanum to the inner ear via the oval window. If one of these ossicles is removed, the organism would be deaf.
quote: And actin alone does not produce flagellar motion. Fibrinogen alone does not cause blood clotting. However, these are parts of IC systems which Behe referrences. In the same way, I am referrencing parts of an IC system that do not produce the function by themselves, but do produce the function in conjunction with other parts in the system.
quote: Actually, I would like your comment on this part of my argument (honest cricisms, I really mean it). My argument is that for Behe to claim that biomolecular IC systems (eg; blood clotting, flagella) came about through intelligent design, he must produce the history of these systems. In other words, he must show how these systems came about through huge steps that could only come about due to ID. Or, what evidence does Behe have that shows these IC systems coming about in "one fell swoop". It is very obvious that he, nor anyone else, has this evidence. Behe's contention that IC systems came about swiftly, and possibly in one fell swoop, is not based on evidence, just on his ad hoc hypothesis. 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. In the case of the middle ear ossicles, it happens over millions of years and in gradual steps. Not only is the integrity of the hearing system kept intact, but the jaw is also able to articulate in ways that won't hinder prey capture or mastication. This is the type of co-aptation that other have hypothesized about possible pathways towards biomolecular IC systems. That it is observable in the fossil record seems to support such a pathway. In conclusion, Behe's contention that IC systems come about in one fell swoop is not evidenced, only hypothesized. IC systems found in the fossil record come about through slow and gradual morphological changes. It seems more likely, through observed changes in the fossil record, that IC systems come about through gradual steps culled by millions of years of evolution.
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DNAunion Inactive Member |
quote: 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?
quote: But I didn't say that. I said the function of the ossicles themselves is not hearing, and that is correct.
quote: 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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NosyNed Member Posts: 9003 From: Canada Joined: |
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.
Are you saying, actually saying, that you don't know what the ossicles do?
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DNAunion Inactive Member |
quote: 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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DNAunion Inactive Member |
quote: 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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DNAunion Inactive Member |
quote: 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
quote: and
quote: 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 Proteins Chapter 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 Chemotaxis Molecular Cell Biology: Fourth Edition: Harvey Lodish, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell, W. H. Freeman and Co., 2000Chapter 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 Stable All 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 Member Posts: 9003 From: Canada Joined: |
But first, is it the ossicles or is it the complete hearing system that's under discussion?
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. The hearing system is a complex enough system that it has some reasonably distinct subsystems. If an overall system has some subsystem that is IC then the overall system is also IC is it not? If that is true we can consider the whole hearing system as the system under consideration. (in fact, thinking about it that isn't really relevant - the hearing system as a whole, without considering subsystems at all is IC since removing an ossicle makes it fail) If any part of it is removed it doesn't work. In particular if one of the ossicles is removed it doesn't work at all. Does that meet Behe's definition of IC? If not why not?
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DNAunion Inactive Member |
quote: 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?
quote: Wouldn't that make the overall hearing system an integrated system of systems? Note the Behe explicitly rejects such as being IC.
quote: 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.
quote: 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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DNAunion Inactive Member |
quote: But by switching to gross anatomy you are demoting your counter down to an argument from analogy.
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DNAunion Inactive Member |
quote: 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.
quote: quote: quote: quote: quote: quote:
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MrHambre Member (Idle past 1414 days) Posts: 1495 From: Framingham, MA, USA Joined: |
DNAunion quotes Michael Behe:
quote:Since he's a biochemist, perhaps Behe should steal the glory from the evo bios and answer the question himself. I'd venture to say he'd be more likely to make his speech in Stockholm through clarifying this developmental pathway than through declaring it nonexistent. Of course, we're not allowed to subject intelligent design creationism to the same scrutiny he demands of Darwinism. If the best we can currently say of Darwinian pathways is that they are plausible, that's more than we'll ever be able to say of intelligent design creationism. Behe and his online acolytes expect us to believe that since the Darwinian mechanism is adequate at some biological levels but (according to him) not at others, we must recognize the relevance of a mechanism that has never produced anything in biology. These passages reminded me how disappointed I was when I read Behe. He formulated tantalizing challenges to biologists and biochemists, giving us glimpses of the solutions to these billion-year-old mysteries, then simply refused to meet the challenges. In one of the passages quoted by DNAunion, Behe is trying to make us believe that the admittedly miraculous world of the cell is just as prosaic and inert as your garage. With a straight face, he tells us that in the magic microworld, certain biological structures (and, after all, only certain ones) need a micromechanic to tinker them into working order. Everything about this approach is unscientific, lacking the thirst for meaningful discovery that motivates empirical evidential inquiry. His utter lack of initiative is truly self-defeating when he says, "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. Maybe I'm wrong in taking the reptilian-jawbones-to-ossicles homology to be just the sort of key someone like Behe could use to unlock these closed doors, but unfortunately Behe has decided to make a career out of declaring them to be shut for good. regards,Esteban "Design This" Hambre [This message has been edited by MrHambre, 03-09-2004]
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Mammuthus Member (Idle past 6496 days) Posts: 3085 From: Munich, Germany Joined: |
First sentence of abstract
Biochem Biophys Res Commun. 2001 Oct 26;288(2):443-7. Related Articles, Links Association between actin and light chains in Chlamydomonas flagellar inner-arm dyneins. Yanagisawa HA, Kamiya R. Department of Biological Sciences, University of Tokyo, Tokyo 113-0033, Japan. Inner dynein arms in cilia and flagella contain actin as a subunit; however, the function of this actin is totally unknown. Here we performed chemical crosslinking experiments to examine the interaction of actin with other subunits. Six of the seven Chlamydomonas inner-arm dynein species separated by anion-exchange chromatography contain actin and either one of the two previously identified light chains, p28 and centrin, in a mutually exclusive manner. Western blotting of chemically crosslinked dyneins indicated that actin is directly associated with p28 and centrin but not with the dynein heavy chains (HCs). In contrast, p28 and centrin both appeared to interact directly with the N-terminal half of the HCs. Thus it is likely that actin is associated with the heavy chains through p28/centrin. These light chains may well function in the assembly or targeting of the inner arm to the correct axonemal location. Copyright 2001 Academic Press. It is also present in flagella Mol Biochem Parasitol. 2004 Mar;134(1):105-14. Related Articles, Links A novel form of actin in Leishmania: molecular characterisation, subcellular localisation and association with subpellicular microtubules. Sahasrabuddhe AA, Bajpai VK, Gupta CM. Division of Molecular and Structural Biology, Central Drug Research Institute, Lucknow 226 001, India. To study the occurrence and subcellular distribution of actin in trypanosomatid parasites, we have cloned and overexpressed Leishmania donovani actin gene in bacteria, purified the protein, and employed the affinity purified rabbit polyclonal anti-recombinant actin antibodies as a probe to study the organisation and subcellular distribution of actin in Leishmania cells. The Leishmania actin did not cross react with antimammalian actin antibodies but was readily recognized by the anti-Leishmania actin antibodies in both the promastigote and amastigote forms of the parasite. About 10(6) copies per cell of this protein (M(r) 42.05 kDa) were present in the Leishmania promastigote. Unlike other eukaryotic actins, the oligomeric forms of Leishmania actin were not stained by phalloidin nor were dissociated by actin filament-disrupting agents, like Latrunculin B and Cytochalasin D. Analysis of the primary structure of this protein revealed that these unusual characteristics may be related to the presence of highly diverged amino acids in the DNase I-binding loop (amino acids 40-50) and the hydrophobic plug (amino acids 262-272) regions of Leishmania actin. The subcellular distribution of actin was studied in the Leishmania promastigotes by employing immunoelectron and immunofluorescence microscopies. This protein 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. Further, the plasma membrane-associated actin was colocalised with subpellicular microtubules, while most of the actin present in the kinetoplast colocalised with the k-DNA network.These results clearly indicate that Leishmania contains a novel form of actin which may structurally and functionally differ from other eukaryotic actins. The functional significance of these observations is discussed. References to actin and axonemes and dynein were also easy enough to find... textbooks are seldom comprehensive or up to date....
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DNAunion Inactive Member |
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).
quote: 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
quote: 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
quote: 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
quote: 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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NosyNed Member Posts: 9003 From: Canada Joined: |
But by switching to gross anatomy you are demoting your counter down to an argument from analogy.
Could you explain your reasoning here in more detail please? What is being shown is that a system which meets Behe's definition of IC can and did evolve. Therefore it is no longer enough for Behe to say that something is IC to show that it can't evolve. He now has to exhaustively show why a particular system can not evolve. There is nothing about the system itself that demonstrates that it can't evolve.
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Loudmouth Inactive Member |
quote: The system is the middle ear ossicles. The function is transfer of sound from the outer tympanum to the oval window of the inner ear. If one of the ossicles is removed from the mammalian middle ear, this function is lost. This is an IC system. Behe himself does not rule out macroscopic IC systems, therefore macroscopic IC systems can be used as direct evidence.
quote: Yes, there function is the transfer, amplification, and attenuation of sound vibrations. This is the function we will focus on. Whether this is related to hearing or not is irrelevant. What is relevant is that mammals depend on this transfer of sound waves in order to survive.
quote: Burden of proof has been met.
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