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Author
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Topic: The Other Flagellum
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Mike Gene
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Member # 149
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posted 31. July 2003 15:11
THE NEGLECTED FLAGELLUM
The first example of an IC system that Michael Behe provided in his book, Darwin’s Black Box , was the flagellum. While the bacterial flagellum has indeed become a focal point in the debates concerning design, Behe focused most of his attention on the eukaryotic flagellum. How is it that the bacterial flagellum quickly overshadowed the eukaryotic flagellum in the debates about irreducible complexity and design?
A charitable interpretation would note that the bacterial flagellum has received more attention because it looks so much like a product of design. Functioning as a nanoscale version of an outboard rotary motor, even flagellar expert David DeRosier acknowledges “the flagellum resembles a machine designed by humans.” ( Cell 93: 17-20). Given the bacterial flagellum looks like something a human might design, more so than many other molecular machines, it is understandable why this particular machine would attract more interest.
A cynical interpretation would note that the irreducible complexity of the eukaryotic flagellum does not really pose an insurmountable obstacle to Darwinian evolution. Two powerful counterarguments have been developed and many in the ID community have thus quietly shied away from this example. Let’s consider the two arguments.
Different Patterns
When Cavalier-Smith reviewed Behe’s book in 1997, he responded to Behe’s claims about the flagellum by essentially setting up a straw man. Cavalier-Smith was under the impression that Behe was arguing that the 9+2 pattern of microtubules represented the IC essence of the flagellum. Cavalier-Smith then easily knocked this down by pointing out that there are functioning flagella that don’t show this pattern. Ken Miller picked it up from here. In his book, Finding Darwin’s God, Miller finds himself “amused” at this argument, adding, “A phone call to any biologist who had ever actually studied cilia and flagella would have told Behe that he’s wrong in his contention that the 9+2 structure is the only way to make a working cilium or flagellum.” (p.141). Miller then cites several examples of flagella that don’t show this 9+2 pattern, including the 9+0 arrangement from eel sperm and the much reduced 3+0 arrangement from the protozoan Diplauxis.
Unfortunately, Behe’s argument never rested on the 9+2 flagellar arrangement. Contrary to Miller’s assertion, not once did Behe contend that the 9+2 structure is the only way to make a functioning flagellum. Behe does include an illustration of the 9+2 arrangement, but this is a standard illustration borrowed from a standard biochemistry textbook. That’s hardly justification for portraying Behe’s argument as being dependent on the 9+2 arrangement as the focus of his discussion of irreducible complexity. This is especially clear in light of the fact that Behe spells out the “IC recipe” of the eukaryotic flagellum on pp. 64-65:
quote:
What components are needed for a cilium to work? Ciliary motion certainly requires microtubules; otherwise, there would be no strands to slide. Additionally, it requires a motor, or else the microtubules of the flagellum would lie stiff and motionless. Furthermore, it requires linkers to tug on neighboring strands, converting the sliding motion into bending motion, and preventing the structure from falling apart. All of these are required to perform one function: ciliary motion.
Behe thus reduces the cilium to a three-component IC system. And given that the examples cited by Miller all include these three parts, they hardly amount to an effective response to this argument. The Cavalier-Smith/Miller response seems to be a classic example of raising a straw man for the purpose of knocking it down. However, there is something here that I will explore below.
The Cooptable Toolkit
If we take Behe’s list of IC components, they really don’t seem to pose much of an obstacle for Darwinian evolution. This is because two of the three components are also known to function apart from the flagellum. Microtubules (composed of the protein tubulin) are needed for ciliary function, as Behe notes, but they also play many essential roles in the cytoplasm of all eukaryotes. For example, microtubules are intimately involved in the organization of the cytoplasm and the separation of chromosomes during mitosis. This means that this IC component could have theoretically existed long before flagella existed. The same holds true for the motor, dynein. Cytoplasmic versions have been identified and they function to transport cargo inside the cell. This basic “house-keeping” function could very well have also existed before the existence of flagella. All that is needed are linker proteins, and there are scores of proteins that fulfill this function inside the cytoplasm. Thus, it would not be hard to imagine these three components, or duplicated (and tweaked) versions of these components coming together through cooption. The standard story here is that some form of protrusion on the cell surface could first be formed, creating some type of selectable function (adherence, increasing cell surface area, enhancing the ability of cells to remain suspended, etc.) We could point to the axopodia,of certain protozoa as examples. This protrusion would then associate with the motor proteins to begin movement. Natural selection would then fine tune the structure over billions of years.
While the story appears quite plausible, it is also worth mentioning that Behe anticipated this explanation in his book and addressed it accordingly (pp. 66-67). He points out that the story is much too vague and it is easy to envision multiple problems were we to get more specific. In another words, if the story breaks down upon attempting to flesh it out, the story ceases to function as a counter-argument against IC. Thus, from Behe’s perspective, until someone fleshes out the story with details, there is no reason to think it maps to reality and the IC obstacle remains.
One can be both critical and sympathetic to this type of response to the cooption story. From the critical perspective, the demand for such details seems excessive, as much of this detail will have been lost in history. Furthermore, the shift to details detracts from the simplicity of the IC-to-ID inference, as we’ve moved from simply scoring IC components to accounting for their history. From the sympathetic perspective, certainly the vague account as listed above cannot be considered a robust explanation. As it stands, it really is a “just-so” story that may only reflect the human brain’s tremendous ability to imagine accounts. After all, the causal explanation for the origin of flagella must be situated in history. Thus, depending on one’s expectations concerning evolutionary explanations, the challenge posed by the IC flagellum will be assessed differently.
But before moving on, I would like to address an element of the story not discussed by Behe. The cooption story conveys the impression that evolving cilia/flagella would be rather easy. All the parts already exist in the cytoplasm and the selective benefit from a protrusion would be widely enjoyed by all sorts of protozoa, who all could benefit from improved adherence, increasing cell surface area, and enhancing the ability of cells to remain suspended. Thus, the story would seem to predict that such proto-flagellar protrusions would be fairly ubiquitous among the various major groups of protists, even independently evolving on many different occasions across deep time. Yet as far as I can tell, such structures are not common at all. That people must point to axopods actually undercuts the argument.
There are three things worth mentioning about axopodia. First, they appear to be largely restricted to two of the eighteen protozoan phyla, Heliozoa and Radiozoa [1]. Secondly, axopodia are not primitive protrusions in any sense. They are very effective organelles used to capture prey, acting much like molecular tentacles. For example, if an protozoan comes into contact with an axopod, the axopod quickly retracts, reeling in the protist for delivery to food vacuoles. In other words, axopodia are rather specialized features. The limited distribution and specialization of such structures argue that they are derived, not primitive. What’s more, the contractile activity of axopodia is not mediated by dynein nor is it ATP-dependent, but instead it appears to be dependent on calcium [2], giving us no reason to connect axopodia to flagella.
The third point related to axopodia is to wonder why they have not evolved into flagella, given they have all the ingredients of the cooption story in play. Long cell extensions built around microtubules. Bending has been observed during contraction. And as one page notes:
quote:
Although this microbe lacks locomotory structures like cilia and flagella, it can move slowly by motion of stiff axopodia or by floating along in the water current. [3]
The axopodia are also moonlighting as motility organelles. There would thus appear to be a smooth slope up the fitness landscape to some form of flagellum. Simply follow the cooption story – duplicate a motor protein and a linker, toss them into axopod, it will start wiggling, and the rest is smooth selective sailing. Yet Actinophryidae have no flagella. Neither do Radiolaria (except when specialized reproductive cells are formed). But there are Helizoans that have both flagella and axopods, indicating that the existence of axopods does not preclude the existence of flagella.[4] The fact that many protozoa with axopodia have not evolved flagella, when the stage has been set to do so for a billion years or so, clearly indicates something is missing from the cooption story. Behe was right in asking for more details.
Return to IC
Behe scores only three part for the flagellum: microtubule, motor, and linker. Yet this list would seem to seriously underestimate the complexity of the flagellum. Behe later recognizes this:
quote:
Above I noted that the cilium contains tubulin, dynein, nexin, and several other connector proteins. If you take these and inject them into a cell that lacks a cilium, however, they do not assemble to give a functioning cilium. Much more is required to obtain a cilium in a cell. A thorough biochemical analysis shows that a cilium contains over two hundred different kinds of proteins; the actual complexity of the cilium is enormously greater than what we have considered. (p. 72)
This count actually comes from the study of the green algae, Chlamydomonas reinhardtii, where approximately 250 proteins were detected in the flagellum.[5] However, about half of these have not been detected through genetic screens using nonmotile mutant strains, suggesting that approximately 125 are both essential and specific to the flagellum. If only 10% of these components form an IC core that resists explanations thought cooption and/or duplication, it would seem IC does indeed pose a serious problem for a Darwinian explanation.
Let’s focus briefly on dynein. Dynein itself is actually a complex motor, typically consisting of two heavy chains, 2-4 intermediate chains, and several light chains. The heavy chains constitute the motor and function in an ATP-dependent fashion, while the other chains function as adaptors for binding/transporting cargo. The modular construct makes sense from a design perspective and would also seem to allow dynein to be a good target for gene duplication/divergence, extending its reach with evolution. Thus, it is not surprising that there are many different variants of dynein playing roles in different processes. Yet all the variants fall into two basic categories – axonemal (flagellar) and cytoplasmic. As noted above, this makes it easy to envision a cytoplasmic variant being duplicated and tweaked to become a axonemal motor. But perhaps things are a little more complicated than this.
If we consider only the dynein heavy chains, Chlamydomonas possesses 16 different versions. Two are cytoplasmic and the other fourteen are associated with the flagellum. [6] The dyneins are situated in specific regions of the flagellum and play different functional roles. This raises the question of whether or not a truly “wiggling” flagellum could be formed from using only one type of dynein (the original duplicated version of the ancestral cytosplasmic form in the cooption story). For example, mutations in two of the axonemal heavy chains resulted in short, paralyzed flagella that would cause the cells to sink in liquid medium. [6] And thus far, comparative data indicate multiple axonemal dynein forms coincided with the origin of flagella:
quote:
The size of the Dhc gene family in Chlamydomonas is comparable with that found in other species such as sea urchin (14), Paramecium (12), Drosophila (>7), rat (13–15), mouse (11), and humans (>8) (Asai et al., 1994 ; Gibbons et al., 1994 ; Rasmusson et al., 1994 ; Tanaka et al., 1995 ; Andrews et al., 1996 ; Vaisberg et al., 1996 ; Vaughan et al., 1996 ; Neesen et al., 1997 ). The remarkable conservation of the Dhc gene family between such diverse organisms is consistent with the proposal that the Dhc gene family diverged into a small number of groups relatively early in the evolution of eucaryotes, but after these groups were established, they remained largely unchanged (Gibbons, 1995 ). [7]
Furthermore, it is also becoming clear that some of the dyneins are not directly involved in motility, but rather in the assembly of the flagellum. Consider the light chain LC8 of outer arm axonemal dynein in Chlamydomonas. It’s a small, highly conserved protein as evidenced by the 90% sequence identity seen in humans, Drosophila melanogaster, Caenorhabditis elegans, and Chlamydomonas . [8]. Genetic deletion of this gene product in Chlamydomonas results in the formation of stumpy, non-functional flagella. Yet the morphology, cell division, and growth of these cells is not altered. A similar phenotype was seen when one of the heavy chain genes, cDhc1b, was deleted. [7]
While gene duplication followed by divergence remains a very plausible explanation for the origin of flagellar dyneins, one has to wonder if a more detailed analysis would detract from the plausibility of this explanation. For example, if a flagellum requires two distinct dyneins, one for flagellar function and one for flagellar assembly, might we have to invoke to separate, concurrent gene duplication events to provide this machinery?
IC Assembly
As we begin to better understand flagellar formation, a distinct IC theme is appearing. Eukaryotic flagella form at the tip, posing a logistical assembly problem. Basically, how do you get about 250 different proteins into the flagellum such that they assemble in a very specific fashion? Many of the pieces are partly assembled at the base of the flagellum and then transported into the flagellum by a specialized pathway known as Intraflagellar Transport (IFT). The basic ingredients are a kinesin-II motor that shuttles precursors into the flagellum, a dynein motor (cDhc1b)that shuttles things back out, and an IFT “raft” that functions much like the trailer on a truck, carrying the material in/out of the flagellum [9]:
The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly. If you knock out the kenesin-II (also known as fla10), no flagella assemble (the phenotype of called “bald”), as the machine for moving the material into the flagellum is missing. If you knock out the transport dynein, stumpy, non-functional flagella form, as material (including the kinesins) is not trucked out of the flagella and thus accumulate into a disordered tangle.
Even more intriguing are the IFT rafts. These particles are composed of 16 different proteins, some large and some small. They can be isolated as two distinct complexes: A and B. Complex A contains IFT 144, IFT140, IFT139, IFT122A, IFT122B, and IFT43. Complex B contains IFT172, IFT88, IFT81, IFT80, IFT74/72, IFT57/55, IFT52, IFT46, IFT27, and IFT20. The sequences of many of these proteins are conserved among the protozoa, nematodes, and vertebrates [10]. Genetic manipulations in green algae, whereby the genes are essentially knocked out, demonstrate the important of these proteins. For example, removal of IFT88, IFT172, IFT140, and IFT52, result in the same bald phenotype as removal of the kinesin transporter [9]. Removal of the IFT proteins have no other effect on the cell, indicating a flagellum-specific function. (I’ll discuss the IFT proteins in more detail at a later time).
If the assembly of flagella require multiple, independent parts shuttling material in and out of the flagellum, then the serious IC challenge posed by the flagellum may not so much reside in the structure described by Behe, but in the manner this structure is assembled.
More later…..
Cites:
1. Cavalier-Smith T. Kingdom protozoa and its 18 phyla. Microbiol Rev. 1993 Dec;57(4):953-94.
2. Arikawa M, Suzaki T. 2002. Reactivation of Ca2+-dependent cytoplasmic contraction in permeabilized cell models of the heliozoon Echinosphaerium akamae. Cell Motil Cytoskeleton. 53(4):267-72.
3. http://www.microscopy-uk.org.uk/mag/artfeb02/ccactino.html
4. http://protist.i.hosei.ac.jp/PDB/Images/Sarcodina/Heliozoa/Dimorpha/index.html
5. Dutcher, S. 1995. Flagellar assembly in two hundred and fifty easy-to-follow steps. TIBS 11: 398-404.
6. Steven H. Mystera, Julie A. Knotta, Katrina M. Wysockia, Eileen O'Tooleb, and Mary E. Portera. 1999. Domains in the 1 Dynein Heavy Chain Required for Inner Arm Assembly and Flagellar Motility in Chlamydomonas . J. Cell Biol., 146: 801-818.
7. Mary E. Porter, Raqual Bower,Julie A. Knott,Pamela Byrd, and William Dentler. 1999. Cytoplasmic Dynein Heavy Chain 1b Is Required for Flagellar Assembly in Chlamydomonas. Mol Biol Cell. 10: 693–712.
8. Gregory J. Pazour, Curtis G. Wilkerson, and George B. Witman. 1998. A Dynein Light Chain Is Essential for the Retrograde Particle Movement of Intraflagellar Transport (IFT). J. Cell Biol. 141: 979-992.
9. Cole, D. 2003. The intraflagellar transport machinery of Chlamydomonas reinhardtii. Traffic 4: 435-442.
10. Gregory J. Pazour, Sheila A. Baker, James A. Deane,Douglas G. Cole,Bethany L. Dickert,Joel L. Rosenbaum,George B. Witman,and Joseph C. Besharse. 2002. The intraflagellar transport protein, IFT88, is essential for vertebrate photoreceptor assembly and maintenance. JCB 157:103-113.
[ 31. July 2003, 15:24: Message edited by: Mike Gene ]
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yersinia
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posted 31. July 2003 21:56
Hi Mike,
Interesting article. I'll wait for your next installment before replying in detail, but for now I have a few questions:
(1) Do you have any idea what specifies (say) the 9+2 pattern? What makes it 9+2 vs. (say) 8+2 or 10+2? What is the molecular difference that results in 3+0 in one organism, 9+2 in another, 15+3 in another, etc.
As far as I can tell, this pattern may be templated by the centriole, but then the question arises of what specifies the pattern in the centriole. It seems that the centriole can self-assemble without being templated by another centriole (another blow to Margulis' views), so probably the components of the centriole self-assemble into the right shape.
(2) What gene codes for nexin (defined as a blurry spot linking microtubules in electron micrographs)?
I've looked for answers to both questions but have not discovered the answers; I think that the answer is currently "nobody knows". So, question (3) is,
(3) It is fair to demand more detail from evolutionary biology, when very fundamental questions about the makeup and assembly of the cilium remain to be answered? Isn't the demand for detail highly ironic given the complete lack of detail in ID hypotheses?
PS: Have you looked for noncilial homologues of the proteins involved in IFT complexes? Without having investigated the issue at all, I predict that they exist.
PPS: You may enjoy the compliments that Julie Thomas has received from some t.o. regulars on a recent talk.origins thread.
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Pim van Meurs
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posted 31. July 2003 23:36
Mike: If the assembly of flagella require multiple, independent parts shuttling material in and out of the flagellum, then the serious IC challenge posed by the flagellum may not so much reside in the structure described by Behe, but in the manner this structure is assembled.
Perhaps, but what if for instance the export mechanism was the original function and the dynein transport mechanism was what allowed for the evolution of flagellar structures? What makes the IFT a more suitable candidate for IC?
As Yersinia comments "Have you looked for noncilial homologues of the proteins involved in IFT complexes? Without having investigated the issue at all, I predict that they exist."
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Mike Gene
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posted 01. August 2003 00:02
Hi Nic,
I’ll take a quick stab at your questions.
1. AFAIK, the microtubule pattern is specified by a fibrous cytoskeleton that extends into the basal body. Apparently, tektin and nexin are the major components. See RE Stephens, S Oleszko-Szuts and RW Linck. 1989. Retention of ciliary ninefold structure after removal of microtubules. Journal of Cell Science 92:391-402. Yes, it would be very interesting to see what is involved in the variant patterns.
2. I think you are right about nexin, in that the gene(s) for this structural component have apparently not been identified.
3. I’m not demanding precise detail, only working with what we have thus far. I am certainly not arguing that “the flagellum is IC, thus it must have been designed.” But as I note, we are starting to get a decent grip on flagellar assembly (over the last 5-10 years) and it does appear that a somewhat solid IC theme is likewise appearing. The mere fact that two different mechanisms are used to transport things in and out is interesting by itself.
4. The lack of detail on ID hypotheses is not of great concern to me for several reasons. Perhaps the main one is that any hypothesis must begin with a lack of detail.
5. I’m not as quick as your are to attribute similarity to homology. But thus far, I have only been able to track down two IFT proteins – IFT52 and IFT88 (I think more sequences will be coming out in the next year or so). IFT52 doesn’t appear to have any non-ciliary “homologs.” IFT88 does. However, the situation with IFT88 is ambiguous, in that it contains TPR motifs (the source of the similarities), a common protein-protein binding domain found in many proteins in eukarya, archaea, and bacteria. Remember, as Denton pointed out, there are only about 1000-or-so domains and this one is particular handy for transient scaffold formation. From a design perspective, we don’t want our ‘cargo raft’ to be too picky or bind too strongly, as this would defeat the purpose of its ability to deliver (and release) 200-or-so different proteins into the flagellum.
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PvM: Perhaps, but what if for instance the export mechanism was the original function and the dynein transport mechanism was what allowed for the evolution of flagellar structures?
But unlike the bacterial flagellum, we’re not exporting things out of the cell. If you send something in, you need a way to get it out (even for simple turnover reasons).
Also, you have to be careful about defining your “function” as something that is needed by a Darwinian account. That’s a classic error of the just-so story.
What makes the IFT a more suitable candidate for IC?
We have a nicely defined “in/out” problem. We have our hands on several of the genes/gene products involved in the process and knock-out experiments have shown at least six to be crucial. The gene products appear to be universal among flagella and highly conserved.
As Yersinia comments "Have you looked for noncilial homologues of the proteins involved in IFT complexes? Without having investigated the issue at all, I predict that they exist."
I should also mention that the “homolog” angle doesn’t really resolve things. For example, the majority of the bacterial flagellar components don’t have non-flagellar “homologs” (sorry, type III secretion doesn’t count). But that doesn’t tip things in the mind of the ID critics. And that both flagellar kinesin and dynein have cytoplasmic “homologs” doesn’t tip things in my mind. I’ll grant that identifying “homologs” that reasonably predate the IC system in question make it much more plausible to think such a system evolved (the story itself becomes a marker for plausibility). But remember, for me, it’s not the “IC=evolution is impossible to imagine” argument. You’ll get confused quickly if you think that is where I am going.
[ 01. August 2003, 00:08: Message edited by: Mike Gene ]
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Mike Gene
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posted 01. August 2003 00:50
I wanted to add one more thing about flagellar assembly, since it will be relevant beyond the issue of IC (I think its cool and I don’t want to forget, as I’m not sure I’ll be able to get back to this soon).
Flagella are assembled at their tips. For example, in one experiment, cells with full-length flagella, but lacking radial spokes, were fused to normal cells. The radial spoke components, provided by the normal cell, entered into the mutant flagella and begin to assemble at the tip. They were then continuously added from there, moving toward the base. This dynamic is associated with IFT. When a temp-sens. mutant of kinesin-II was shifted to the non-permissive temperature, the fully formed flagella began to shrink and were eventually reabsorbed. With nothing new going in, the only thing happening was that stuff was coming out. The flagella are dynamic structures such that assembly and maintenance blur into one. The wisdom of tubulin.
[ 01. August 2003, 00:51: Message edited by: Mike Gene ]
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Pim van Meurs
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posted 01. August 2003 01:06
Mike: You reject my question as a "just so story" but I would argue that such a just story is not different from the ID hypothesis so far. After all as you said yourself " Perhaps the main one is that any hypothesis must begin with a lack of detail". Or does this not apply to Darwinian hypotheses?
Let me see if I can make myself more clear here. Lets presume that initially the use of kinesin export was not to build a flagellum but rather to export proteins (toxins?) such as for instance the type III secretion? What if dynein was a later addition allowing for flagellar function to evolve. You suggested that
quote:
If the assembly of flagella require multiple, independent parts shuttling material in and out of the flagellum, then the serious IC challenge posed by the flagellum may not so much reside in the structure described by Behe, but in the manner this structure is assembled.
Unless you can eliminate alternative pathways, and science has so far perhaps identified few if any, how can we infer IC or even consider this to be a 'serious IC challenge'?
When asked why the IFT is a more suitable candidate for IC you respond:
quote:
We have a nicely defined “in/out” problem. We have our hands on several of the genes/gene products involved in the process and knock-out experiments have shown at least six to be crucial. The gene products appear to be universal among flagella and highly conserved.
None of these seem to be particularly relevant to identifying IC. Although I agree that the results for the knock-out experiments are necessary for IC, they are not necessarily sufficient. Certainly the cytoplasmic homologogs and the phylogenetic position of the flagellar dynein proteins seems to be quite interesting.
Certainly your suggestion that
quote:
The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly.
seems begging the question since it has not been established that a kinesin only motor could not have a selectable function altough different from flagellar function but unless you want to use the limited definition of IC to refer to 'original function', any suggestions of ICness need to deal with all possible pathways not just the concurrent duplication scenario proposed by you.
I do appreciate your efforts in researching the flagellum but I believe that some of your claims, in absence of much of the necessary data, may be a bit early.
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Mesk
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posted 01. August 2003 05:44
Hi Mike,
Nice post - like yersinia, I'll wait until your second instalment before I comment in detail. I would like to comment on one point that bugged me, however:
quote:
The axopodia are also moonlighting as motility organelles. There would thus appear to be a smooth slope up the fitness landscape to some form of flagellum. Simply follow the cooption story – duplicate a motor protein and a linker, toss them into axopod, it will start wiggling, and the rest is smooth selective sailing. Yet Actinophryidae have no flagella. Neither do Radiolaria (except when specialized reproductive cells are formed). But there are Helizoans that have both flagella and axopods, indicating that the existence of axopods does not preclude the existence of flagella.[4] The fact that many protozoa with axopodia have not evolved flagella, when the stage has been set to do so for a billion years or so, clearly indicates something is missing from the cooption story. Behe was right in asking for more details.
Your reasoning here seems dangerously close to an all-too-common fallacy - the notion that a particular evolved structure represents some Platonic ideal towards which all organisms must be striving. A flagellum is no doubt useful to some organisms, but there is absolutely no reason to expect that it would be advantageous for all organisms. You suggest that the fact that axopodia have not evolved into flagella suggests that co-option cannot readily explain flagellar evolution, but in fact there is a far more straightforward explanation from an evolutionary point of view: for many protozoons, flagellar-like motion is not required and axopodia serve their purposes admirably.
There is (AFAIK, anyway, but feel free to correct me) no particular reason to believe that there are actually any strong selective forces acting to promote the evolution of greater independent motility in these taxa, but even if there were the result would not necessarily closely resemble the standard eukaryotic flagellum. Evolution only "cares" about outcomes, not structural details.
I'm also interested to see how you can make sense of these data from a frontloading perspective, but I imagine that will come in the next instalment.
Mesk.
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Pim van Meurs
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posted 02. August 2003 14:21
It seems that my initial hunch may have some experimental support
quote:
Much of the flagellum lies outside the cell, and so the corresponding protein subunits must be exported. They use a pathway that involves a central channel in the nascent structure itself, and a specialized type III flagellar protein export apparatus that is closely related to the apparatus for exporting virulence factors of many pathogenic bacteria such as Yersinia pestis.
Source
So there is a specialzied type III flagellar protein export apparatus which is used to export the necessary proteins in the flagellum. Could the ancestral form have been merely an 'export apparatus' for proteins for exporting virulence factors?
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Mike Gene
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posted 03. August 2003 12:53
PvM,
I’m not rejecting your question as a just so story. I’m simply pointing out the problem of inventing vague functions for the sole purpose of making just so stories. In this case, you raise the possibility of the export mechanism as the function. Was there independent evidence that led to this hypothesis? Or was it simply an ad hoc reaction to the IC problem? You write:
quote:
Lets presume that initially the use of kinesin export was not to build a flagellum but rather to export proteins (toxins?) such as for instance the type III secretion?
Recall that we are talking about the eukaryotic flagellum. In bacteria, the type III secretory system shuttles proteins out of the cell . In eukaryotes, where does kinesin export proteins out of the cell? Furthermore, unlike bacterial flagella, all of the machinery of the eukaryotic flagellum is contained within the cell.
We approach this differently. Your approach would have me prove “that a kinesin only motor could not have a selectable function although different from flagellar function.” That is, you want me to prove yet another negative. But I don’t view IC as a Rorschach Inkblot Test, assessing your ability to imagine just so stories. If you propose, as a way out of the IC quagmire, a pathway that employs kinesin to export proteins (toxins?) out of the cell, the burden is yours (just for starters) to ground this function in reality.
[ 03. August 2003, 12:54: Message edited by: Mike Gene ]
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Mike Gene
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posted 03. August 2003 13:05
Mesk,
I’m not demanding/expecting that axopodia evolve into the typical 9+2 eukaryotic flagellum. Any form of analogous wiggling motility structure would do.
You write:
quote:
You suggest that the fact that axopodia have not evolved into flagella suggests that co-option cannot readily explain flagellar evolution, but in fact there is a far more straightforward explanation from an evolutionary point of view: for many protozoons, flagellar-like motion is not required and axopodia serve their purposes admirably.
Actually, what I am trying to point out regarding axopodia, cooption, and flagella is that the cooption story may be misleading as a function of its vagueness. Here we have a biological example with all the ingredients of the cooption story. Taking the cooption story at face value, we would predict these structures would evolve into more robust motility structures.
Now, there are two possible evolutionary explanations. There is the environmental explanation that you propose – flagella failed to evolve because the right type of selective pressure never arose. There is also the biological explanation. Flagella failed to evolve for the same reason mice never evolved an exoskeleton – there are intrinsic developmental/genetic constraints.
While the environmental explanation you propose is plausible, it has a couple of things that count against it (in my mind).
First, improved motility would seem to provide a selective advantage across a wide range of environments, given this function would feed into several basic life events – finding mates, catching prey, dispersal, escaping predators. It would be surprising, that over the last millions (billions?) of years, none of the axopodia-containing lineages ever explored these niches given it would be so easy to evolve flagella (as predicted by the cooption story).
Secondly, the environmental explanation seems to take us out of the realm of testing. Raphidiophrys don’t have flagella because there was never selective forces working to make one. How do we know this? Because they don’t have flagella? But many diverse eukaryotes have flagella becaue there were selective forces that worked to make it. How do we know this? Because they have flagella? How can we test the environmental explanation?
The advantage of the biological explanation is we can test it. Let’s dissect the axopodia and compare/contrast to the flagellum. Are axopodia “dead ends” with regard to flagella evolvability? One way to do some serious damage to the biological explanation is to dissect the flagella of Dimorpha. If they are structurally different from the typical eukaryotic flagellum, such that we can infer they evolved independently, yet also similar to the axopodia, the argument of biological constraint has been handed a serious blow. BTW, this is just more of the type of reseach that ID theorists could do.
[ 03. August 2003, 13:09: Message edited by: Mike Gene ]
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Pim van Meurs
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posted 03. August 2003 14:58
Mike: I’m not rejecting your question as a just so story. I’m simply pointing out the problem of inventing vague functions for the sole purpose of making just so stories.
But this applies equally well to ID namely that 'just so stories' become hypotheses etc. ID has the not very enviable task however of calculating the probabilities for all such hypothetical pathways, even 'just so stories'.
Mike: In this case, you raise the possibility of the export mechanism as the function. Was there independent evidence that led to this hypothesis?
Yes.
Mike: Or was it simply an ad hoc reaction to the IC problem?
May I ask if IC was an ad hoc reaction to Darwinism? Perhaps that will answer your question? But let me elaborate somewhat further:
My hypothesis was based on your description of the IFT and was spurred by your claims of ICness which rely after all on the (im)plausibility of (hypothetical) pathways
Mike hits the proverbial nail on the head when he states that 'We approach this differently. Your approach would have me prove “that a kinesin only motor could not have a selectable function although different from flagellar function.” That is, you want me to prove yet another negative. "
Is that not the whole foudation of IC and in fact of the more popular form of intelligent design namely rejecting alternatives to infer a negative? If you are interested in IC from an ID perspective then you should be very interested in people who can provide you with 'just so' stories since the ID inference depdends on being able to reject any and all such stories (chance and regularity pathways).
Of course the burden is on science to find 'just so stories' extend them to hypotheses and test said hypotheses. But your approach seems inherently to depend on rejecting any such attempts at 'just so stories' that may lead to 'hypotheses' while lacking any hypothesis your self. In this case the ultimate 'just so' story seems to me to be 'it could not have evolved but just do not give me any possibilities to explore the validity of this negative claim'.
When you suggested, without much supporting evidence (isn't the burden on you in this variant of 'just so stories'?) that "The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly."
I provided with one (of undoubtfully) many scenarios in which the need for concurrent duplications can be rejected.
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Mike Gene
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posted 03. August 2003 15:42
PvM: When you suggested, without much supporting evidence (isn't the burden on you in this variant of 'just so stories'?) that "The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly."
I provided with one (of undoubtfully) many scenarios in which the need for concurrent duplications can be rejected.
Sure, but you ought not stop here. The next step is to determine if your scenario is grounded in reality. You seemed to recognize this, but unfortunately, appealing to type III systems in bacteria are not relevant. A good place to start is to find an example where eukaryotes use kinesin to export things out of a cell that in someway, foreshadows flagella. Either that, or put a little bit more detail on your story.
Look at it this way. You don’t assign much meaning to ID just so stories, right? Why should I assign much meaning to your just so story?
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Pim van Meurs
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posted 03. August 2003 16:00
Mike asks: Look at it this way. You don’t assign much meaning to ID just so stories, right? Why should I assign much meaning to your just so story?
Because I am not arguing that the IFT seems to require a coinciding gene duplication?
Additionally, IC needs to take 'just so' stories very seriously since ID inference strongly depends on the plausibility of such stories. Once ID presents its own hypotheses beyond elimination of alternatives, such 'just stories' may be evolved in scientific hypotheses and perhaps even theories. Until then I am not sure what to do with 'just so' stories which assert a negative. But when you propose that 'The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly' just so stories are quite relevant.
Thus you are of course free to reject my 'just so story' (which I interpret to be darwinian pathways for IFT are complicated by the perceived need for concurrent duplications) but that would merely affect the plausibility of your 'just so story'. In the mean time science goes on as they say. Until ID's just so stories go beyond a negative claim, they are not of much interest (to me). YMMV or course.
I could spend my time exploring additional 'just so stories' but my intent was merely to address your claim of concurrency which seems to not be a requirement.
[ 03. August 2003, 16:04: Message edited by: Pim van Meurs ]
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Mike Gene
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posted 03. August 2003 16:25
PvM,
I take just so stories seriously if there is supporting evidence for the story. In this case, it is clear you reached into thin air to invent a purpose simply because the IC nature of this assembly process poses a problem. In other words, if you approach the topic expecting a Darwinian solution, you are compelled to invent the bare bone outline of such a story as you have. After all, did anyone suggest this prior to my posting? Thus, the question becomes whether the account you propose is a function of the evidence? Or is it a function of metaphysical needs? It certainly seems the latter is in play.
You write: But when you propose that 'The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly' just so stories are quite relevant.
They become relevant once we get the faintest hint that the story is more than an ad hoc response. Note that I said “we would seem to require.” That is, there isn’t anything in the data that would lead us to choose the gradual explanation you favor (and is required by the Darwinian perspective). The data show that cells require (at least) two different motors to assemble and maintain the flagellum. You need data that shows where eukaryotes use kinesin to export things out of a cell that in someway, foreshadows flagella. Without this, you don’t even have a just so story.
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Pim van Meurs
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posted 03. August 2003 17:24
Mike: I take just so stories seriously if there is supporting evidence for the story. In this case, it is clear you reached into thin air to invent a purpose simply because the IC nature of this assembly process poses a problem. In other words, if you approach the topic expecting a Darwinian solution, you are compelled to invent the bare bone outline of such a story as you have. After all, did anyone suggest this prior to my posting?
It was not meant as much to provide for a Darwinian solution but rather to address your claim about concurrency. Concurrency may be as good a 'just so story' as 'non-concurrency'.
Certainly your accusation that it is a function of metaphysical needs, can be equally well applied to the original claim. Or am I wrong? This seems to be a good example of psychological typecasting :-)
Did anyone else suggest such a pathway? I don't know but that seems irrelevant here. I am not compelled to 'invent a just so story' other than the proposal of your 'just so story' which seems to require concurrency where there may or may not be such a need. That concurrency would complicate Darwinian pathways and non-concurrency would not seems incidental.
Mike: They become relevant once we get the faintest hint that the story is more than an ad hoc response.
It's an ad hoc response to an ad hoc proposal of yours related.to concurrency of the duplication event.
That's all. Do you have any data that support your suggested 'just so' concurrency requirement?
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