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Author
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Topic: Still Spinning Just Fine: A Response to Ken Miller
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Rex Kerr
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Member # 632
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posted 18. February 2003 20:05
quote:
Call me a stick in the mud, but it seems to me that all you've done with your 14 steps is break down an assembly problem based on a preexisting design and then list some assembly instructions in order.
Yep. Because every such story needs to be ruled out: "7) S calculates the probability of the rejection region R conditional on each of the chance hypotheses in {H_i} (i in I) and determines that P(R|H_i) < alpha for all i in the index set I"
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Indeed, there's no reason to think that there's a selective advantage going from one of your steps to the next.
All right, I'll come up with an example of where each type of interaction appears to increase fitness in at least one known system, where I can find it in two minutes or less. (I don't want to spend forever on this hypothetical example.)
- There are many types of voltage-gated calcium channels, each of which is important to survival. Hence, duplicated pores with different properties can provide a survival advantage.
- There are multiple different associated subunits of calcium channels, and different ones are expressed in different tissues and modulate the channels in different, functionally important ways.
- Protein secretion is found and important in both gram-positive and gram-negative bacteria (using different mechanisms).
- TTSS goes through all three layers; this improves its function.
- TTSS goes through all three layers; this improves its function.
- Can't find an example of a separate pore-lining subunit in two minutes for a protein export system. Nuclear pore, I'd imagine, but it's taking me too long to find details.
- Talking about extensions of lining without talking about lining is silly.
- The flagellar cap in Psedomonas binds mucin, which is important for virulence (even without the filament).
- Integrins contain long extracellular domains that make cell-cell adhesion mechanically easier and enhance adhesion.
- Same answer.
- There exist bacterial toxins that inject peptides into host cells by undergoing conformational change (can't find details in 2 minutes).
- Added in edit: forgot this one! Oops. I'll have to look for an example later of where rotational motion is better than more limited motion, but both are OK. Incidentally, this is the step I'm least confident of right now.
- The flagellum itself--all the different types of flagella, actually--suggests that low-friction improves function.
- Likewise with the hook in the eubacterial flagellum.
Is this conclusive? Good heavens, of course not! But the burden is to show that it is less probable that these factors could have played a role in evolution than 10^(-150). (Or 10^-110 or something, if you account for the replicational resources used by the evolutionary process I described.)
And in fact, the burden is to show that every possible such pathway has a probability of less than 10^(-150).
Simply calculating a probability of 10^(-2954) for de novo construction of an entire flagellar-type complex is not good enough. You must also rule out any path where de novo construction is unnecessary.
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As for the probability you calculate for the scenario, it is literally pulled out of the air.
Well, I could have given better justification for the probabilities rather than relying on memory and experience.
Gene duplication frequency: under stress it can happen as often as 10^(-3) per generation (!), with 10^(-8) being more typical. Apparently I was far too conservative here. Reference--Menez, Remy, and Buckingham, "Suppression of thermosensitive peptidyl-tRNA hydrolase mutation in Escherichia coli by gene duplication." Microbiology 2001 Jun;147(Pt 6):1581-9
Adding a domain frequency: Bacterial genomes tend to be a few Mbp in size. When adding domains by hand, there are typically 5-10 amino acids of flexibility in where the attachment point is. If duplication inserts randomly into the genome which it does not, the probability would be no worse than 10^(-6) of picking up a domain that exists exactly once.
Specific binding for another protein: Half of the genome is in the "wrong orientation", so if you duplicate into there you will pick up a short random mess of peptides. This would happen about half the time. People can find medium-affinity specific peptide-binding peptides with libraries only about 10^6 in size, so my estimate of frequency of 10^(-9) may have been too low. Reference: Zhang, Zhu, and Kodadek, "Selection and application of peptide-binding peptides" Nature Biotechnology 2000 Jan;18(1):71-74.
Signal sequence frequency: can just be a specific binding site. The 10^-6 number above is consistent with my estimate.
Chance to lose function: about 10^(-5) according to a web site that I have no particular reason to trust. I don't want to spend the time to find a proper reference, since I have observed spontaneous loss of genes in undergraduate lab experiments, where we were using fewer than 10^8 cells.
Chance to coevolve increased affinity: I explained the numbers before, except for the 1/100 to improve the interaction, which comes from personal experience observing that interactions tend to be improved by or rely upon having one of 2-3 amino acids on each side.
Chance to get mechanical coupling: If you randomly stick calmodulin into GFP, you will get a usable calcium sensor at least 1/900 of the time (reference: look up "camgaroo" or "pericam", and note that when people intentionally made the construct it worked). I was being very conservative.
So all of the components of the scenario are no longer pulled out of the air.
Of course, the entire pathway is, but if we cannot find functional intermediates in extant organisms--and there is no particular reason to expect that we should be able to--then we have no choice but to pull the pathway out of thin air.
The question is: can we evaluate the probability of these hypothetical pathways, and do they fail the UPB?
quote:
Take your step 2: "This pore acquires several associated subunits to regulate what is exported through it." Oh, really. How many subunits? And what exactly do they do? And how do they contribute to the fitness of the organism?
This was unnecessary; I was just trying to build up something as large as the existing flagellum. But even though these proteins are needed in the actual flagellum, a flagellum without so many that still was functional would meet our specification, presumably. So one is free to leave out that step.
However, if this really was an export channel, maybe each associated subunit binds to a substance that is to be exported out.
Finally, I would just note that in arguing against the TTSS as a precursor to the flagellum, Mike Gene said:
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For starters, evidence has surfaced that the basal body of the flagellum already works to secrete proteins other than the flagellar proteins, including virulence factors.
This pretty obviously means that the flagellum has a selectable function that does not require it to work as a motor!
Why, then, is it so implausible that the secretion function is primordial, the flagellum was a somewhat later addition (but so advantageous that it took over--it could provide both motor and secretion functions), and that in some organisms the flagellar portion was lost again to produce the TTSS?
This may not be your preferred means of explanation, but it must be seriously considered and ruled out, not just waved away.
[ 19. February 2003, 05:51: Message edited by: Rex Kerr ]
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yersinia
Member
Member # 324
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posted 18. February 2003 23:58
Mike Gene writes,
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What is interesting about this logic is that we already know that the mousetrap was intelligently designed. We also know that it did not first exist as a clipboard, then a tie clip. Thus, while it is logically possible to see the mousetrap as Miller does, that is, as a modified clipboard and tie clip, such perceptions are not tied to history nor the origin of the mousetrap. Thus, coming up with imaginary accounts that tap into our ability to imagine cooptional origins, by itself, is rather meaningless.
'Tis an analogy, not an explanation. Most people's eyes glaze over when you start talking about flagella parts.
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If we can successfully come up with such explanations where they are known to be false(the mousetrap), how do we know that our ability to do likewise with things like the flagellum are not also inherently flawed?
The Type III secretory system, MotAB homologs, Che homologs, etc. were not created by humans, they were observed in biology. With the biological systems the alternative functions are not being invented like Miller invented the mousetrap tie-clip. That's the difference.
Plus, we have rather a lot of evidence that cooption is a ubiquitous process in evolution.
quote:
[snip]
Thus, it would seem that we'd need to establish two things for the plausibility of the EFM hypothesis.
1. Would "any ol' transporter" really do? That is, could we take the framework of any ol' transporter and put the type of flesh on it that is exhibited by the bacterial flagellum? Or would most of these transporters be dead-ends in the sense that their transport mechanism entails a constraint that would prevent the evolution of something like the flagellum-as-we-know-it? Again, this latter point seems to be the case since none of the other transport systems evolved something comparable to flagellum among eubacteria.
This is an exceedingly misleading statement, because unless a reader is a major nerd like me, (s)he is being left unaware of the following rather important facts:
1) A homolog of the Type IV secretion system is used in "twitching" (crawling) motility in various eubacteria.
2) A homolog of the Type IV secretion system is used in the archaeal flagellum; and before Mike Gene protests, the resemblence between the two systems is significant enough that the world expert on archaeal flagella, Ken Jarrell, wrote in JME in 1998:
quote:
We feel that the discoveries of archaeal flagella-related putative gene products with similarity to type IV pilus accessory proteins indicate that the archaeal flagella also share this common origin and have evolved it to function as the primary motility apparatus. Although the function of the common origin can only be speculated, this system must predate the last common ancestor of extant life. ("Further Evidence to Suggest That Archaeal Flagella Are Related to Bacterial Type IV Pili", Journal of Molecular Evolution, 46: 370-373, 1998)
3) Some forms of gliding motility also appear to be based on other secretion systems (carbohydrates, in this case). See e.g. Wolgemuth et al. 2002, "How myxobacteria glide and Hoiczyk & Baumeister 1998, "The junctional pore complex, a prokaryotic secretion organelle, is the molecular motor underlying gliding motility in cyanobacteria".
So it looks like for four of the major forms of active prokaryotic motion, two of them are flagellar, based on two of the four different protein transport systems (and Type IV and Type II are probably homologs, so then it's 2/3). A crawling form of motility is also based on the Type IV system, and yet another form of motility is based on another kind of secretion, of carbohydrates.
Certainly "sticking something out and moving it" is not the only way to move, other prokaryotes have transport mechanisms that are wholly mysterious (anyone care to invoke ID to explain their motion? No? You dirty methodological naturalists, you...). But it appears that homology between motility systems and nonmotility transport systems is a widespread pattern rather than a single odd fact.
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2. Is there any reason to think the type III export system, complete with the ancestors of flhA, flhB, fliR, fliQ, fliP, fliI and others, existed as a "cooptable part." Thus far, the answer is no, as there are good reasons to think the type III system evolved from pre-existing flagella.
Yes, yes, I'm perfectly happy to conceed that the currently-known Type III secretion systems are derived from flagella. The main point about the current Type III secretion systems, however, is simply that Behe was wrong, because his premier, tightly integrated, interacting irreducibly complex system was in fact reducible. It's as if we walked out in nature and discovered Beheian mousetrap subsets that poisoned mice instead of trapping them.
In addition, the independence of the secretion system lends plausibility to the idea that a *primitive* type III secretion system, either with a nonvirulence function (or maybe an anti-prokaryote function, there are some predatory bacteria) once existed. Before 1994, the possibility of an independently-functioning nonflagellar subset of flagellar components would probably not even have occurred to anyone. After the discovery of T3SSs in 1994, it is firmly on the table of possibilities.
Prokaryotes make use of dozens of transporters (a more specific sub-list) for various things, furthermore they often have multiple copies of Type I-IV transporters. So postulating one more is perfectly reasonable.
It does, of course, remain a postulate. It is, however, a testable one, e.g. when we get the structures of the various components of the various secretion systems, we might discover homology at the structural level just like we did with tubulin-ftsZ and dynein-AAA ATPases.
This however, is interesting:
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d. It's much easier to envision the evolution of the type III system from flagella than vice versa. For starters, evidence has surfaced that the basal body of the flagellum already works to secrete proteins other than the flagellar proteins, including virulence factors. Thus, the basal body is already poised to evolve into a type III system from the start.
But wait! Dembski and others have repeatedly said of cooption that it is wildly unlikely, an appeal to massive amounts of chance, etc. Which is it? Cooption only when one thinks it helps the ID side of the argument?
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Evolution apparently would only have to duplicate and tweak the type III virulence protein secretion activity already existing in flagella. . In my opinion, this view is far more parsimonious than to propose that something like the type III system evolved long ago, was lost by all bacteria but gram-negative animal/plant pathogens and then was used to evolve the flagellum so that horizontal transfer could spread flagella far and wide (despite the lack of evidence for such transfer).
This is not the hypothesis being advocated. The reasonable hypothesis is:
1) ancestral secretion system (primitive type III, perhaps homologous to a primitive version of another transport system)
2) flagellum develops at (or near; Cavalier-Smith thinks there might be some basally nonflagellate eubacteria) the base of the eubacterial tree
3) When eukaryotes arise, flagellum is coopted as a virulence system (it should be noted that Type I, II, and IV transport systems also serve as virulence systems in various bacteria). Reversal is common in evolution, Exhibit A: the return of numerous tetrapods to the water.
Now as you love to point out, we currently have no direct evidence for #1. The place to look is in new genome sequences (genome projects are heavily biased towards disease-causing organisms) and at structural studies of known transport systems. Call it a prediction of the hypothesis if you like. Type III secretion was only discovered in 1994, I'm not sure why you have such high expectations that if a basal precursor was going to be found it would have happened already.
After all, a prokaryotic tubulin (Jenkins et al. 2002, "Genes for the cytoskeletal protein tubulin in the bacterial genus Prosthecobacter," PNAS) was only published a month or two ago (an interesting contradiction of your essay Tubulin and ftsZ: More than One Way to View Something). You never know what might turn up.
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Is there any evidence that supports transporting this system, or something like it, back in time? The type III system is one of at least four different bacterial protein transport systems. And it appears to be the most complex of the bunch. The key here is that the type III/flagellar cytoplasmic export system does not show clear homology with any of these other transport systems. But we also know that evolution builds on and modifies what already exists rather than create de novo. Thus, if these other transport systems were already in place (and they probably were), why didn't evolution simply build on one of the simpler versions
...it did, it's called the Type IV secretion system. The relative complexity of Type III vs. Type IV appears to be up for grabs to me. Like I said, bacteria appear to be quite happy to have all kinds of transport systems, and often multiple copies of particular classes, with divergent or similar functions. Some bacteria even have multiple motility systems.
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rather than create a whole new method of protein secretion de novo? The type III-from-flagellum scenario better fits with what we know about evolution - that it uses what already exists rather than inventing de novo. Thus, not only is there no evidence to support putting this transporter (or something closely homologous) back in pre-flagella days, there is reason to think it wouldn't be there.
Well, there are various suggestive bits and pieces:
1) the nonflagellar MotAB homologs which appear to be basally distributed,
2) as well as nonflagellar homologs of the key chemotaxis proteins (see "Evolution of two-component signal transduction," Koretke et al. 2000, Mol Biol Evol).
...both of which would have to have been around if the flagellum-evolved-from-a-primitive-Type III-secretion-system hypothesis is correct.
3) Furthermore, the Type III secretion virulence system makes use of an outer-membrane pore (a secretin) produced by the Type II secretion pathway (and two of the flagellum components are are similarly secreted, see Fernandez & Berenguer 2000, Secretion and assembly of regular surface structures in Gram-negative bacteria), indicating that (1) The Type II system preceded the flagellum (likely for other reasons as well, the T2SS is ubiquitous) and (2) the bridge from inner membrane to outer was passed by "cheating" and snarfing outer membrane proteins from T2SS. Why an independently-designed flagellum would have this odd feature is beyond me.
4) Finally, the homology between the flagellum/T3SS FliI gene and the F ATPase is easily recoverable with a highly significant e-value with protein BLAST, indicating that some chunk of the Type III secretion system existed way back at the LCA.
Just bits and pieces, I know, but it's not nothing.
[ 19. February 2003, 00:08: Message edited by: yersinia ]
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VonRSmith
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Member # 671
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posted 19. February 2003 01:04
William A. Dembski writes in response to Rex Kerr:
quote:
Yes, selection always operates. But there needs to be a selective advantage in going from one step to the next, and there's no reason to think that obtains in your scenario
Dr. Dembski:
It was my understanding that the methods you use to infer design depend on a rigorous elimination of *all* relevant alternative chance hypotheses. The rigor claimed for this method seems to me to depend on this eliminative inference, and it is this and only this which makes your IC argument potentially more than just another argument from personal incredulity. Am I correct so far? If I have misunderstand your design inference, please set me straight.
I understand (and to a certain degree applaud) your skepticism of Rex's speculative scenario. And of course the question of the working of selection is crucial to his claim, since it is what justifies his drastic upward revision of the probability of his scenario. But that does not justify rejecting it out of hand. If anything, I would think that the interests of rigor would dictate erring on the side of inclusiveness in considering his proposed scenario.
If you do discount such an evolutionary hypothesis because you don't find it intuitively convincing, rather than doing a relevant probability calculation on it, it seems to me that you are guilty of exactly what Ken Miller has accused you of: engaging in an argument from personal incredulity.
In short, you aren't finished with Rex's proposed scenario, or others like it, simply by being skeptical of it. You must be able to justify *eliminating* it as a relevant hypothesis. I don't see that you have done that, especially since the selective advantange of several of Rex's proposed steps seem pretty self-evident, even to a layman such as myself (steps 1, 4, 5, and 11-14 come to mind).
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Mike Gene
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Member # 149
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posted 21. February 2003 08:13
Upon reading Nic's reply, it is becoming quite clear to me that several points of clarification are needed.
1. Nic writes "Now as you love to point out, we currently have no direct evidence for #1 (where #1 is the notion that a primitive TTSS existed prior to the flagellum). Instead of saying "Now as you often point out...," the focus is on my emotional state while pointing out. Thus, I suppose I better clarify that I don't "love" to point out we have no direct evidence for #1. I point it out because I think it is quite relevant to the issue at hand. If the TTSS evolved from the flagellum, then the TTSS no longer provides evidence for a "primitive TTSS." So why propose the existence of such a thing, apart from the fact that a gradualistic viewpoint mandates something like this?
Perhaps I can reassure people about my emotional detachment by reminding them of my working hypothesis - an original consortium of cells was both bioengineered and used to seed this planet. An aspect of this bioengineering may have entailed front-loading. Nothing in this hypothesis mandates that the bacterial flagellum was designed. In fact, there are several possibilities concerning the make-up of this consortium which follow from trying to ensure the success of a seeding event in a distant environment that is largely unknown:
a. Several different generic motility structures were included. Increasing the number of motility structures would increase the odds that useful means of motility would be available.
b. Flagella were the only motility structures included, since life would fare best under the water (due in large part to the missing ozone layer). However, multiple secretion systems were front-loaded to evolve motility structures (many that would come in handy to movement over solid matrices) where the environment could untap the designs that best suited the bugs.
c. No motility structures were included, instead they were all front-loaded. If the original cells were endowed with "the Type III secretory system, MotAB homologs, Che homologs, etc.," then we might have a state poised to evolve the flagellum.
Currently, I lean towards b., but not because of any emotional attachment. I can be just as happy with a or c. ![[Smile]](smile.gif)
2. My point concerning Miller's analogy was explicitly spelled out: "But keep in mind that whenever you are dealing with a machine, it is always going to be possible to imagine the various parts existing without the machine, as long as you keep your explanation vague and are free to imagine simpler states with imaginary selective benefits and ad hoc functions." It's one thing to deconstruct a machine and imagine the individual parts existing independent of the machine and the run this imagination in reverse to "evolve the machine." But it's quite a different thing to translate this imagination into history. Thus, I am not at all impressed by any success in coming up with a way to imagine a way how something "could have evolved." That we can imagine a mousetrap as an evolving clipboard, then tie-clip, shows that we have an ability to project evolution onto the world. This is not all that surprising, since just as much of the evidence for design boils down to "it looks designed," so too does much of the evidence for evolution boil down to "it looks evolved."
3. There are three main points where Nic and I don't share common ground and it is important to recognize these to appreciate our lack of agreement on issues that stem from these unshared assumptions.
a.) Homology. Nic writes, " It does, of course, remain a postulate. It is, however, a testable one, e.g. when we get the structures of the various components of the various secretion systems, we might discover homology at the structural level just like we did with tubulin-ftsZ and dynein-AAA ATPases."
Yet I don't recognize the "discovery" of homology between tubulin and ftsZ (for example). Homology is only an interpretation of patches of similarity. We went through all this the last time we discussed this matter. In mainstream science, there are three possible explanations for similarity - common descent, convergence, and coincidence. When Nic quotes scientists who conclude a homologous relationship between proteins on the basis of structural data, we must remember that this is done simply by excluding convergence and coincidence (and often times, no real effort is made to exclude convergence, I point to return to when I eventually get around to discussing Denton's recent paper). But from a teleological perspective, there is also the possibility of "common design" (as Jay describes it). And published conclusions of homology are not made by also excluding this possibility. Thus, while Nic concludes homology on the basis of structural similarity, I consider this an example of jumping to a conclusion.
b.) Related to a.) is where Nic seems to be working under the assumption that a designer would never reuse a design in another context. This leads to the conclusion that every aspect of an IC machine must be unique, such that any similarity with any other cellular component works against a design inference and instead reflects "homology." The 'homologous" relationship between FliI and the alpha/beta subunits of the F-ATPase is a good example. That two proteins share a common nucleotide-binding motif supposedly counts against design as, I assume, a designer "should have created a unique nucleotide-binding motif for the flagellum and F-ATPase. But why? What we do know is that this motif has been an outstanding success for both machines, surviving and functioning well for billions of years. It would seem to me that a sign of good design is not found in its uniqueness, but in its ability to work well and survive being put to the test over and over again.
c.) Finally, there is Nic's appeal to cooption - " cooption is a ubiquitous process in evolution." Murder is ubiquitous too, but that doesn't mean we invoke it willy-nilly to explain every death. We invoke it when certain data patterns call for it. And that is a serious problem I have with Nic's appeal to cooption - it is often too ad hoc. Keep in mind I accept cooption, as it is an important ingredient in front-loading. But cooption can be invoked to explain anything, regardless of whether or not it was behind the origin of something.
Let me provide a biological example to drive this point home. One could also say that genomic deletions are ubiquitous. Yet when we align sequences, a "gap penalty" is figured into the analysis. Since any two randomly generated sequences can be aligned if we insert enough gaps between amino acids, a penalty is introduced to constrain the number of gaps to prevent the alignment from becoming biologically meaningless. Thus, when aligning sequences, a positive score is given to matched residues and a negative score is given for introducing gaps. Yet when Nic invokes cooption, there is no penalty assessed. Without a consideration of such penalties, we are essentially aligning sequences through the arbitrary employment of gaps.
Furthermore, the common nature of cooption does not mean all proteins (and all functions) are equally prone to cooption, which undercuts the attempts to extrapolate "cooption here and there" to "cooption everywhere." Take the flagellum. Because it is IC, a loss-of-function mutation in one gene ends up taking all the flagellar genes out of the picture. As a result, they all decay (a loss-of-function in one sequence turns the other functioning sequences into "pseudogenes"). Now, flagella have been lost many times over among eubacteria. In fact, there are some species of pathogens where we can catch of snapshot of this decay. But here's the point. If you have, say, 30 flagellum genes, and one is lost by some deletion, that leaves 29 functioning sequences which can be fed into the cooption mill. Yet when I poked around in some of the genomes of nonmotile bacteria, there are no flagellar homologs that were coopted into another non-flagellar function. I would not surprise me entirely if there exist a few, but the fact that the typical fate of flagellar genes, after removal of the flagellum, is extinction, ought to warn us against invoking cooption simply because it fills in the blanks of some story.
Thus, if we stand back, we can see what Nic expects from a designed flagellum - an IC structure where are parts are unique and a world where cooption does not exist. But this is an appeal to epistemological evidence (discussed on my web page). Positing the design of the flagellum does not lead me to expect all its parts would be unique and that cooption would not exist elsewhere. And this is why Nic and I will continue to talk past each other.
4. I argued: "Would "any ol' transporter" really do? That is, could we take the framework of any ol' transporter and put the type of flesh on it that is exhibited by the bacterial flagellum? Or would most of these transporters be dead-ends in the sense that their transport mechanism entails a constraint that would prevent the evolution of something like the flagellum-as-we-know-it? Again, this latter point seems to be the case since none of the other transport systems evolved something comparable to flagellum among eubacteria."
Nic labels this an "exceedingly misleading statement." But, judging by his reply, I don't think Nic understands the argument. First of all, as I explain in my web page, it is not surprising that motility structures tend to have secretion subsystems embedded in them. Since motility structures transact with the extracellular environment, there must be a way of getting them outside the cell. Thus, I don't find it that meaningful (from an origin perspective) that motility structures and secretion systems have a functional relationship. And my argument is not about evolving "motility structures." It is about accounting for the existence of the bacterial flagellum. What I am highlighting is the fact that there are dead-ends in evolution. The whole concept of evolvability comes into play. For example, Rex starts his story as follows: A pore duplicates in an early bacterium and becomes associated with an enzyme whose products provide a fitness advantage when transported outside the cell. Yet for this to actually account for the historical origin of the flagellum, this "pore" can not be a "frozen accident" that amounts to a dead end as far as flagellar evolution is concerned. We cannot invoke just any ol' pore. And the fact that the myriad of other pore complexes that exist (and have existed) in bacteria did not spawn the evolution of dozens of different flagellar variants suggests any ol' pore will not do. The story that Rex and others tell would be more convincing if we had a few dozen types of flagella among eubacteria rather than the universal flagellum (and yes, I'll deal with the exception of Archaea in more detail later), where all those functional, historical states from steps 1-13 are now missing.
Outta time. More later.
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Clay Schentrup
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posted 15. March 2003 13:59
I don't know why Dembski and others in his camp continue to press evolutionists for an "explanation" of how things like flagella arose. The worst case scenerio for an evolutionist is that every single codon to for the flagella alleles mutated randomly all at once. Evolution doesn't _have_ to be gradual. It's just a matter of how likely a given mutational step between a parent and offspring is. The probability of flagella genes mutating in one single macro-mutation event might be small, but they are obviously greater than zero. And there is no other known process besides normal non-intelligent mutative processes, that can even in _theory_ cause such a thing.
Dembski believes in intelligent design. The onus is on him to demonstrate any verifiable processes which are both intelligent and have a propensity to create things like flagella DNA. Until he and/or his constituents provide this there is no need of any explanation other than mutation/selection for any observed biological feature. The intelligent design argument is so ridiculously illogical its a wonder that prominent scientists feel the need to provide evolutionary explanations for them.
For a more elaborate exrpanation of the holes in the ID argument see my debate with Michael Behe at:
[edit - new posters can not post links, especially if they are shameless self-promotion ]
[ 15. March 2003, 17:58: Message edited by: Moderator ]
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Moderator
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posted 15. March 2003 17:54
Clay, perhaps you aren't familiar with the standards at Brainstorms . It just so happens that this ain't your mama's battle ground.
Comments like the following, about anyone, or anyone's thought system, just aren't permitted. We like to call them "fire starters", and well, we just don't like fires.
"so ridiculously illogical"
The next time you post here, post in a spirit of cooperation. Battlewarriors need not apply.
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Mike Gene
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posted 02. January 2005 22:10
Okay, I said I’d add some more later. Sometimes, “later” can mean years.
Yersinia: quote:
After all, a prokaryotic tubulin (Jenkins et al. 2002, "Genes for the cytoskeletal protein tubulin in the bacterial genus Prosthecobacter," PNAS) was only published a month or two ago (an interesting contradiction of your essay Tubulin and ftsZ: More than One Way to View Something). You never know what might turn up.
There is nothing in the Staley paper that contradicts my essay. In fact, I think it obliquely strengthens my essay. Let me explain.
In my TeleoLogic essay, I noted:
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And one of the facts not mention thus far in this thread is that although both ftsZ and tubulin have very different amino acid sequences when compared to each other, the sequences of both ftsZ and tubulin are highly conserved in bacteria and eukarya, respectively. In other words, when we compare ftsZ sequence within bacteria and tubulin sequence with eukarya, we find strong sequence conservation. FtsZ, for example, shows 40-50% identity when very different forms of bacteria are compared and I believe the tubulin conservation is even higher. In fact, one paper on my desk states "tubulins are among the most conserved proteins known."
This pattern is consistent with independent origins by design. That is, the first bacteria were endowed with a GPD variant known as ftsZ that has been conserved for billions of years due to its important design objective. Similarly, the first eukaryotes were endowed with a GPD variant known as tubulin that has been conserved for billions of years due to its important design objectives.
On the other hand, if we try to force common descent on the two distinct, highly conserved proteins, we face a strange situation. For prior to the evolution of ftsZ and tubulin from this hypothetical ftsZ/tubulin-like precursor, there was no apparent functional constraint. If there was, it is difficult to explain how the two sequences so radically drifted from each other only to be locked into place (of all places) in the last common ancestors of eukaryotes and bacteria. But wait a minute. The 3-D structure was being conserved. That's the basis for inferring the common descent. Yet what was it doing prior to the two sequences getting locked into place? Nothing bacterial. Nothing eukaryotic.
Actually, this is a cut-n-paste job from an ARN posting from 2001 (you can still find it in the archives). Now, the 2002 PNAS article makes a very similar argument:
quote:
At present, the leading candidate for an evolutionary precursor of tubulin in the bacterial/archaeal domains is the cell division protein, FtsZ. Although there is strong evidence from their 3D structures that tubulin and FtsZ are homologous proteins (5, 6), they share only very low sequence identity, most of which is confined to the GTP-binding region (7). The strikingly low sequence identity is difficult to reconcile with the fact that tubulins and FtsZs are among the slowest-evolving proteins known and raises the question of whether any more closely related homologs of tubulin exist in members of the Bacteria or Archaea (8, 9).
It is this very “difficulty” that served as the impetus to look for tubulin in these relatively uncharacterized bacteria with MT-like structures. Thus, the Staley paper effectively confirms the seriousness of my argument. Thus, the question will turn on whether or not they truly isolated a prokaryotic tubulin.
They did find two tubulin genes, btuba (for bacterial tubulin A) and btubb (for bacterial tubulin B). btuba is homologous to eukaryotic alpha tubulin, with 31-35% sequence identity. btubb is homologous to eukaryotic beta tubulin, with 34-37% sequence identity. While this is a much better match that ftsZ (around 20% identity), it is still a long way from the highly conserved tubulin among eukaryotes. For example, if we compare the beta-tubulins (445 amino acids in length) from humans and mice, the sequence identity is 92%. The sequence identity is also 92% between humans and fruit flies. It ranges from 80-82% when human sequence is compared to dozens of different fungi. And it we compare human beta tubulin with to its homolog in the unicellular Giardia lamblia, the sequence identity is 85%.
The researchers failed to find any evidence of these tubulins being involved in forming MT-like structures. And modeling, along with the sequence data, led the researchers to conclude that the tubulins in bacteria don’t form characteristic dimers.
There are thus two possible explanations for the origin of these bacterial tubulins. These genes either arose via a horizontal gene transfer from a eukaryote or the bacterial tubulins are ancestral to eukaryotic tubulins. The researchers rule out a recent horizontal transfer as a consequence of the sequence divergence. However, if you take eukaryotic tubulin and express it a bacterial context, many of the functional constraints may have been lost, allowing for a rapid burst of molecular evolution. The authors of the PNAS paper admit their research cannot distinguish between the two hypotheses.
Nevertheless, I think the hypothesis of horizontal transfer is the stronger of the two.
First, Prosthecobacter belongs to the division, Verrucomicrobia, bacteria that partake in an intimate symbiotic relationship with ciliates in the genus Euplotidium. The bacteria act as ectosymbionts to defend their host against a ciliate predator. Because of this intimate relationship, a horizontal transfer event at some point in the past is likely.
Secondly, the tubulin genes are restricted entirely to Prosthecobacter. This is significant because there over 200 bacterial genomes that have been completely sequenced. If these tubulin genes are “bacterial,” then they have been lost everyplace else except among Prosthecobacter. Because of this restricted distribution of these tubulin genes, if they are ancestral to their euakaryotic homologs, we would have to place Prosthecobacter as the members of eubacteria closest to eukaryotes, suggesting that they should harbor other eukaryote-like genes. Yet as the Staley lab explains:
quote:
Two hypotheses involve horizontal gene transfer (HGT) either from the Eucarya to the Verrucomicrobia or vice versa. An alternative hypothesis is that a member of the Verrucomicrobia or a closely related group evolved to become the founding ancestors of the Eucarya. Based upon partial genome sequences that are available, we are currently trying to determine which of the three hypotheses seems most reasonable. The most readily tested hypothesis is the last one. If it is correct, then we would expect that a substantial number of eukaryotic genes would be found in the genomes of the Verrucomicrobia. Preliminary results based upon BLAST searches of genes of the Verrucomicrobia indicate, however, that fewer other eukaryotic genes have been found in the Prosthecobacter genome than expected based on the simplest variant of this model.
Here
I do not have any ideological opposition to scoring ftsZ and tubulin as true homologs, as such a relationship would be very friendly to front-loading evolution. But the fact that their sequences are so strongly conserved within bacteria and eukaryotes, yet so distant between groups, is a real problem, as confirmed by the Staley paper. That horizontal transfer from eukaryotes remains a plausible, even most likely, explanation for their origin would mean that we are left without clear tubulin homologs in bacteria and the problem I have mentioned. These “bacterial” tubulins can thus be viewed as a degenerate/stream-lined state after being freed from the constraints of their ancestral eukaryotic tasks.
[ 02. January 2005, 22:14: Message edited by: Mike Gene ]
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Jim Skipper
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posted 06. January 2005 21:46
William A. Dembski wrote:
quote:
My argument, always, is that evolutionary pathways to irreducibly complex systems, even if they exist, are non-Darwinian.
Not to backtrack too much I hope, but the above quote caught my attention and I feel it is quite important.
Dembski, if you claim that your only concern is that the evolutionary vectors cited are non-Darwinian, then your argument seems rather pointless. The pathways are non-Darwinian.
Evolutionary theory, through the accumulation of observational and experimental evidence has grown far beyond Darwin. There are multiple evolutionary vectors, many more valid that Darwin's original theory.
To require that all evolutionary pathways be expressed in terms of Darwin's theory is nonsense. It is like saying that you will only believe quantum theory if it can be explained by Newtonian physics, or perhaps, more to the topic, if a scientist required that the only acceptable arguments for Intelligent Design are those expressed in Aramaic or Hebrew quoting the Bible.
Or perhaps I am misunderstanding your point.
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