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Author
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Topic: Organisms using GAs vs. Organisms being built by GAs
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Paul A. Nelson
Member
Member # 26
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posted 18. September 2002 22:01
Yersinia wrote:
quote:
Paul, earlier in this very thread, in rebuttal to an earlier assertion by Dembski, I gave a rather extensive list of sources documenting how well-understood the origin of new genes is. Ignoring this literature when considering scenarios that posit the progressive origin of genes this is sticking your head in the sand, and no one who has read this literature is going to be able to take rebuttals like yours seriously. The post-adaptive immune system evolution of e.g. MHC diversity is yet another case of massive new gene evolution and which is yet more evidence that the immune system is particularly prone to favoring new genes (for increased diversity), which you would have seen if you followed up the references which I've been "literature-bombing" you with.
None of this bears on my question. I asked simply that you provide the exact formulation of natural selection that you’re using (i.e., as a general theory, not a particular scenario), and show how the evolution of the vertebrate immune system, or some part of that system, is explained by selection. Natural selection is not a magical force that strings together bits of this and that and makes them work. It is a biological process, the invocation of which requires evidence. (See John Endler, Natural Selection in the Wild, Princeton University Press, 1986.) It is impossible for me, or anyone, to judge the merits of your many assertions above, made in the name of natural selection, because you appeal to selection (as a cause) wholly without regard to its evidential requirements.
You say it’s too much trouble to get into the details yourself; others have done the work already. OK –- let’s look at Matt Inlay’s article. Here’s a paragraph from the middle. I’ve numbered the major claims:
quote:
(1) A transposon containing the RAG genes and flanked by RSSs integrates itself into the gene for a primordial antigen-receptor gene, splitting it into two gene segments (V and J).
(2) The locus itself is transciptionally inactive in most cell types, and prevents the expression of the RAG genes and removal of the integrated transposon. However, in a lymphocyte-like cell, the locus becomes transcriptionally active, and the RAG genes express themselves and remove the transposon, reuniting the two gene segments.
(3) The imprecise joining process generates a level of receptor diversity that favors the organism bearing this transposon, and its descendants thrive with the increased immune capabilities.
Let’s focus on claims (2) and (3).
(2) Transcription is a tightly regulated process. What evidence shows that the novel RAGs would be expressed only "in a lymphocyte-like cell," and not in other cell types? Inlay’s hypothesis turns on the genes only where he wants them expressed. How?
(3) Organisms lacking V(D)J recombination -– i.e., that do not possess an adaptive immune system –- get along just fine without it. What evidence shows that receptor diversity (supposing [2] occurred) nevertheless conveyed a fitness difference?
Maybe you could direct these questions to Matt Inlay.
You wrote:
quote:
The basic selection pressures for diversity and control are roughly constant
And you know this how?
[ 18 September 2002, 22:05: Message edited by: Paul A. Nelson ]
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andyg
Member
Member # 415
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posted 18. September 2002 22:29
Paul Nelson wrote:
"I asked simply that you [.....] show how the evolution of the vertebrate immune system, or some part of that system, is explained by selection."
That's not really a simple question, is it? I think your question is deliberately phrased to put the respondent between a rock and a hard place. We do not have a molecular fossil record. Period. Therefore, the most ideal evidence - a record of the genome of every vertebrate that ever lived, together with the lineal relationships between each genome - is simply not available. Even if this were available, we have no idea of the historical selection pressures that every vertebrate was faced with at any given point. You seem to be asking for something that you know cannot be produced, and feigning horror when it is not made available. A good-faith explanation might take examples of modern day immune systems, establish phylogenetic relationships between them and propose scenarios as to how ancestral forms could arise. You will then dismiss this as mere storytelling. I think it is rather disingenuous to imply that the evidence is somewhere out there, and that biologists lack the wit either to gather it, or to string it together in a way that could be verified historically.
I may, on the other hand, have misunderstood your request. Are you asking for something different to what I describe above?
AndyG
[ 18 September 2002, 22:31: Message edited by: andyg ]
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Paul A. Nelson
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Member # 26
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posted 18. September 2002 23:14
Andy wrote:
quote:
You seem to be asking for something that you know cannot be produced, and feigning horror when it is not made available.
Yersinia says the vertebrate immune system evolved via natural selection. I'd like to know how he learned that.
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yersinia
Member
Member # 324
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posted 19. September 2002 00:21
Hey Mike,
I think I'll start another thread to discuss the criteria issue...
Regarding the capabilities of mutation acting alone, I still don't see the point of indulging you, like I said the limits are reasonably well known. Probably about the most that mutation alone can accomplish is the fashioning of a crudely functioning protein out of a noncoding (or unrelated-coding) sequence (e.g., nylonase by frameshift, Turf-13 from an rna gene IIRC). If you would like to start another thread and lay out your reasoning then I might have more to say.
nic
PS: Just so this doesn't get misinterpreted, the above is my estimation of the approximate limits of what mutation can do "starting from scratch", basically random (or perhaps periodic/statistically-biased-but-unselected) sequences. Art has discussed this fairly extensively in various threads in terms of the low "information content" of proteins. The main action of mutation is in modifying already functional stuff, i.e. when not starting from scratch, and here the results can be more impressive (and then we add cumulative selection...)
[ 19 September 2002, 02:43: Message edited by: yersinia ]
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yersinia
Member
Member # 324
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posted 19. September 2002 02:36
Hey Paul,
Not all evidence of natural processes requires demographic studies. Evidence for the action of natural evolutionary processes (including natural selection and the various kinds of random mutation) in the long-distant past can be found by looking at how patterns of evidence match up with the predictions made by the hypothesized action of said mechanisms.
This was already discussed back on page 1 of this thread and in the therein referenced ARN thread on ancient gene duplications and other ancient events where the predictions of the RM&NS model regarding what we should observe in ancient evidence are laid out. Many of these, particularly e.g. the cooption prediction, apply quite well to the immune system situation.
yersinia
[ 19 September 2002, 02:45: Message edited by: yersinia ]
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rafe gutman
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Member # 134
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posted 19. September 2002 05:55
quote:
by dr. dembski:
As for your example, I'm not going to take the bait. You're asking me to play a game: "Provide as much detail in terms of possible causal mechanisms for your ID position as I do for my Darwinian position." ID is not a mechanistic theory, and it's not ID's task to match your pathetic level of detail in telling mechanistic stories. If ID is correct and an intelligence is responsible and indispensable for certain structures, then it makes no sense to try to ape your method of connecting the dots. True, there may be dots to be connected. But there may also be fundamental discontinuities, and with IC systems that is what ID is discovering.
hmmm, dembski calls my model "pathetic", nelson says it's "storytelling", and yet neither would advance their own opinion of how these systems originated. let he who has their own model cast the first stone...
dr. dembski, i never asked for a mechanism, just something more than, "poof!" it's really not that hard. surely you must think something happened. the question is, what? was it a single design intervention, or multiple? was the design introduced through natural means, or did it supernaturally appear? was it a modification of an existing design, or completely novel? did it require the "creation" of a new organism?
i will not reveal any more details of my model until someone outlines an alternative one. it seems totally hypocritical to attack aspects of one model, when you don't have a clue what to replace it with. does ID have anything to offer here?
we can look high or low, in books or in person, but the result is the same. the ID community has no answers to the question of the origin of the immune system.
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Mike Gene
Member
Member # 149
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posted 19. September 2002 07:54
Hi Nic,
You write:
quote:
Regarding the capabilities of mutation acting alone, I still don't see the point of indulging you, like I said the limits are reasonably well known. Probably about the most that mutation alone can accomplish is the fashioning of a crudely functioning protein out of a noncoding (or unrelated-coding) sequence (e.g., nylonase by frameshift, Turf-13 from an rna gene IIRC). If you would like to start another thread and lay out your reasoning then I might have more to say.
But I'm not questioning the existence of the limits. Nor am I questioning where we place the limits. The question is - why do these reasonably well-known limits exist?
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Mike Gene
Member
Member # 149
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posted 19. September 2002 08:19
Hello Andy,
You write: A good-faith explanation might take examples of modern day immune systems, establish phylogenetic relationships between them and propose scenarios as to how ancestral forms could arise. You will then dismiss this as mere storytelling. I think it is rather disingenuous to imply that the evidence is somewhere out there, and that biologists lack the wit either to gather it, or to string it together in a way that could be verified historically.
I think this is why Jerry Coyne noted:
quote:
In science's pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics. For evolutionary biology is a historical science, laden with history's inevitable imponderables.
http://www.tnr.com/040300/coyne040300.html
That is, the most we can get (and ever hope to get) from such a good-faith explanation is "the immune system looks like it evolved and it's reasonable to think natural selection could have been behind its evolution." The problem comes when some (many?) people insist that all knowledgeable, intelligent, sane, and honest people would admit that the immune system did in fact evolve by natural selection.
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Deanne M. Taylor
Member
Member # 274
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posted 19. September 2002 08:45
Mr. Dembski writes:
quote:
Nonetheless, you've redefined the problem. Scale invariance occurs hierarchically, but unlike with fractals, the "self-similarity" here cannot be pushed down the hierarchy indefinitely -- eventually we reach a level of material constitution that cannot support biologically functional hubs.
For the record, straight off...when I spoke of a scale-invariant "hierarchy", it could be taken to mean "order of supremacy". I don't mean that. I mean "order of connections on a node". Sorry not to be clear. In hierarchy, I meant that there were hubs with many many many connections, then hubs with many many connections, then hubs with just many connections, then a wild branching out all over the "network space" down to a majority of nodes that only have a few or one connection.
If you have a node that starts off in "pre hub" form, as an outlier, and you add more connections to that node, then it turns into a hub. Remove connections from a hub one at a time, and you get a non-hub eventually. How you define hub is, of course, not defined by how many absolute connections it has, but relative to the whole network. It's interesting to note that out of the vast majority of proteins that show sequence drift in eukaryotes, there are only a few
proteins or protein complexes that show a higher level of fixation, and they are invariably hub-type positions in networks with conserved sequences. In fact, biologists can use the level of conservation through species to determine the functional similarity between species, and positional (in a network) importance of a protein or part of a protein. That's a common way of studying proteins and they function.
In evolution, co-adaptation among various interacting components is important. Molecular evolution believes that when you fix a new component though gene duplication you throw an evolutionary stable network into a wild pendulum swing. See the gene duplication that led to human chorionic gonadatropin and the need for longer human gestation for instance. In these instances, you'll see evidence for a scramble in the components of that network to adjust to the change by accelerated evolution within the components of that network. The components are restrained by their existing function yet must also supply the new function with support when it confers an advantage. Swing the pendulum, things scramble for the swing back.
One of the interesting things about the data coming out of genomics projects is that it doesn't need whitewashing to fit into evolutionary theory. When you analyse the raw data, you can find things that support evolution without looking for them. For instance, Eichler found segmental duplications in the human genome when studying the Celera genome for assembly errors. He then went further and found more evidence for evolution within those duplications.
Mr. Dembski writes:
quote:
If a certain minimal number of hubs are necessary for life to exist at all (as minimal complexity considerations suggest), then your scale invariance argument at best works for trying explain things up the hierarchy. But even here there are serious problems.
I don't see the origin of any serious problems.
Nobody has ever established that there are a minimal or maximal number of hubs for life to exist at all. Certainly in a scale-invariant network measured to be some degree "N" there have to be a minimal number of hubs of a certain number of connections, as related to the total connections in the network and the total number of players in that network. (for the graph geeks, that'd be edges and nodes). But that's just definition. There have been no observed rules as to how complex this network must be, and in looking at gene counts in various organisms, there doesn't seem to be a set "this many genes, this many hubs" rule (thus far!) which cannot disagree with evolutionary theory which suggests opportunistic development of biological networks.
Thus far, life seems pretty capable of using the same protein molecules in various ways to accomplish various things. Which is back to the multi-use proteins of the previous post.
But a measure of "minimal complexity" has no meaning in out of context of a particular species. I had not addressed the maximal numbers of connections that can be knocked out of an organism before it starts to catastrophically fail, because in a scale-invariant network, that has little meaning. You can hit a hub the first time you do the experiment and fail the organism. Or, you can knock out a dozen nodes before you hit something important. If you deliberately start pruning back only outliers, it's likely that you can excise quite a few before you get a catastrophic failure. And every organism has its own strategy, so there's no comparing an overall, "generic" organism for "minimal complexity". Again, no meaning attached to that.
I was stating, before, that you can measure the importance of any ONE connection in an organism by knocking it out. The more you knock out, the less able that organism is going to be able to function. My point was that there are very few "important" connections taken on their own. Which also supports the idea of robust networks, but I'll leave that argument aside for another post.
If you mean to say by "minimal complexity" that a eurkaryotic organism has to have ATP synthetase, and a few other basic members of a citric acid cycle in eukaryotes, then it could be argued that you also need the entire mitochondrial function to accomplish that, which includes the cellular nucleus, which requires the rest of the cell by association. "Minimal Complexity" therefore has no meaning in this context. You could possibly prune off several outlier branches and get no appreciable change in an organism. But the more you prune, the less and less able the organism will be to function, as the network makes the organism, and the nodes within the organism show differing magnitudes of connection.
Mr. Dembski writes:
quote:
As with so much of the self-organizational literature that I've seen applied to biology, I see in your post the attempt to make some global property make all the pieces suddenly fall into place and all the problems disappear.
Actually, I'm asking you to examine scale invariance as evidence for piecewise addition of molecular components in biological networks.
I'm positing a theory that scale-invariance is the smoking gun for the same sequential series of events that you desire proof of. Can you show me how scale invariance makes piecewise addition through evolution and selection unlikely, AND/OR requires IC?
Mr. Dembski writes:
quote:
You write: "The QUALITY of the network, the very essence of the biological network, speaks to the very same mechanism you are demanding proof of." How does a "quality" that "speaks to" some mechanism explain anything or provide a proof?
One could ask the same kind of proof in a criminal trial. How is anything proof? I argue that scale invariance across all biological networks is sufficient evidence that complex biological networks grew in a sequential fashion by gene innovation, co-evolution and co-opting of inter-pathway assocations with subsequent evolution that renders your demand for the evidence of sequential co-evolution unnecessary .
I can show evidence for my supposition. I'd like to hear an argument to the contrary.
Mr. Dembski writes:
quote:
I asked for a detailed Darwinian pathway for IC systems, not a feature that biological systems should have if the Darwinian mechanism is taken for granted as having the power to produce IC systems. And it seems to me that's all you're doing.
I'm showing that Darwinian evolution predicts the appearence of scale-free networks as a consequence of the step-by-step process you are demanding proof of. Is there any other process you can think of that can create these scale-invariant networks (short of *poof they appear*)? What else can create a functioning biological network with scale invariant properties, with minimal numbers of highly connected hubs with greater numbers of less-well-connected nodes linked together by these hubs?
Mr. Dembski writes:
quote:
Again you write: "In the case of biological networks, there is a footprint laid down in the very qualities of these networks, furnished by scale invariance, that points to the source of that scale invariance in simpler progenitor networks." Okay, so there are some footprints that these networks that exhibit scale invariance leave behind (let's grant that all these concepts are well-defined). What of it? These are just words. Where are the bridge principles that connect these concepts to actual biological systems and provide concrete insights into the nuts and bolts of IC systems?
Let's seed the proto-system with a simple network to start, to avoid the side argument of abiogenesis for the moment, though I'm prepared for that discussion as well. Now, these are all "how" a seemingly IC system can evolve. Expanding on the examples in each of the following is kept at a minimum to save space. I'm always available for questions).
Mr. Dembski writes:
quote:
Where are the bridge principles that connect these concepts to actual biological systems and provide concrete insights into the nuts and bolts of IC systems?
Here goes...
1) A simple network exists.
2) A gene within that network is duplicated (see Eichler's work on segmental duplication and Gerstein's pseudogene work) and is expressed in such a way that the network is now "double dosed" in that one component. We'll call the duplicate PROTEIN A.
3) PROTEIN A is either free to, or pressured to, drift away from its twin which still functions happily along as usual (see human chorionic gonadatropin as one example), and multiple copies of various proteins as another example.
4)If drifting, PROTEIN A can assume a new function through the following (admittedly subset of possible) events:
4a) PATHWAY LINKER. PROTEIN A can assume a functional association with a component in another pathway and maintained association with its parent pathway. See papers on promiscuous protein-protein binding. These generating associations are common even before mutations put the entering proteins in the headlights of the new pathway. Therefore PROTEIN A can mutate and connect two pathways and in that way confer an advantage, especially if it improves two set processes.
4b) IMPROVED FUNCTION OF ORIGINAL SYSTEM. Enhancement of the current pathway. PROTEIN A establishes, in its greater freedom to mutate, a better version of its parent component, which then conveys an advantage on that mechanism, and PROTEIN A replaces the original parent component in the original mechanism. This can happen several times in sequential evolutionary time. The original, so-so functioning parent component is lost to mutational drift. See for example the many disabled copies of proteins in various protein families across the human genome.
4c) LOSS OF ORIGINAL FUNCTION. PROTEIN A's gene is disabled by mutational drift as it is just a duplicated copy, and is lost into the background of the genome.
4d) GAIN OF NEW LOCATION SPECIFICATION. PROTEIN A acquires a new transcription binding factor site that allows it to be expressed in another tissue, in another area, under different conditions, etc, leaving it open for a new round of cooperation and selection under different conditions.
4e) GAIN OF NEW PATHWAY. A new pathway gains an association with PROTEIN A, but at the same time PROTEIN A loses the ability to associate with its parent pathway, therefore being coopted into a new pathway and establishing a new function.
5) If that new function acquired by PROTEIN A conveys a reproductive advantage, it's "fixed" (pressured to remain relatively the same against mutation). If PROTEIN A's new function has no particular advantage, it stays in its new function as long as mutational drift will allow it to, which is an average function of change over time.
6) PROTEIN A now can generate more connections within the network. This involves generation of scale-invariant properties: Development of binding associations onto PROTEIN A from outside venues occurs and turns it into what we would define as a "hub protein", or "irreducibly complex".
This is accomplished by additional connections are made onto PROTEIN A from outside pathways in their own right. See #4 for mechanisms, although #4 was specifically addressing PROTEIN A's ability to change, you can apply #4 to every other protein in the organism, and this time PROTEIN A is the recipient of another protein's change.
Now that PROTEIN A is a hub in its own right, let's call it HUB A.
Some of these new associations on HUB A don't provide much evolutionary pressure if any, in that they're not critical to the function of the organism.
Some associations are high-pressure and functional in ways that can be construed as "irreducibly complex" in that they stabilize the hub in the places where it functions for that particular important pathway. That is, if a hub protein has a binding surface specific for one particular crucial pathway, you won't see that binding surface change much at all, while the rest of the hub structure is free to drift along and acquire mutational change. If you "break" one of those components in the conserved region, you kill the organism. So, certain protein-protein interactions on the same hub protein can be defined as IC, while other associations are certainly not IC as they are not critical to the function of the organism. A hub is not required to be IC in every pathway it is involved in, though it most certainly can be.
7) Co-evolution of seemingly irreducibly complex machineries during critical moments in a species' history.
This is the important point, this step #7, and is a bit long, so bear with me.
Our HUB A, in step #6, has acquired several new binding partners and is now a hub onto itself. It might be considered to be "irreducibly complex" in that monkeying around with the system would make it impossible to function. But that doesn't force other proteins to come in "from outside" the immediate functional environs of HUB A and associate with it. It's still fair game.
Because proteins can have so many non-specific interactions, at one point, HUB A becomes subject to a link into a pathway that heretofore was only mildly interesting to the organism. But suddenly, before that new connection to another pathway has a chance to mutate off into obscurity, that link suddenly becomes critical to the organism's survival.
HUB A suddenly has pressure to optimize in a new direction -- to support a new pathway that is absolutely or even occasionally important for survival, for instance during a once-a-year loss of available oxygen in the water during the algal summer bloom, etc. Else the system will fall under the knife of selection because our hub cannot optimize for these new stringent environmental conditions.
Our organism is, therefore, on the edge of destruction. The hub protein, its once-stable, happy function as an important part of a system of pathways has now had the crushing weight of "live or die" function in a new environment added to it.
The system will therefore be pressured to evolve, and evolve quickly to optimize that pathway over several generations. But there are already important components that rely on that system (it's "IC"), and will NOT like our hub component to change else the entire organism goes kaput if the change is too radical and disrupts the existing associations already keeping the organism alive.
So what does HUB A do, if it needs to change in a certain direction to optimize a newly important function/pathway to promote survival in these new difficult circumstances, but also must uphold its already-important pathway?
We can go to a specific example.
Let's start with a population, a few billion, bacteria in a warm and oozy pool who suddenly find that overcrowding has removed resources from one pathway (sulfur compound 1, SC1 ) while there seems to be quite a bit of free sulfur compound 2 (SC2) that nobody is utilizing. Suddenly, a bacterium, through the processes outlined in #4 above, aquires the ability to process (SC2) *weakly* by coopting SC1's pathway, while it simulatanously ekes out an existence on the measly bit of SC1 it's been living off of, all along.
Any small change which disrupts the weakly efficient but very important SC2 pathway will put the bacterium back into the pool of the have-nots, who are still struggling to survive in an overcrowded population.
A small change in the direction towards optimization of the new SC2 function but away from the current and very efficient SC1 function destroys the bacterium, since obviously small changes towards SC2 are most likely not going to be enough to make up for the energy availble from the wildly successful SC1 metabolic pathway, and the bacterium removes itself from the experimental gene pool.
But bacteria that can optimize SC2 while maintaining SC1 will have the advantage. First off, the bacterium who first established the weakly efficient pathway is free to reproduce, and admittedly at a faster rate than the other, older population, because even a weakly efficient pathway gives it more of an energy advantage for reproduction.
Then, from that pool of progeny, evolution experiments on adaptation to that new gene that allows SC2 to be processed along with SC1. But remember, our hub protein cannot evolve too far from the original SC1 function, so there's a pushme-pullyou going on in the system. Small incremental changes, and the failures dying off, are the only ways TO evolve a seemingly IC system. They're such small changes they could be called "adaptations" at that point, because each adaptation in the SC1-SC2 pathway allows more energy, and lots of it! to be given to that population of bacteria. Soon there is enough energy produced from the once-weakly-successful SC2 pathway that the pressure to hold onto its earlier function for SC1 production is tossed aside and the system completely roars into evolutionary high gear to completely optimize the system for SC2 utilization.
Or, if the bacterium takes the easy way out or if it has enough evolutionary time to duplicate the hub itself, it could duplicate the hub, and therefore evolve the duplicate to for SC2 processing. This addition would add to a scale-free network as it would evolve away from SC1 pathway into an entirely new hub structure surrounded by SC2 processing machinery.
I cannot see how all this cannot be a plausible and supported mechanism connected with scale invariance, gene innovation, genetic drift, and opportunistic evolution, all phenomena we have observed in the laboratory.
In this example, I have taken a previously IC system using observed mechanisms from throughout molecular biology and converted this IC system into another form without destroying the original system, in a stepwise fashion.
Now, if you'd like biochemically relevant mutations, we can talk about that. I am a biophysicist (protein structuralist) by training, and I'd enjoy discussing evidence for pathway cooptation and the "mutability" of active sites, and the generic structure of protein-protein interaction sites.
Mr. Dembski writes:
quote:
Or consider: " I argue scale-free invariance in networks is the smoking-gun evidence for exactly what you're asking for." But where's the argument?
The argument is that the networks were formed by local additions and changes (small incremental steps) under global pressures (fixation and selection) to produce scale invariance, as in the small example of the bacterium above.
Mr. Dembski writes:
quote:
Where's the causal specificity? It's all fine and well to model an evolutionary process computationally and get hierarchical systems exhibiting scale invariance.
I present my causal specificity above.
Mr. Dembski writes:
quote:
But scale invariance is a global property that can be modeled without ever introducing irreducible complexity (indeed, the work you cite has proceeded quite nicely without Behe). IC is a local property. That's why it needs to be assessed system by system.
In SCALE INVARIANT networks, local is the same as global, that is the definition of "scale invariant". The behavior of the network on a local level is the same as the behavior of the network on a global level, one interpretation is that the network was built up using "local" factors under "global pressures" so that no matter how far out, or how far in, you examine the network, it has the same properties. So, locally, yes, scale invariance is important.
You will certainly need to introduce IC into a model to test if it is supported by scale invariance. I can think of a few ways that you can describe scale invariance supporting IC, but only if you assume IC systems evolve!
Perhaps someone else with less observational bias can come up with a way that scale invariance produces evidence of IC as a counter-argument to sequential addition of once-unnecessary components into a growing and evolving complex network.
One can attempt to prove that models such as my model above, of an IC system in a bacterium evolving a new function and therefore changing an already-IC system in the direction of a new function is mathematically improbable. This would have to be in the context of generating a scale-free network, using all the evolutionary mechanisms we observe or find evidence of in a laboratory (cooptation of pathways, non-specific protein interactions, gene duplication, retrotransposons, gradual adaptation, opportunistic mutation, selection, competition).
Mr. Dembski writes:
quote:
I find your conclusion remarkable: "I await eagerly the contrary proof that scale invariance is not sufficient proof of sequential addition and redeployment on a ancestral, simpler network, given that Darwinian evolution proposes such changes over the span of evolutionary time." In other words, given that Darwinian evolution is compatible with (there's no requirement here) scale invariant networks at whose principal nodes sit IC systems, there's no need to supply actual detailed Darwinian pathways of how these IC systems arose. This is like saying we can believe that lead gets transformed into gold without ever seeing how the alchemist effected the transformation. And why? Because scale invariance is simply posited as the new philosopher's stone.
Not exactly. I'm saying that scale invariance shows that lead HAS been turned into gold. It's ironic that you should use the philsopher's stone to criticise my approach, as I shall show in a minute.
I say that the fact that lead was turned into gold is proof that there was a mechanism, containing a logical sequence of events, that turned that lead into gold. Using the alchemist analogy, I am NOT claiming a philosopher's stone that can transmute lead into gold, in one fell swoop.
The irony is that, using that analogy, ID is the mechanism that claims a philosopher's stone!
Evolution does not claim a mystical, magical mechanism. It claims a chemical, logical sequence of events to turn the lead into gold. Something like, "LEAD -> compound A -> compoud B -> compound N -> GOLD." using mechanisms within those arrows that are logical and progressive, and not always at the same rate.
You must admit that ID posits "LEAD -> MIRACLE -> GOLD". which is the exact essence of the philosopher's stone you accuse me of using.
I'm asking you for proof as to other explainations outside of Darwinian evolution that can explain the lead-> gold transition.
If you want to posit an instantanous design, a miracle of disbelief, then that cannot be proven, and there is no science in your examination.
I'm not saying that there can't be other explanations, and I'm waiting for an alternate, better explanation of the import of scale invariance in biological networks outside of sequential, gradual addition of local components (including assembly of protein "machines").
We have proof of scale invariance. We have proof of mechanisms that are implicated in generating that scale invariance. I would like to discuss why scale invariance (observed) coupled with genetic mechanisms (observed) can not result from the sequential addition of components within "irreducibly complex" systems, proof that you demand and I insist are satisfied by the inferences above. If you disagree with my inferences, you should be able to say why, for instance, segmental duplication is not real, or why it cannot produce new genes, and why incremental evolution and gene duplication cannot explain scale-invariance in biological networks.
Mr. Dembski writes:
quote:
I'm afraid I won't be able to do anything on this thread till the weekend.
We're all patient adults. Please take your time!
Deanne
[ 19 September 2002, 08:49: Message edited by: Deanne M. Taylor ]
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charlie d.
Member
Member # 159
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posted 19. September 2002 13:15
Boy! Away one week, and immunology hell breaks loose. It took me a while to catch up with this thread! In general, I noticed the very open disdain of some ID supporters for accurate descriptions of published data and testable hypotheses, as if science could be made just out of generalizations and broad concepts. Face it, if one really wants to know whether and how the immune system evolved, one has to deal with "minutiae" like the existence of Ig domains and ITAMs in invertebrates, or the function and mechanisms of innate immunity in insects, and the biochemistry of transposases. Simply, one needs to know it all. To say that one cannot be bothered to keep up with the literature, while at the same time making claims on what the literature can or cannot explain, is simply mind-boggling arrogance. This is, in fact, what surprised me of Behe's DBB chapter on immunology (the only one I was qualified to judge) when I first read it: it was so dense in misconceptions, lack of basic facts, and misrepresentations that my conclusions were that if that was the level of scholarship in the entire book, it was abismally low indeed.
Now, I see Nic, rafe and others have made a good job at dismantling the original concept of the immune system's ICness - to the point that, like the old creationist ploy regarding transitional fossils, every new element discovered that supports evolution is just used as a starting point for a request for more, and more finely grained, intermediates. How self-defeating that strategy is, is obvious from the long history of creationist retreat from claims on the evolution of birds or cetaceans.
Finally, a couple of technical points, in response to Paul, who said:
quote:
Let’s focus on claims (2) and (3).
(2) Transcription is a tightly regulated process. What evidence shows that the novel RAGs would be expressed only "in a lymphocyte-like cell," and not in other cell types? Inlay’s hypothesis turns on the genes only where he wants them expressed. How?
(3) Organisms lacking V(D)J recombination -– i.e., that do not possess an adaptive immune system –- get along just fine without it. What evidence shows that receptor diversity (supposing [2] occurred) nevertheless conveyed a fitness difference?
As for (2), there is very solid evidence from the study of transcriptional regulation: expression of most genes is regulated by both proximal elements (the promoters), and enhancers which exert their activity at a distance, and work to control larger chromatin regions, sometimes including multiple genes. In the case of immunoglobulin genes, the major elements controlling their expression are a set of enhancers, usually one located in the first major intron of the gene, and one (sometimes more) located distally, 3' of each locus. These enhancer elements all can work by controlling expression not only of the immunoglobulin promoters, but also of any other promoter that may happen to be - through natural or artificial rearrangement processes - located in the vicinity (enhancer activity is rather spurious in its specificity for promoters). Thus, for instance, many chromosomal translocations are known that transfer cell growth-controlling genes in proximity to Ig loci. These growth controlling genes are then dysregulated in their expression, taking on the pattern of expression of Ig loci (constitutive, high level expression in B lymphocytes), resulting in uncontrolled cell growth and cancerogenesis (giving rise to lymphomas or leukemias). Any transposon gene inserting itself into a primordial Ig locus, like the translocated oncogene promoters in lymphomas, would find itself under the control of such enhancer elements, and would become expressed in teh same cells as the proto-Ig genes themselves.
Paul's point (3), on the other hand, falls more into the vague, unsatisfiable requirements ID advocates are so fond of. How would one reasonably show a fitness difference deriving from a novel gene whose detailed structure and function we cannot know, in an organism that simply does not exist any more?
Just to amuse Paul, I would say I think there is little doubt that antigen receptor diversity confers an advantage to organisms. There is also much evidence that in organisms that do not have mechanisms for the combinatorial generation of antigen receptors, diversity is generated evolutionarily by the common mechanisms of gene duplication and divergence, such as in the case of the multiple, broad specificity soluble receptors in insects. This clearly suggests the existence of selective pressures favoring receptor diversity, by any means necessary.
Therefore, transpositional recombination of gene segments may just be one of the mechanisms that can efficiently add extensive diversity. The interesting issue is, it may not be the best one. Indeed, there are at least 2 vertebrates that have essentially "opted out" of the classic combinatorial rearrangement process in favor of other alternatives: rabbits and chickens. With some differences, in both rabbits antibody heavy chanis and chickens (all chains) the role of the combinatorial assembly of variable region segments is extremely limited, with only one or at best a few variable segments used, and most of the variability deriving from other processes, such as gene conversion from V region pseudogens, or somatic hypermutation of rearranged segments. That 2 such distant organisms would reach similar solutions to antibody variability is intriguing because it may suggest that these alternative systems could indeed be more efficient than the classic one. This raises two interesting design conundrums, I think. First, if the "classic" system of combinatorial diversity is a marvel of design, as it seems, why would some species require such a radical re-engineering of the entire system (and in the rabbit case, why only on some Ig genes and not others)? Doesn't this look haphazard to say the least? And second, assuming that the alternative system is indeed better: why would a designer favor rabbits and poultry, over us?
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Deanne M. Taylor
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posted 19. September 2002 13:18
An interesting quote (and a derivative of Barabasi's research on scale-free networks), text in brackets is mine, from New Scientist:
"They found two vital ingredients [in the qualities of scale-free networks]. First, a scale-free network must be growing -- so that the Web needs new pages to be added every day, and the actors' network needs a constant supply of raw talent. Second, these new recruits must show some form of preference as they attach to the network...[various examples deleted for brevity]... With proteins, one candidate for this "preference" mechanism is gene duplication -- a rare occurance during cell division when genes are copied twice. Every time this happens, all the proteins that interact with the duplicate protein get another link."
If you want more on this article, go to the bottom of this post. The whole PDF is available.
For those who enjoy visuals, here's a simplified picture of what a scale-free network looks like. Biological networks tend to follow this kind of appearence.
Some might make the connection between this pattern and how networks of this kind can spring up from simple networks that see duplication, addition, and evolution over time.
This particular picture of a scale-free network is one that represents a airborne spreading contagion through a population. However, this same kind of scale-free network appears in biological networks.
Picture of a scale-free network (simplified)
I might also add that Barabasi has a book out now on networks in the popular press:
Barabasi's book, "Linked"
New Scientist's cover story on scale-free networks (I had no idea this subject was getting so popular!)
New Scientist Article on Scale-Free Networks
And one more paper...the preprint PDF of Barabasi's study on scale-free networks in yeast including actual measurements of degree of connectivity vs. how important that protein is to actual knock-out experiments. (Yeast is a eukaryote, and while it is a simple organism it exhibits function similar to higher organisms which, coincidentally, also have scale-free network behavior in their protein networks).
Barabasi's paper on function of proteins in scale-free networks (read for yourself!)
[ 19 September 2002, 23:29: Message edited by: Deanne M. Taylor ]
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Paul A. Nelson
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posted 19. September 2002 15:03
Charlie wrote:
quote:
As for (2), there is very solid evidence from the study of transcriptional regulation: expression of most genes is regulated by both proximal elements (the promoters), and enhancers which exert their activity at a distance, and work to control larger chromatin regions, sometimes including multiple genes. In the case of immunoglobulin genes, the major elements controlling their expression are a set of enhancers, usually one located in the first major intron of the gene, and one (sometimes more) located distally, 3' of each locus. These enhancer elements all can work by controlling expression not only of the immunoglobulin promoters, but also of any other promoter that may happen to be - through natural or artificial rearrangement processes - located in the vicinity (enhancer activity is rather spurious in its specificity for promoters). Thus, for instance, many chromosomal translocations are known that transfer cell growth-controlling genes in proximity to Ig loci. These growth controlling genes are then dysregulated in their expression, taking on the pattern of expression of Ig loci (constitutive, high level expression in B lymphocytes), resulting in uncontrolled cell growth and cancerogenesis (giving rise to lymphomas or leukemias). Any transposon gene inserting itself into a primordial Ig locus, like the translocated oncogene promoters in lymphomas, would find itself under the control of such enhancer elements, and would become expressed in teh same cells as the proto-Ig genes themselves.
Some questions:
1. My original comment/question (2) was poorly phrased. Let me try again. Presumably the proto-RAG transposon could land anywhere in the genome, and be expressed (or not). What evidence shows that the proto-RAG transposon would insert only into a primordial Ig locus, and be expressed only in the cell types where that locus was active?
2. What evidence shows that the normal function of the primordial Ig locus -- i.e., its function prior to the RAG insertion -- would not be disrupted or compromised by the RAG transposon?
Charlie continued:
quote:
Paul's point (3), on the other hand, falls more into the vague, unsatisfiable requirements ID advocates are so fond of. How would one reasonably show a fitness difference deriving from a novel gene whose detailed structure and function we cannot know, in an organism that simply does not exist any more?
The “vague, unsatisfiable requirements” aren’t mine. They are set by the theory of natural selection itself. In the thread above, Yersinia argued that selection explained the origin of the immune system. To support that claim, he needs to provide the relevant evidence.
Charlie continued:
quote:
Just to amuse Paul, I would say I think there is little doubt that antigen receptor diversity confers an advantage to organisms. There is also much evidence that in organisms that do not have mechanisms for the combinatorial generation of antigen receptors, diversity is generated evolutionarily by the common mechanisms of gene duplication and divergence, such as in the case of the multiple, broad specificity soluble receptors in insects. This clearly suggests the existence of selective pressures favoring receptor diversity, by any means necessary.
Or not. Bacteria have nothing resembling the vertebrate immune system, and they're doing just fine.
In his talk.design article, Matt Inlay said that the descendants of the original RAG mutant "thrive with the increased immune capabilities." But how does he know this?
I suggest that he doesn't know it. Rather, he's simply waved the wand of "natural selection" over a (putative) historical episode, postulated an entirely hypothetical selective advantage, and called it an explanation.
Charlie concluded:
quote:
Therefore, transpositional recombination of gene segments may just be one of the mechanisms that can efficiently add extensive diversity. The interesting issue is, it may not be the best one. Indeed, there are at least 2 vertebrates that have essentially "opted out" of the classic combinatorial rearrangement process in favor of other alternatives: rabbits and chickens. With some differences, in both rabbits antibody heavy chanis and chickens (all chains) the role of the combinatorial assembly of variable region segments is extremely limited, with only one or at best a few variable segments used, and most of the variability deriving from other processes, such as gene conversion from V region pseudogens, or somatic hypermutation of rearranged segments. That 2 such distant organisms would reach similar solutions to antibody variability is intriguing because it may suggest that these alternative systems could indeed be more efficient than the classic one. This raises two interesting design conundrums, I think. First, if the "classic" system of combinatorial diversity is a marvel of design, as it seems, why would some species require such a radical re-engineering of the entire system (and in the rabbit case, why only on some Ig genes and not others)? Doesn't this look haphazard to say the least? And second, assuming that the alternative system is indeed better: why would a designer favor rabbits and poultry, over us?
Yes, it's terribly unfair. I can see gulls from my office window, winging along swiftly at several hundred feet, and thus avoiding the miserable afternoon traffic here in the northern suburbs of Chicago. The designer shortchanged me. I want my wings!
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andyg
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posted 19. September 2002 15:52
QUOTH Paul Nelson:
Andy wrote:
quote:
You seem to be asking for something that you know cannot be produced, and feigning horror when it is
not made available.
Yersinia says the vertebrate immune system evolved via natural selection. I'd like to know how he learned that.
END QUOTE.
Just out of interest, what evidence for Yersinia's statement would you find convincing?
AndyG
(answering a short post with another short post)
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charlie d.
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posted 19. September 2002 17:02
quote:
1. My original comment/question (2) was poorly phrased. Let me try again. Presumably the proto-RAG transposon could land anywhere in the genome, and be expressed (or not). What evidence shows that the proto-RAG transposon would insert only into a primordial Ig locus, and be expressed only in the cell types where that locus was active?
None - there is no such requirement. Transposons insert themselves pretty much anywhere. They are probably doing that, right now as I type, in my genome and yours. In most cases they do no harm, in others they cause disease, in a few cases, they may create new functional combinations by moving stuff around. However, once a transposon inserts itself in proximity to a certain locus, its genes can fall under the regulation of that locus' transcriptional control elements, and become expressed in that locus' specific pattern, just like translocated oncogenes do.
quote:
2. What evidence shows that the normal function of the primordial Ig locus -- i.e., its function prior to the RAG insertion -- would not be disrupted or compromised by the RAG transposon?
None, but that's not a scientifically testable question, is it? In other words, what kind of evidence are you thinking about exactly? How would one meaningfully test that?
quote:
The “vague, unsatisfiable requirements” aren’t mine. They are set by the theory of natural selection itself. In the thread above, Yersinia argued that selection explained the origin of the immune system. To support that claim, he needs to provide the relevant evidence.
Wrong: the theory of natural selection does not require that every single trait be testable for its adaptive value. That's just an artificial hurdle set by skeptics of the theory. It's as if gravitation skeptics were asking to prove that Jupiter's moons are held in orbit by that planet's gravitational attraction by directly measuring it, and then by somehow blocking it to see if the moons fly away.
quote:
In his talk.design article, Matt Inlay said that the descendants of the original RAG mutant "thrive with the increased immune capabilities." But how does he know this?
I suggest that he doesn't know it. Rather, he's simply waved the wand of "natural selection" over a (putative) historical episode, postulated an entirely hypothetical selective advantage, and called it an explanation.
You are playing the same trick again. Unless we clone and genetically modify extinct early vertebrates, and reconstruct their ecosystems, including their common pathogens, there is no way this can be tested. However, we can be reasonably sure that one of a number of scenarios that do not contradict what we can observe every day about evolution and molecular biology, could have happened. Just as we can be reasonably sure that Jupiter's moon's orbits do not work in any different way than our own moon, or for that matter by any law different from that applied on falling apples.
Let me be very clear: I am quite positive Matt Inlay did not intend his scenario as an accurate description of the actual events in the evolution of the immune system. As several people have pointed out before in this thread, however, the whole point of DBB's chapter 6 was that no such scenario existed or could even be envisioned: how could antibodies exist without recombination, or recombination without antibodies? The 2 had to appear together, and that was essentially impossible: IC! In fact, Behe should have already known, had he looked at the relevant literature, that functional antigen receptors that do not rearrange do in fact exist. He should have also known, had he bothered to at least ask any immunologist, that the transposase cooption hypothesis already existed. It also happened that within a couple of years from DBB, that hypothesis found strong experimental confirmation: such luck! So, do antigen receptors and their rearrangement machinery form an IC system? No, they don't. Neither does the complement system, for that matter: examples of partial complement cascades are now well known. Neither is the change from membrane to secreted immunoglobulins (the third of the immunological "misteries" of DBB chapter 6): antigen receptors can work effectively as entirely soluble, or entirely membrane-bound, molecules.
Basically, the IC edifice for the immune system has crumbled. What ID advocates are left to ask about the immune system, and other once-(supposedly)impenetrable IC examples, is something that anyone could ask about almost anything in biology: how did insulin evolve, step by step, with all intermediates defined and their selective advantages proven? How about nails, or nose hair? What's so special, then, about the immune system, or the flagellum? What's so special about IC, or CSI? If we know that jaw bones can turn gradually into a hearing system, that enzymes can turn into crystallins, or molecular antifreeze, why not other apparently unlikely scenarios?
Do we know how the immune system evolved? Only in a very sketchy way. Will we ever know all, or even most, details? Almost certainly not. Is there anything about immune system evolution that appears insormountable with respect to what we know about evolution, genetics, molecular biology? Not even close.
[ 19 September 2002, 20:30: Message edited by: charlie d. ]
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andyg
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posted 19. September 2002 17:42
Mike Gene wrote:
"That is, the most we can get (and ever hope to get) from such a good-faith explanation is "the immune system looks like it evolved and it's reasonable to think natural selection could have been behind its evolution." The problem comes when some (many?) people insist that all knowledgeable, intelligent, sane, and honest people would admit that the immune system did in fact evolve by natural selection"
This smacks of a straw-man argument to me. Who are these people who "insist" that ALL (emphasis mine) knowledgeable, intelligent, sane, and honest people would admit that the immune system evolved by natural selection? The only possible candidate I could think of offhand would be Richard Dawkins.
My own guess, for what it's worth, would be that most scientists would say something along the lines of "well, I'm not an immunologist myself, and I don't spend much time thinking about molecular evolution either. Until someone comes along with a more plausible explanation, my default, lay-scientist position is that the vertebrate immune system liekly evolved. Once I finish writing this grant, I'll see if I can get over to the library and do some Medline searches to see if anyone has had any bright ideas".
It's a fair question ask what sort of molecular evidence would satisfy Mike Behe or Bill Dembski that a particular system likely evolved. Would their evidentiary criteria be qualitatively different from a consideration of, say, whether birds evolved from a reptilian ancestor? Is it fair for people to resort to a Designer-of-the-gaps argument in either case?
AndyG
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