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Author
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Topic: Organisms using GAs vs. Organisms being built by GAs
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yersinia
Member
Member # 324
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posted 16. September 2002 16:37
Dr. Peonie,
Very briefly,
quote:
1. I do not think that Yersinia made their case in any direct sense. I pointed out two examples where predictions did not hold.
A. The RAG genes are not derivative from lower eukaryotes
B. The vertebrate class I and II MHC do not show homology to molecules in lower eukaryote rejection reactions
(A) I agree with, rather we have a well-supported hypothesis for the origin of RAGs. You even appear to agree, below, that the explanation has strengthened in recent years. I'm not sure how this causes difficulties for evolution in any way...
(B) I posted some indications from the literature that, first, research is just beginning (give me that tunicate genome sequence!) and second, even extant literature hints that success is expected in terms of discovering MHC homology in basal deuterostomes. Again, I don't see the problem. Call the discovery of strengthening indications of MHC homology another future prediction of RM&NS if you like.
quote:
But the futility of this thread and the arguments go deeper.
A. First, I think the argument of irreducible complexity is well nigh impossible to defend, regardless of the possible truth or falsity of its premise. It will always be subject to the creativity of “this or that might have happened”. Thus I would not want to enter into a defense of that notion.
Neither would I, but not because of the mere imagination of evolutionary biologists. The real problem with the IC argument is lots of physical evidence that contradicts it, as is being demonstrated in the thread.
quote:
B. Second, I believe that the arguments made by Yersinia and most antagonists in this debate carry with them a hidden assumption. That assumption is this: any scenario wherein the DNA of an organism might have been altered, whether known now or yet to be discovered is in the domain of natural evolution, natural design or whatever one wants to call it and, by the same token, not it the domain of a designer.
Like I said above, sure, it's possible that the putative IDer mimicked known natural processes. But why propose an IDer if natural processes are sufficient? The processes invoke in explaining the origin of the vertebrate immune system are not anything really wild, rather they are things like gene duplication, subsitution, insertion/deletion, etc., or more generally speaking, cooption and specialization. These are all things that we are observing in modern genomes as occurring naturally, so why invoke ID over these natural processes in the past? It's unparsimonious.
quote:
Finally, there was this bit about the flagella. The argument of the flagella hinges on where
Aquifex is located in the scheme of things. From my perspective this is simply impossible to sort out.
And archaea also. I agree that the question of the deep phylogeny of microbes is currently unresolved. Given the known capabilities of prokaryotes for LGT, the fact that these are the absolute oldest events in the history of life, and the short history of serious investigation of the question compared to metazoan phylogeny (decades vs. centuries), I think this is to be expected.
quote:
However, given the status of things, hinging an argument on deriving the flagella from “older” Aquifex or something like that seems weak. I am not calling this into question as a defense of irreducible complexity, I am simply commenting on the character of these arguments.
Sure, but then all phylogeny-dependent inferences are going to be weak for these very ancient events, including Mike Gene's argument that the flagellum is basal and was included in the (designed) LCA of bacterial. Cavalier-Smith (2002), for example, proposes a bacterial phylogeny that he says includes a possible nonflagellate outgroup.
I would be perfectly prepared to shrug and leave the whole case of the flagellum aside until more phylogenetic information is available (e.g. comparable to our knowledge of metazoan phylogeny), but the Intelligent Design movement has picked the single most ancient of Behe's IC systems as their emblem, somewhat protected from scrutiny (for the moment) by a few billion years of time. So I feel compelled to look at the limited available evidence and point out even there we have indications of just what the ID folks are demanding in the form of precursors.
Returning to the Main Point, though, Dr. Peonie: don't you agree that the arguments of the ID movement are best tested in systems that are much more recent, where the evidence regarding their origin is much more accessible? Wouldn't you agree that the success of evolutionary immunology is a point in favor of modern evolutionary biology and a point against the hypothesis that direct intervention by an unknown designer must be invoked to explain complex structures?
yersinia
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rafe gutman
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Member # 134
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posted 16. September 2002 17:44
dr. poenie,
quote:
But the futility of this thread and the arguments go deeper.
A. First, I think the argument of irreducible complexity is well nigh impossible to defend, regardless of the possible truth or falsity of its premise. It will always be subject to the creativity of “this or that might have happened”. Thus I would not want to enter into a defense of that notion.
i agree, michael behe's argument from irreducible complexity requires that no natural pathway be possible in order to make a design inference. remember, dr. behe attacks both the adaptive and the innate immune system. the complement system is on his list of IC systems. you apparently don't question its evolution, would you agree that dr. behe was wrong in this case?
quote:
B. Second, I believe that the arguments made by Yersinia and most antagonists in this debate carry with them a hidden assumption. That assumption is this: any scenario wherein the DNA of an organism might have been altered, whether known now or yet to be discovered is in the domain of natural evolution, natural design or whatever one wants to call it and, by the same token, not it the domain of a designer.
i agree, i personally can't think of any evidence that couldn't be explained by intelligent design. this lack of falsifiability is a serious weakness of ID.
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Paul A. Nelson
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Member # 26
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posted 16. September 2002 19:37
Yersinia,
You wrote:
quote:
The processes invoke in explaining the origin of the vertebrate immune system are not anything really wild, rather they are things like gene duplication, subsitution, insertion/deletion, etc., or more generally speaking, cooption and specialization.
Can you explain -- in your own words, and avoiding extensive quoting -- the specific selective advantages invoked (in the relevant literature) for these events? Please give the formulation of the theory of natural selection that you are employing.
[ 16 September 2002, 19:38: Message edited by: Paul A. Nelson ]
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yersinia
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Member # 324
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posted 16. September 2002 21:13
Hi Paul,
quote:
Can you explain -- in your own words, and avoiding extensive quoting -- the specific selective advantages invoked (in the relevant literature) for these events? Please give the formulation of the theory of natural selection that you are employing.
Hi Paul,
I'm not sure why having it in my own words is important, I'm not an evolutionary immunologist. My point is that ID has completely failed to deal with the experts and their literature in this field, despite Dembski et al. making continual claims that such literature does not exist.
Why should I, as a nonexpert, take ID seriously when it's quite clear that there are entire fields of extensive research on the evolution of complex systems that the IDists have straight-out denied the existence of for years, let alone refuted in any way?
Regarding the role of natural selection, it's pretty clear that the basic selection pressure way back from basal bilaterans to the adaptive immune system of vertebrates is simply enhanced immune function, especially in terms of enhancing (1) diversity of receptors and (2) regulation of an increasingly powerful system. Inlay's article already provides as close to a layman's exposition of the literature as you're going to get and already contains more material than will ever get discussed in a bulliten board thread regarding the advantages of particular mutational steps. The benefit of improved immune response seems rather obvious to me, and indeed there is a pretty huge literature on natural selection and the immune system, e.g. on MHC diversity (lots of articles) which proves the constant influence of natural selection for improved immunity.
The question is not really what the selective pressures were, that is pretty obvious in this case: diseases are continually trying to eat you alive. The assertion that Dembski has been making is that you "can't get to here from there" because the intermediates were not functional, but as we've seen, this appears insupportable.
yersinia
PS: Gluttons for punishment can however check out this peer-reviewed article all about the selective forces guiding the evolution of the vertebrate immune system:
quote:
Cohn M. Immunol Rev 2002 Jul;185(1):24-38
The immune system: a weapon of mass destruction invented by evolution to even the odds during the war of the DNAs.
(link includes related articles)
Living systems operate under interactive selective pressures. Populations have the ability to anticipate the future by generating a repertoire of elements that cope with new selective pressures. If the repertoire of such elements were transcendental, natural selection could not operate because any one of them would be too rare. This is the problem that vertebrates faced in order to deal with a vast number of pathogens. The solution was to invent an immune system that underwent somatic evolution. This required a random repertoire that was generated somatically and divided the antigenic universe into combinatorials of determinants. As a result, it became virtually impossible for pathogens to escape recognition but the functioning of such a repertoire required two new regulatory mechanisms: 1) a somatic discriminator between Not-To-Be-Ridded ('Self') and To-Be-Ridded ('Non-self') antigens, and 2) a way to optimize the magnitude and choice of the class of the effector response. The principles governing this dual regulation are analyzed in the light of natural selection. [outline]
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Argon
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Member # 276
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posted 16. September 2002 23:04
Yersinia,
Hopefully I'll be corrected if wrong, but I believe that what Paul Nelson and Bill Dembski are asking for is really no different from Behe's request in _Darwin's Black Box_. Essentially, that is to see fairly detailed calculations about specific biochemical interactions involved in the evolution of system by means of mutation and natural selection. To quote from DBB (wrt explanations about the evolution of the blood clotting system - page 94):
quote:
Nothing is said about the amount of clotting material initially available, the strength of the clot that would be formed by a primitive clotting system, the length of time the clot would take to form once a cut occurred, what fluid pressure the clot would resist, how detrimental the formation of inappropriate clots would be, or a hundred other such questions. The absolute and relative values of these factors and others could make any particular hypothetical system either possible or (much more likely) wildly wrong.
Bill writes:
quote:
Pathways are continuous trajectories that connect the dots. The issue is not whether the dots are in place but how to connect them.
It is one thing to consider sequence similarities as possible indicators of common descent, but are Behe, Dembski and Nelson being unreasonable to demand that evolutionists provide calculations about how specific mutations would affect the performance of an earlier system undergoing evolution? Is it unreasonable to conclude in favor of an ID explanation when the detailed mathematical models of cell functions, such as outlined above by Mike Behe, are not presented? Should one be wary of a "scientific explanation" that lacks transparent mathematical clarity?
I hope that Bill and Paul can comment further.
[ 16 September 2002, 23:52: Message edited by: Argon ]
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Martin F. Poenie
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Member # 10
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posted 16. September 2002 23:35
Gosh, dragged back to this again
I will post a little more later, can't do it now. I only want to say to Rafe is if Mike Behe wants to defend IC on blood clotting then more power to him. What I know about platelets and blood clotting is that when Tim Rink tried to quickly pull 50cc of blood out of me to get platelets I passed out and it ruined the experiment.
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Mike Gene
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Member # 149
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posted 17. September 2002 00:01
Hi Nic,
You write:
If RM & NS can produce the vertebrate immune system in all of it's glorious, IC (Behe 1996) complexity, then asserting that some extra factor such as ID must be introduced to explain the flagellum is unparsimonious.
I am aware that Mike-Gene-ID is prepared to concede the natural evolution of certain complex, IC things like blood clotting and the immune system and yet maintain the ID inference for other cases of complexity such as the flagellum where the origin events are far more remote and the available evidence is much spottier, but (a) I think that is highly unparsimonious and (b) in any case, this kind of inconsistency is not a part of Dembski's argument, which is what we're talking about.
Well, as I have explained before, there is no inconsistency on my part. That you think inconsistency is involved is a function of at least two faulty assumptions. And the complaint about "spottier available evidence" has already been answered. But I'd rather not fray the thread any more by going into these and instead stick to the topic-relevant point.
Above, Dembski asked you to put your "hallmarks of evolution" on the table. You then listed three criteria. I found this encouraging. However, in light of your parsimony argument above, it's starting to look like your hallmarks have no teeth. Above, you seem to be arguing that you accept the evolution of the flagellum because of the evolution of blood clotting and the immune system. In other words, you don't need any hallmarks in the case of the flagellum. Instead, you appeal to philosophical arguments about parsimony.
As I see it, a rigorous hallmark would be used to score something as evolved or not. That is, biological features that fail to exhibit any of your hallmarks should not be scored as "evolved." But how can this be when the non-teleological approach begins by assuming every biotic feature arose through evolution? That is, since you already believe every biotic feature arose through evolution, and use parsimony arguments to justify extrapolating evolution here from evolution there, your hallmarks appear to be nothing more than window dressing that are applied, post-hoc, if they can be applied. Put simply, your hallmarks do not appear to have any scoring power since failure to find hallmarks does not dislodge or even weaken the evolution belief. It seems to me you are trying to draw from two different methodological approaches that don't mix very well - one approach scores and the other approach generalizes.
I do think the scoring approach is a better way to address a history full of contingency. Attempts to generalize end up smearing all biotic data into a blurry, homogenous whole, such that changing wing colors in moths becomes evidence for the Darwinian origin of the bacterial flagellum. I prefer the investigative method that scores; one that is open-ended, looking for the best explanation rather than merely looking for facts to support preconceptions. This is why your leading attempt to highlight hallmarks of flagellar evolution (motA-exbB homology) is much better than the philosophical arguments revolving around parsimony. That's why I will try to get to it in the next few busy days.
PS: In the meantime, you wrote:
Surely the reasons that the capabilities of mutation alone are considered limited are well-known to everyone from Dawkins to Dembski, do I really have to repeat it here?
Yes, please do. I'd rather not assume anything here. I think it might be instructive to consider why is it that the capabilities of mutation alone are so limited. The ties in are numerous.
[ 17 September 2002, 00:08: Message edited by: Mike Gene ]
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rafe gutman
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posted 17. September 2002 01:10
quote:
yersinia: The processes invoke in explaining the origin of the vertebrate immune system are not anything really wild, rather they are things like gene duplication, subsitution, insertion/deletion, etc., or more generally speaking, cooption and specialization.
paul: Can you explain -- in your own words, and avoiding extensive quoting -- the specific selective advantages invoked (in the relevant literature) for these events? Please give the formulation of the theory of natural selection that you are employing.
i'd like to answer this for the complement system. the original complement protein contained a thioester group that is cleaved by serine proteases. when an infectious agent's serine proteases cleaves this protein, it exposes the thioester group, which then binds covalently to the pathogen's serine protease, inactivating it. later, the system evolved it's own serine protease (perhaps co-opted from the blood-clotting cascade), and could activate the complement protein by itself. now the system could protect itself from pathogens by attaching large amounts of complement to them, neutralizing them (agglutination). later, receptors appeared that facilitated the elimination of these complement-bound pathogens by phagocytosis (opsonization). later, the complement proteins evolved the ability to induce local inflammation (anaphylatoxins). finally, the complement system evolved a cytolytic ability (lysis). all of this proceeded through the mechanisms that yersinia initially described.
i'm not sure if this is detailed enough for you, but many of the details are out there in the literature. if you'd like more specifics, you'll first have to present a model for how this system could have originated via intelligent design, with at least as much detail as a i presented.
"quid pro quo, clarisse"
[ 17 September 2002, 01:13: Message edited by: rafe gutman ]
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yersinia
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posted 17. September 2002 01:18
I'm probably past 3 posts so I will be brief.
Forgive me Argon but I'll leave aside blood-clotting for Rafe Gutmann or another poster, but briefly I think that Behe's arguments on blood-clotting have just as many problems as his immune system chapter (critiqued in detail by Inlay; and if you read the Inlay article, you will discover that indeed blood-clotting and the complement system have common origins if you go far enough back). Ken Miller among others has written at some length on the issue. A fairly thorough list of articles and web links is online here. I think that Mike Gene for one more-or-less concedes the case on blood-clotting, and as Peonie has indicated that he is amenable to the gradual origin of the innate immune system (specifically declared IC by Behe 1996, let us not forget) I expect that he would feel similarly about the origin of blood-clotting as the nature of the evidence is quite similar.
Regarding math, Argon writes,
quote:
It is one thing to consider sequence similarities as possible indicators of common descent, but are Behe, Dembski and Nelson being unreasonable to demand that evolutionists provide calculations about how specific mutations would affect the performance of an earlier system undergoing evolution? Is it unreasonable to conclude in favor of an ID explanation when the detailed mathematical models of cell functions, such as outlined above by Mike Behe, are not presented? Should one be wary of a "scientific explanation" that lacks transparent mathematical clarity?
Like ID for instance?
Mathematical models are only meaningful in very restricted situations where one has very high confidence in the input assumptions. Otherwise it's garbage-in, garbage-out. A great deal of science proceeds by the much more generally applicable method of hypothesis proposal and testing. Geologists didn't employ probability calculations to determine whether or not an asteroid hit the earth 65 million years ago or to construct the theory of plate tectonics, they just followed the usual observe-hypothesize-predict-test cycle.
Basic reasoning about evolutionary models uses several methods to justify assumptions that certain hypothesized stages and events are high probability:
1) Extant organisms and systems (i.e., Miller and others have made the point to Behe that you can't say that simpler blood-clotting systems are unlikely, because current organisms get by today with just such simpler systems; the requirement for a blood-clotting system are less demanding if you have, for instance, a low-pressure circulatory system with but a rudimentary heart).
2) Extant observed (or inferred from the evidence-rich recent geologic past) processes. The various forms of e.g. gene duplication and cooption or specialization, other mutations, polyploidy, transposon activity, etc. -- all of these are common enough in the lab or the recent past and therefore would appear to be quite likely events anytime in the past that life-as-we-know-it (ie DNA/RNA/protein) exists.
3) Phylogenetic reconstruction. This gives us an outline of roughly what happened, in what order. A lot more could be said here but for a summary of why phylogenetic methods are generally speaking reliable see here and particularly the bit on the statistics of generating independent congruent trees by chance.
There are probably more but you get the idea. Origins-of-complex-systems hypotheses are not built in some world where nothing is known about how biology works, but are rather are constructed in a world -- known to the biologists who published all of those articles on the origin of new genes and cooption of systems -- where things like the origin of new genes and cooption of systems are known to happen basically all of the time out there in the real world of biology.
Thanks, yersinia (nic)
[ 17 September 2002, 01:20: Message edited by: yersinia ]
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yersinia
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posted 17. September 2002 01:38
Hey Mike,
I agree that it would be useful to formalize what we might call "relative likelihood reasoning" or some such thing, perhaps even with some attempt at scoring.
Perhaps it would be best to start another thread to do this. Briefly, several distinctions that would probably be useful in such an endeavor:
Positive evidence (evidence for some hypothesis) vs. negative evidence (evidence against some hypothesis), perhaps vs. "neutral" (e.g., perhaps no evidence either way).
Evidence for "it did happen this way" vs. evidence for "it could happen this way". E.g. the known Type III secretion systems, which are derived, are not particularly good evidence for "it did happen this way" but (IMO) are certainly evidence for "it could happen this way" ("it" = evolution of flagellum from a transport system).
A consideration of *expectation* of evidence, i.e. we can expect more evidence regarding the evolution of things that fossilize easily than we can for the evolution of things that fossilize poorly. E.g., chimps live in rainforests with acidic soils that dissolve bones so the lack of chimp fossils compared to hominid fossils is not particularly surprising.
(Along a similar vein, billions of years older = less expectation of evidence; this is an argument I advanced earlier regarding the flagellum vs. the immune system)
Another variation on the above would be length/amount of study. Short version that often causes woe to those of us interested in evolution: relevant to medicine = lots and lots of study (a plus in the case of the immune system, however); not relevant to medicine = take a hike. Bombadier beetles just aren't going to get quite the amount of attention that the immune system does.
There's probably more ("length of time since reasonably complete understanding of system"), but that's a start.
Obviously complete agreement might be difficult but perhaps it would be useful. Feel free to quote/use this in another thread if you are so inspired, Mike.
Thanks, nic
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rafe gutman
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posted 17. September 2002 05:52
quote:
from the original post:
It seems that the immune system, for instance, is a general purpose GA that targets an interloper, sets up a gradient that tracks the interloper, and then runs a GA adapted to that gradient whose output is a molecular assemblage that vanquishes the interloper.
i don't mean to disrupt the direction this thread is going in, but i had a question about dr. dembski's original post. is he saying that the immune system can create complex, specified information? after all, in the course of fighting off any given infection, the immune system will create immunglobulins and T cell receptors with at least 50 amino acids that are unique to that defense. if an organism acquires immunity to several different pathogens, we're talking about immunological information in the 100s (of specified amino acids), surely that must constitute CSI.
is there an increase in information of an organism after it acquires immunity to a pathogen? is this information both complex and specified?
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Martin F. Poenie
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posted 17. September 2002 09:49
Yersinia
So I will post a little more on the topic. I entered this thread because of the argument that you were making that I thought were somewhat misleading. So analyze the way you have been arguing this point. It begins with a paper by Louis Du Pasquier on the Immune system of Vertebrates and Invertebrates where he looks at the variety of proteins as possible precursors vertebrate Ig genes. He finds a little bit of similarity to this or that protein but nothing that he can confidently assert as the precursor. So how does Du Pasquier summarize that analysis?
“Whatever the causes for, and the order of appearance of its essential elements, the immune system became constituted in the ancestors of the jawed vertebrates. “
Now, Matt Inlay cites Du Pasquier
The steps of this model are based on comparisons between these genes and between those genes in different jawed vertebrates, the details of which will not be discussed in this article (for review see Du Pasquier 2000).
So now, it becomes a model.
And then Yersinia comes in and triumphantly says “see Inlay”.
Again Inlay refers to ITAMs in a tunicate gene. This is a reference to a protein called A74 that has no similarity to any other known protein. So what are ITAMs? ITAMs are an arrangement of two tyrosines in a peptide with a certain spacing between them. Tyrosines are widely used in cell signaling. When phosphorylated, they can become ligands for proteins with SH2 domains. What makes ITAMs special is that there are proteins such as ZAP70 that contain dual SH2 domains and bind to the ITAM phosphorylated tyrosines as a unit. At present, no such protein has been identified in tunicates. The ITAM motif is based on four residues. It is possible that these are ordinary SH2 binding sites and that no dual SH2 domain-containing will be found. Until and unless one does find such a protein this is not a compelling argument. If proteins with these dual SH2 domains are found in tunicates, then it becomes a good argument.
So having said this does it mean that I think there was no precursor to the Ig gene. My answer is, No, of course not. Does it mean that I predict that no dual SH2 domain containing protein will be found in tunicates? No again. I am not sure, it seems like at this point it seems like the story could go either way.
But let’s suppose that eventually a precursor to the current TcR and Ig genes is identified. Does that solve the problem of the immunological “big bang”? Hardly, we are talking about a system that involves 1% of the vertebrate genome. The T cell receptor signaling system is the most complicated signaling receptor system I know of and we still do not know all the parts or what they all do. Beyond that once you can generate combinatorial immunity you now have the potential to damage or kill or damage yourself. Thus it is hard to see how combinatorial immunity can operate without the clonal deletion / selection systems in place and indeed, given the present resolution that is available to us, the thymus appears at the same time (i.e. in sharks) as the combinatorial immune system.
So this is one of the most startling developments I can imagine. From the little review by Laird et al. (2000) I quote,
“Agnathans, the most primitive chordates, are poised at a fascinating point in evolution. In the 50million years between agnathan and chondrichthian divergence, something mysterious, even miraculous occurred: the adaptive immune system evolved.
Now I do not infer from that statement any religious sentiment. I take it to reflect their deep appreciation of the magnitude and sweeping scope of this event. I get no sense from your posts that you do understand or appreciate what happened.
Having said that, do I now postulate materialization of genes and magic events by a designer? The answer is still No. What I see here is a striking conspiracy of coincidences. It has nothing to do with whether or not one will successfully find precursors. It is quite possible that we will find many more proteins for which no homologues can be found in lower vertebrates. It is also likely that we will find many that do have homologues in lower vertebrates. And having found them we will still be left with and event that is no less amazing.
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Paul A. Nelson
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posted 17. September 2002 10:05
Yersinia,
I know you're not an immunologist or an evolutionary biologist. But you're writing about both topics here, in considerable detail, so it's reasonable to assume that you understand them.
The reason I ask for your own writing is to slow down, and to focus, what Bill Dembski calls the "torrent of words" (abstracts, URLs, etc.) that you're posting.
I asked about role of natural selection in the evolution of the immune system. You wrote:
quote:
Regarding the role of natural selection, it's pretty clear that the basic selection pressure way back from basal bilaterans to the adaptive immune system of vertebrates is simply enhanced immune function, especially in terms of enhancing (1) diversity of receptors and (2) regulation of an increasingly powerful system.... The benefit of improved immune response seems rather obvious to me, and indeed there is a pretty huge literature on natural selection and the immune system, e.g. on MHC diversity (lots of articles) which proves the constant influence of natural selection for improved immunity.
The question is not really what the selective pressures were, that is pretty obvious in this case: diseases are continually trying to eat you alive.
Yes, an immune system is a good trait to have, all things considered. But that's not evidence that the process of natural selection explains the origin of the system.
It would be immensely helpful if you could give, in brief outline, the exact formulation of natural selection that you're using in this discussion.
For my part, I've downloaded Matt Inlay's article, and will read it carefully.
[ 17 September 2002, 10:19: Message edited by: Paul A. Nelson ]
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Bonnie A. Mallard
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Member # 286
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posted 17. September 2002 15:13
Paradox or Symbiosis? An Immunologist's point of view.
Yersinia contents that "high-tech designs are
working in direct opposition" but couldn't this be better described as each
organism striving to strike a point of balance - or equilibrium to facilitate
ordered mutualism as may have been the origin intention. That the immune system
as a whole functions to discriminate self from non-self or to detect danger
does not detract from the notion that the optimal outcome of an immune response
for both the host and parasite is development of a symbiotic relationship. Many
have argued for the so called hallmarks of evolution within the immune
system; nonetheless, there are features with this GA which can not be reduced
before function is lost. For example, genes encoding MHC molecules (whether
many or few - depending on the organism) must maintain the basic features which
allow presentation of self and foreign antigens to other highly defined
structures, such as the T-cell receptors, which in turn must maintain the ability
to transduce complex intracellular signals which facilitate particular
immunological responses. Although various organisms may differ in terms
of which elements of the immune system they require in order to respond
to a variety of stimuli each of these responses must display a set of
minimum specifications to remain functional.
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yersinia
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Member # 324
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posted 17. September 2002 17:49
Dr. Peonie,
I'm not sure where we're going with this, since we appear to agree on my main points, to wit:
(1) that the immune system considered as a whole emerged fairly gradually, contra the implications of the Dembski/Behe argument from IC that subsets of the system would be nonfunctional
(2) That this is particularly true for the complement system, even though Behe explicitly declared it IC in Darwin's Black Box. (And by comparison to the similar case with blood-clotting for which extensive literature also exists, I have assumed you feel similarly about the blood-clotting case although you have not advanced a considered opinion on it yet)
(3) That even for the adaptive immune system, which did emerge relatively rapidly (which I and the Inlay article conceded already, so I'm not sure why you are making a further point of it) -- geologically speaking (~50 million years, and lets not forget all of the extinct basal vertebrates that are *known* to have existed across this transition from the fossil evidence) -- there is significant evidence of functional, phylogenetically basal homologs of parts of the system, again in contradiction to the IC argument which says that subsets of the IC system are functionless. Even for the RAGs, certainly the most striking feature of the adaptive immune system, you have conceded that a decent and increasingly well-supported hypothesis for their origin exists.
(4) A very large literature and indeed an entire field exist on the topic of evolutionary immunology, which I think you would conceed has experienced substantial success although of course (as with any science) not all questions have been answered.
Therefore, it seems to me that you would agree that the leaders of the ID movement have badly misstepped in the case of the immune system, for example when Behe wrote in Darwin's Black Box that:
quote:
"We can look high or we can look low, in books or in journals, but the result is the same. The scientific literature has no answers to the question of the origin of the immune system." (Darwin's Black Box, p. 138)
As Dembski has recently made his entire argument for ID in biology dependent on Behe's IC argument, and has made similar assertions about the lack of literature explaining the origins of complex systems like the immune system, then I think you would have to agree that his thesis is similarly wounded by extant research about the evolution of the immune system.
I would appreciate your comments on whether or not my interpretations and deductions from your previous comments in the thread are correct. Rather than take up your whole day, perhaps you could just give us a thumbs-up or thumbs-down on the truth of this statement:
quote:
"We can look high or we can look low, in books or in journals, but the result is the same. The scientific literature has no answers to the question of the origin of the immune system." (Darwin's Black Box, p. 138)
nic
PS: some more specific comments in the next post...
[ 17 September 2002, 17:52: Message edited by: yersinia ]
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