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Topic: Organisms using GAs vs. Organisms being built by GAs
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RB
Member
Member # 263
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posted 09. October 2002 09:56
Paul,
In your mere creation paper, you apply Intelligent Design, post hoc, for explaining origin (lack of natural origin) to Bicoid in Drosophila. Have you followed the literature lately concerning Bicoid evolution? (in particular the complete lack or need for biciod in non-dipterans, bicoid being a recent gene duplication of the Hox3 (zen) gene of insects.)
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Paul A. Nelson
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Member # 26
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posted 09. October 2002 11:52
Hi Randy,
Why don't you start a new thread, on bicoid? I've been talking with Bill Wimsatt recently about this, and would be interested in participating in a discussion on the topic. Thanks.
P.S. To answer your question -- yes, I've been following the literature.
[ 09. October 2002, 11:54: Message edited by: Paul A. Nelson ]
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RB
Member
Member # 263
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posted 09. October 2002 20:19
Hey Paul, nice detective work (on the Randy) since I haven't used my name here or ARN (not that I have hidden it, just RB is an old nickname, I hate typing so the shorter the name and password the better, that has stuck on internet)(Not that there are too many mormon RBs in the evo-devo literature.) That said....
I need to know from you (before I begin the new thread), where I need to start. In your opinion, is there evidence for common ancestry of insects, or holometabola in particular? What is your opinion on what is required to build an argument for orthology (or paralogy) of genes? (Do you think orthology or paralogy can be established?) Those at least are beginning questions I would like to know a prelim answer to before starting the thread.
[ 09. October 2002, 22:28: Message edited by: RB ]
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rafe gutman
Member
Member # 134
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posted 10. October 2002 06:52
quote:
paul:
I've been looking at the primary literature cited by Matt Inlay and others in this thread, and see no reason to revise my earlier opinion that "natural selection" is invoked post hoc as a magic wand.
paul, given that the original mutation events occurred in organisms that are no longer around, and given that natural selection takes thousands to millions of years to occur, is there any evidence that can reasonably be obtained by scientists that would make you think that evolution is a better explanation for the origin of the immune system than ID?
what seems to be happening on this thread is that the evolution supporters list evidence that supports the evolution of the immune system. the IDists then state that the evidence doesn't prove evolution, and demand evidence that does so. considering the fact that behe et al. claim that evolution cannot produce IC systems, our goal was simply to show that it can, not that it did (in the case of the immune system). you've made some pretty hefty demands, but so far you've failed to give any reason why ID is a better explanation than evolution here.
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Mike Gene
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Member # 149
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posted 10. October 2002 07:36
Hi Rafe,
You write: what seems to be happening on this thread is that the evolution supporters list evidence that supports the evolution of the immune system. the IDists then state that the evidence doesn't prove evolution, and demand evidence that does so.
Of course, I have found that ID critics take this approach when it comes to the claim that life itself was designed (i.e., nothing less than proof counts). What is more interesting to me, however, is the essence of the support you speak of. Doesn't it simply boil down to - "these data make it look like the immune system evolved."
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Jules
Member
Member # 181
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posted 10. October 2002 08:16
Sorry for not answering sooner, Charlie, but your arguments forced me to go back and reread Chap.6 of DBB more carefully.
Charlie:
"1. Clonal selection: Behe argued that antibody molecules work because antigen-specific clones are selected on the basis of their membrane antibody by their ability to recognize antigen, and only the clones that are selected are then able to secrete antibodies in their soluble, "active" form. Take away the antibody membrane form, he said, and secreted antibodies alone would not work, because the specificity would be lost. Take away the secreted form, and antibodies, as membrane proteins, would be useless. Thus, the antibody mebrane/secreted form "switch" occurring during clonal selection seems IC.
Alas, this argument completely ignores 2 facts, both well known in 1996:
a) that membrane-only antigen receptors exist and are used during immune responses in both vertebrates (T cell receptors), and invertebrates (some innate immunity receptors).
b) that secreted-only broad-specificity antigen receptors exist in the innate immune system of both vertebrates and invertebrates. Indeed even antibodies themselves work quite well as soluble-only molecules: individuals with immunodeficiencies that hamper antibody production are often given i.v. antibodies purified from the plasma of healthy subjects for therapy. No clonal selection, no membrane-secreted switch, yet those antibodies are protective to a reasonable extent. Clonal selection and membrane/secreted antibodies are not IC."
Me: But Behe isn't saying that membrane-antibodies or secreted antibodies wouldn't be useful. He's saying that the clonal selection system wouldn't work without all three components. And that still looks IC to me.
"2. Antibody diversity. Here the argument was simple: there can be no antibodies without rearrangement-mediated variability, but on the other hand there is no way to evolve the enzymatic machinery for antibodies, before antibodies exist. Again, Behe was simply ignorant of the facts: first, as stated above, there are several innate immunity recpetors that are broadly specific to bacterial and viral antigens, and act the same way as antibodies do, without gene rearrangments. Second, the idea of the recombination machinery arising from co-option of a transposase (i.e. recombination enzymes pre-dating antibodies) had already been advanced by the time of DBB's publication - as any respectable immunologist would have gladly told Behe. It was elegantly confirmed just a few years later. The recombination/antibody system is not IC."
Me: From Behe's comments, it seems he was already aware of the recombination machinery arising by co-option. I assume we're talking about things such as the RAG genes? The fact that parts of the machinery already existed in other functions does not explain how they all came together to form the antibody diversity system. But Dr.Poenie already commented on this.
"3. The complement pathway was discussed as a classic example of IC-ness: a series of interacting proteins (although the interaction here is more temporal than spatial, as in the flagellum), forming a cascade in which each component is necessary. Again, there were examples already suspected in 1996, and confirmed later, of complement cascades that lack individual components but work effectively, such as that in certain protovertebrates."
Me: This might be your strongest argument. Cascade systems, being essentially linear in nature, seem to me to be the ones most available for evolutionary development, by simply adding on to either end of the system. I would predict that if the complement system has evolved it has done so either at the beginning of the cascade, or the end, but probably not in the middle. However, this leaves open the question of how the simplest complement system first originated. I'm willing to bet that the simplest system we can imagine will be IC.
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Paul A. Nelson
Member
Member # 26
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posted 10. October 2002 08:46
Hey Randy,
It was easy to figure out that "RB" was you (you were at the U of C evo-devo meeting; I wish you would have come by the Nelson/Wells poster and said hello). Anyway, why not just start with my Mere Creation chapter? I make some pretty strong claims about bicoid there, which Bill Wimsatt thinks the recent literature certainly challenge.
Don't miss P.J. Shaw et al., "Coevolution in bicoid-dependent promoters and the inception of regulatory incompatibilities among species of higher Diptera," Evolution and Development 4 (2002):265-277.
Note to Rafe: I don't think my skepticism about the role of natural selection in the origin of the immune system is any stronger than what one frequently finds in the literature. Example: just off the top of your head, what sort of theorist would you say wrote the following?
quote:
As far as I can see, statements of the type that "phenotype x is an adaptation, evolved via the agency of natural selection," are thoroughly untestable. The necessary data needed to refute such an assertion cannot be gathered, and we are more or less forced to accept it as an article of faith rather than a scientific statement.
[ 10. October 2002, 09:39: Message edited by: Paul A. Nelson ]
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rafe gutman
Member
Member # 134
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posted 10. October 2002 17:32
mike, i should point out that nowhere in this thread did i demand proof of ID. i've asked for models and explanations, but not proof. so far, all my requests for ID explanations have been either dismissed or ignored. meanwhile, the IDists on this thread continue to move the goalposts further and further back, and now we are required to demonstrate natural selection on events that occurred half a billion years ago. otherwise what? evolution is a myth and ID is therefore true? i have no problem with skepticism. i understand that if you keep probing, eventually you will reach the end of our current knowledge. but why should that be considered a victory for ID? those who display such skepticism for evolution must also concede that evolution is still the better explanation. if they don't want to concede that, then they should put forth an ID explanation and see how it holds up under scrutiny. otherwise, they're just being hypocritical.
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rafe gutman
Member
Member # 134
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posted 10. October 2002 17:48
jules, thanks for taking the time to respond. i don't want to steal your questions from charlie, but let me respond briefly (i'll just include your quotes):
quote:
regarding clonal selection:
"But Behe isn't saying that membrane-antibodies or secreted antibodies wouldn't be useful. He's saying that the clonal selection system wouldn't work without all three components. And that still looks IC to me. "
actually, behe did say that:
"Secreting a little bit of antibody into the great outdoors is a waste of resources if there's no way to tell if it's doing any good. Ditto for making a membrane-bound antibody. And why make a messenger protein first if there is nobody to give it a message, and nobody to receive the message if it did get one? We are led inexorably to the conclusion that even this greatly simplified clonal selection could not have come about in gradual steps." (page 125)
the clonal selection system is how the cell tells whether or not the antibody is "doing any good". behe is implying that without the clonal selection system, producing a membrane bound antibody would be a "waste of resources" (i.e. functionless).
quote:
regarding antibody diversity:
"From Behe's comments, it seems he was already aware of the recombination machinery arising by co-option. I assume we're talking about things such as the RAG genes? The fact that parts of the machinery already existed in other functions does not explain how they all came together to form the antibody diversity system. But Dr.Poenie already commented on this. "
the whole purpose of the argument from IC is to say that IC systems can't evolve. essential to that idea is that subsets of these systems cannot be functional. otherwise they can evolve gradually (i.e. one or two components at a time). of the three components behe lists as part of the antibody diversity system, two can function without the third in transposition systems. so all three components did not need to come together simultaneously.
we seem to be in agreement regarding the complement system, so i won't go into it. if you have any more questions, i'd be happy to answer them to the best of my abilities.
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rafe gutman
Member
Member # 134
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posted 02. November 2002 18:13
a couple of interesting papers on the immune system have popped up recently:
1. Mayer WE, Uinuk-Ool T, Tichy H, Gartland LA, Klein J, Cooper MD.
Isolation and characterization of lymphocyte-like cells from a lamprey.
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14350-5.
this paper presents evidence for the existence of lymphocytes (cells intimately involved in the adaptive immune response) in lampreys, which don't have an adaptive immune system. previously, one could have argued that rearranging antigen receptors and lymphocytes were irreducible. now it doesn't look like that is the case.
2. Uinuk-Ool T, Mayer WE, Sato A, Dongak R, Cooper MD, Klein J.
Lamprey lymphocyte-like cells express homologs of genes involved in
immunologically relevant activities of mammalian lymphocytes.
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14356-61.
this article, the complement to the previous article, shows that the lamprey lymphocytes express genes similar to ones expressed in mammalian lymphocytes. these genes are also involved in the adaptive immune response in mammals, so it's strange that they are present in lamprey. incidently, both these articles are freely accessible online.
3. Dodds AW.
Which came first, the lectin/classical pathway or the alternative pathway of
complement?
Immunobiology. 2002 Sep;205(4-5):340-54.
this article provides a model for the evolution of the complement system. if paul wants to call the author's model "storytelling", he's free to do so, but now it's not just some random internet poster's idea.
i won't quote his model (it spans 2 pages), but he does say this about the model:
quote:
the scheme outlined in figures 5 and 6 involves a stepwise increase in effectiveness of the system, each step giving benefit to the species involved.
since the time this thread began, probably a dozen articles have been published that support the notion that the immune system evolved. has ID advanced in any way since then?
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yersinia
Member
Member # 324
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posted 14. November 2002 02:07
Nature Immunology just came out with a special focus issue on the web, "Focus on Immune Invasion".
http://www.nature.com/ni/special_focus/immune_evasion/
It includes an overview essay outlining diverse ways in which Darwinian evolution has been a fruitful theory in the study of invaders, who very often have "ingenious" features designed to evade the immune system:
quote:
Nature Immunology 3, 987 - 989 (2002)
Immunology taught by Darwin
Rodney E. Phillips
The Peter Medawar Building for Pathogen Research, University of Oxford, South Parks Road, Oxford OX1 3SY, UK. rodney.phillips@ndm.ox.ac.uk.
This Focus issue brings together the cornucopia of strategies that pathogens and tumors utilize to avoid immune recognition. Here Rodney Phillips discusses some general principles that emerge from this analysis.
[...]
I believe that the issue is free online after (free) registration.
yersinia
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yersinia
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Member # 324
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posted 17. February 2003 18:34
I just took another look at this thread, I think it might be worth adding a few bits just to show what else has been published on the evolutionary origins of the vertebrate immune system in the few short months since November.
E.g.:
quote:
Proc Natl Acad Sci U S A 2003 Jan 21;100(2):622-7
Urochordates and the origin of natural killer cells: Identification of a CD94/NKR-P1-related receptor in blood cells of Botryllus.
Khalturin K, Becker M, Rinkevich B, Bosch TC.
Zoological Institute, Christian Albrechts University Kiel, Olshausenstrasse 40, 24098 Kiel, Germany Europe; and National Institute of Oceanography, Tel Shikmona, P.O. Box 8030, Haifa 31080, Israel Asia.
Transplantation immunity based on the recognition of MHC molecules is well described in vertebrates. Vertebrates, however, do not undergo transplantation reaction naturally. The phylogenetically closest group in which transplantation reactions can occur is the Urochordata. Therefore, these animals occupy a key position for understanding the evolution of the vertebrate immune system. When screening for genes differentially expressed during allorecognition in Botryllus schlosseri, we isolated a gene coding for a type II transmembrane protein with a C-type lectin-binding domain and close similarity to vertebrates CD94 and NKR-P1. Here we show that the gene, BsCD94-1, is differentially regulated during allorecognition and that a subpopulation of blood cells carries the corresponding receptor on its cell surface. Southern blot analysis with DNA from individual colonies and intronless BsCD94-1 probe reveal variation between individuals at the genomic level. CD94 in vertebrates is one of the markers for natural killer cells and binds to MHC class I molecules. Natural killer cells play a major role in recognition and elimination of allogeneic cells. Their evolutionary origin, however, remained unknown. The results presented here indicate that the elaboration of the vertebrate immune system may have its roots in an ancestral population of cells in the urochordate blood.
(bold added)
Another gap closed...
(a bunch of related articles)
And here is one on the "ingenious" strategies viruses use to avoid the immune system (although you never know, perhaps such creativity was front-loaded in as according to certain notions natural selection has no creativity):
quote:
J Gen Virol 2003 Jan;84(Pt 1):1-15
Virus complement evasion strategies.
Favoreel HW, Van de Walle GR, Nauwynck HJ, Pensaert MB.
Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium.
The immune system has a variety of tools at its disposal to combat virus infections. These can be subdivided roughly into two categories: 'first line defence', consisting of the non-specific, innate immune system, and 'adaptive immune response', acquired over time following virus infection or vaccination. During evolution, viruses have developed numerous, and often very ingenious, strategies to counteract efficient recognition of virions or virus-infected cells by both innate and adaptive immunity. This review will focus on the different strategies that viruses use to avoid recognition by one of the components of the immune system: the complement system. Complement evasion is of particular importance for viruses, since complement activation is a crucial component of innate immunity (alternative and mannan-binding lectin activation pathway) as well as of adaptive immunity (classical, antibody-dependent complement activation).
...obvious clinical relevance.
Also appears to support the "Diversity in Immune System Molecules is a Highly Selectable Trait" thesis I was advocating earlier in this thread.
[edit to add link to virus article]
[ 17. February 2003, 19:14: Message edited by: yersinia ]
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Nel
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Member # 614
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posted 11. March 2003 22:40
I noticed this thread wasn't closed, and I have a bunch of free time opening up. I hope I'm not dredging up old arguments, but I've been reading Inlay's essay and have been studying the amazing immune system. I have several questions about it that is bugging me. Inlay's essay states:
quote:
Behe is totally wrong to assert that receptors with single specificities are useless to the immune system. There are many non-rearranging, innate receptors very important to host defense, such as the LPS receptor. Others include the glycan receptor, the mannose receptor, and the macrophage scavenger receptor; which together recognize many different bacterial constituents.
But germline encoded receptors are not a part of the V(D)J recombination system. Secondly, it is unlikely that any of them have single specificities. For example, the scavenger receptor A recognizes ac-LDL, altered forms of bovinew serum albumin, pI:pC, etc. TLR4 has LPS and RSV-fusion protein, a still unidentified lipid from TB, Hsps, etc.
quote:
When Behe states that "A primitive system with only one or a few antibody molecules would be …. not sufficient to make a difference", he is dead wrong. Insects, echinoderms, tunicates, lancelets, and agnathans have all been able to survive without the benefit of an adaptive immune system, relying on an array of innate receptors specific to common bacterial surface constituents.
Toll receptors and other innate immune molecules are not antibodies. So I don't understand how pointing to innate receptors in insects,echinoderms, etc shows "A primitive system with only one or a few antibody molecules". The term "innate" reflects those components of the immune system that are available in the absence of antigenic experience. In other words, if you were born into a sterile environment, you would still have these defense systems fully functional and ready for your first microbial exposure. The simplest and most important innate immune organ is skin. Burn victims who have lost all of their skin will die long before AIDS patients who have lost all of their T cells.
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charlie d.
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Member # 159
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posted 12. March 2003 08:17
I think Inlay's point is that you can have effective soluble or membrane antigen receptors without somatic recombination. Thus, the ICness of the antigen receptor/VDJ recombinase system (you can't have one without the other), as proposed by Behe, dissolves. You can have antigen receptors that do not rearrange, and recombinase that doesn't recombine antigen receptors (as a transposase), and there are good examples of both.
That innate immunity receptors are not antibodies is semantics: we only call antibodies molecules that share the characteristics of vertebrate immunoglobulins (even if we found with absolute certainty the non-rearranging precursor of vertebrate antibodies, it wouldn't be called an antibody). Innate immunity receptors are however functionally equivalent to antibodies in that they recognize antigens with some specificity, and activate immune reaction pathways as a result of their binding.
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Nel
Member
Member # 614
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posted 12. March 2003 17:10
Charlie:
I think Inlay's point is that you can have effective soluble or membrane antigen receptors without somatic recombination. Thus, the ICness of the antigen receptor/VDJ recombinase system (you can't have one without the other), as proposed by Behe, dissolves.
Nelson:
I don't see how it does. It is clear that you absolutely need the Rag genes for the development of both T and B cells. Mice lacking one of these genes are deficient in T and B cells. Without RSS, as Behe said, "it' s like expecting a machine that's randomly cutting paper to make a paper doll". If the function of the V(D)J recombinase is to mediate the rearrangement of receptor genes in B and T cells, then you absolutely need these receptors or the whole thing is pointless. I think that this is an accurate way of saying what Behe said. It looks like ICness of the VDJ recombinase hasn't dissolved, it's still stands right in your face begging you to mess with it.
Charlie:
You can have antigen receptors that do not rearrange, and recombinase that doesn't recombine antigen receptors (as a transposase), and there are good examples of both.
Nelson:
Showing me receptors that have nothing to do with recombination isn't relevant. Even Matt Inlay admits that none of these receptors are homologous to the receptors that V(D)J recombination is concerned with.
Also, AFAIK, Rag-mediated transposition has never been found to be able to occur in cells. The point about in vitro experiments was made by Julie Thomas a while back:
quote:
2. The similar activity should exist at biologically relevant states. This is important as in vitro evidence can be misleading. For example, if actual player C is a DNA-binding protein, but binds to RNA in the test tube under conditions that are not seen in the cell, the similar activity is biologically suspect and may simply be an artifact of the unnatural in vitro conditions.
Also, if the transposase is also IC, not only are we begging the question of the origin of both systems, we are now arguing in a circle. A point also made by Julie:
quote:
The similar activity should not be part of another IC system. Otherwise, the argument travels in a circle. For example, single-stranded binding (ssb) proteins are involved in DNA replication and DNA recombination. If one explains away the role of ssb proteins in replication by appealing to recombination, yet explains away the role of ssb proteins in recombination by appealing to replication, we have gotten nowhere and have only the appearance of a refutation of actual player C's role in an IC system
[ 12. March 2003, 18:22: Message edited by: Nelson_Alonso ]
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