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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 17. September 2002 18:00
Dr. Poenie,
PS: In the case of Igs in the adaptive immune system, you posted some concerns about some of the peer-reviewed articles cited by Inlay. This is well-taken but it appears to be a minor quibble about The Main Point regarding Igs which is that the general case for the existence of Ig precursors is quite strong, e.g. I previously quoted two of the references that you yourself cited when arguing that the evidence was weak, but found:
quote:
E.g., ref 15 abstract:
quote:
We have isolated, characterized, and partially sequenced immunoglobulin from the most primitive extant nonvertebrate craniate, the hagfish, a jawless fish that may have diverged from the vertebrate lineage more than 500 million years ago. The 160-kDa protein, which is a minor serum component, is composed of two different heavy chains of 69 and 74 kDa and a light chain of 29 kDa and resembles known immunoglobulin on the basis of an equimolar ratio of heavy and light chains, N-linked glycosylation of heavy chains, presence of intra- and interchain disulfide bonds, and polydispersity of each peptide chain. High molecular mass (polymeric) as well as low molecular mass (monomeric) forms were isolated from serum. The hagfish immunoglobulin is unique in that each heterodimer is composed of two different heavy chains and two light chains. The partial peptide maps and amino acid compositions of the two heavy chains differ; the chains do not crossreact immunologically. Slight crossreactivity of the 74-kDa heavy chain with antisera against purified shark immunoglobulin and some conservation of amino acid sequences, including those surrounding a cysteine, suggest that the isolated protein is an immunoglobulin.
Returning to Laird et al., in addition to the quote you include, directly before it we have Laird et al. citing more evidence of Ig and TCR precursors:
quote:
Ig and TCR molecules feature a structural motif comprised of ß-pleated sheets, known as the “Ig fold,” whose archtypical presence in receptors and adhesion molecules through phylum Chordata and even in invertebrates (13, 14) dates it before the entrance of RAG.
In the first reference the authors go so far as to identify their molecular as "a hagfish immunoglobin" which would appear to contradict your previous statement that:
quote:
The TcR and Ig genes make their first appearance in Sharks.
...although I suppose it depends mostly on definitions.
Here and here are some articles citing Ig domains in tunicates.
quote:
“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”.
I am not sure that your characterization of Du Pasquier's work is accurate. The man coedited an entire volume:
Origin and Evolution of the Vertebrate Immune System (Current Topics in Microbiology and Immunology, 248)
by L. Du Pasquier (Editor), G. W. Litman (Editor)
...on the topic (too bad we don't have such books regarding ID hypotheses on the origin of such complex systems, eh?), and in addition to Du Pasquier (2001) cited by Inlay (Inlay's in-text citation to Du Pasquier 2000 should say 2001, hopefully that wasn't confusing) Du Pasquier has a 2002 article as well:
Du Pasquier L. Several MHC-linked Ig superfamily genes have features of ancestral antigen-specific receptor genes. Curr Top Microbiol Immunol. 2002;266:57-71.
...and Du Pasquier's work has evidently served as the basis for at least one webpage presenting a model for the origin of Igs:
Origin and evolution of the immunoglobulin module
Briefly, in conclusion you write:
quote:
Having said that, do I now postulate materialization of genes and magic events by a designer? The answer is still No.
However, ID does. You will be happy to know that you are now part of the Vast Dogmatic Darwinian-Naturalist Conspiracy...
quote:
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.
I agree that the events we are considering are amazing -- but then I think that the origins of stars, continents, mammals, and orchid contrivances are also amazing. I don't see the need to invoke the intervention of a mysterious unknown designer to explain their origin however, and I am afraid that a major component of the strong support the ID idea receives in some quarters is due to a failure to confront the scientific literature in a serious fashion.
Thanks, yersinia
Laird, D.J., A.W. De Tomaso, M.D. Cooper, and I.L. Weissman. 2000. 50 million years of chordate evolution: Seeking the origins of adaptive immunity. Proc. Natl. Acad. Sci. U.S.A. 97:6924-6926. (Also full text free online)
[added in edit]
PPS: In the interests of maximum accuracy:
The claim of a hagfish immunoglobulin made in Varner, Neame, and Litman 1991 (the ref 15 quoted above) is not supported by later work by Litman and colleagues. E.g.:
quote:
Rast JP, Litman GW. Immunol Rev 1998 Dec;166:79-86
Towards understanding the evolutionary origins and early diversification of rearranging antigen receptors.
The rearranging antigen binding receptors, immunoglobulin heavy (IgH) and light (IgL) chains and the four classes of T-cell antigen receptors (TCR) are found in all contemporary species of jawed vertebrates examined thus far. Ig genes have undergone marked changes in organization and mechanisms of diversification during vertebrate phylogeny; whereas TCR genes, which are found in species as phylogenetically removed as man and cartilaginous fishes (e.g. skate), are generally similar in terms of structure, diversification and, presumably, function. The patterns of Ig divergence in cartilaginous fish are informative as to both the potential for genetic variation and the mechanisms that bring about such change. No evidence has been found for homologs of either Ig, TCR, recombination activating gene (RAG)1 or RAG2 in jawless vertebrates or invertebrates. Thus, a phylogenetic demarcation exists in terms of the presence and absence of the rearranging antigen binding receptor genes. It is presumed that the rearranging antigen binding receptors arose from a non-rearranging predecessor. The recent discovery of non-rearranging homologs of antigen binding receptor genes in several species offers insight into alternative forms of recognition, relationships between adaptive and innate mechanisms of immunity, and the origins of antigen recognition.
I will therefore stipulate that it is entirely correct to say, as Peonie did:
quote:
The TcR and Ig genes make their first appearance in Sharks.
...although it is apparent from e.g. Rast and Litman 1998 quoted above that they have evidence that non-rearranging receptors are viable and therefore that they think that a non-rearranging ancestor is out there somewhere.
PPPS: (last one I promise)
Regarding the role that the Ig domain/fold plays in Igs and other immune system molecules (the former is found in both invertebrates and vertebrates), here is a good introduction:
Immunoglobulin Structure
yersinia
[ 17. March 2003, 02:04: Message edited by: yersinia ]
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rafe gutman
Member
Member # 134
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posted 18. September 2002 00:44
dr. poenie,
sorry to drag you back into this, but it's good to have you back. i agree with much of what you have to say, particularly in acknowledging the "abruptness" of the appearance of the adaptive immune system. it is indeed quite mind-boggling how quickly all those components came together in the common ancestor to the jawed vertebrates. i am not, however, daunted by the this mystery, and i assume that you are not either. i think the only place we differ in is our propects for the future. i'm much more optimistic that precursors will be found, while you remain neutral. i respect your opinion on the matter, but i must stress again how much it differs from dr. behe's. i don't think you share his sentiment that the scientific community is "shrugging its shoulders", nor that the literature has "no answers to the question of the origin of the immune system". and behe includes the complement system here. i think it's safe to assume no one here is going to defend behe's statements in regards to complement.
earlier you said:
quote:
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.
i'm not an expert on signal transduction, but it seems pretty clear that A74 is involved in immune-related signal transduction, and that tyrosine phosphorylation of the ITAM is part of it. as for the SH2-containing proteins, i should point out that homologues for syk and ZAP70 have been discovered in organisms as distant as hydra [1], and as similar (to tunicates) as sea urchin [2]. additionally, a CD45 homologue, which can augment signaling through ITAMs, was found in hagfish [3]. so while we don't have a tunicate syk-family homologue, many of the other pieces are already in place. it's not unreasonable to think that the downstream targets of A74 will be identified soon, i guess we can reserve judgement til then. do you think it will be homologous to syk/ZAP70?
references
[1] Steele RE, Stover NA, Sakaguchi M.
Appearance and disappearance of Syk family protein-tyrosine kinase genes during
metazoan evolution.
Gene. 1999 Oct 18;239(1):91-7.
[2] Sakuma M, Onodera H, Suyemitsu T, Yamasu K.
The protein tyrosine kinases of the sea urchin Anthocidaris crassispina.
Zoolog Sci. 1997 Dec;14(6):941-6.
[3]Nagata T, Suzuki T, Ohta Y, Flajnik MF, Kasahara M.
The leukocyte common antigen (CD45) of the Pacific hagfish, Eptatretus stoutii:
implications for the primordial function of CD45.
Immunogenetics. 2002 Jul;54(4):286-91.
[ 18 September 2002, 00:47: Message edited by: rafe gutman ]
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William A. Dembski
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Member # 7
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posted 18. September 2002 01:32
Yersinia,
Perhaps we need to institute some controls on the ISCID discussion board about "literature bombing" by overenthusiastic users of the PubMed search engine. What I see in your posts are dozens of thinly-explained citations, underlain by a sloppy understanding of the evidential requirements of evolutionary explanation. I come back to Paul Nelson's challenge to you: Give a sustained argument in your own words of how some IC system of the sort that I or Mike Behe cites came about. Thus far you have been bluffing.
You've charged me with moving the goalposts and adjusting the definition of irreducible complexity because I require of evolutionary biologists to "connect the dots" in a causally convincing way. The dots here are functional precursors that could conceivably have evolved into the final system of interest. You state that previously I claimed that the dots couldn't exist because they wouldn't be functional. Please show me in Michael Behe's writings or my own where we deny that IC systems can be made up of subsystems that can be functional in their own right. The point is not whether subsystems can be functional on their own but whether they can exhibit the same function in the same manner as the system in question. You misrepresent our position.
Let me spell out what's needed for a detailed Darwinian pathway to explain an IC system. The problem is similar to that of connecting two organisms in the fossil record. Given organisms X and Y, if they are related by common descent via the Darwinian mechanism, there must be a continuous chain of organisms X(0) --> X(1) --> ...--> X(m) = X and Y(0) --> Y(1) --> ...--> Y(n) = Y where X(0) = Y(0) is a common ancestor. In the best circumstance, each such X(i) and Y(j) must be explicitly exhibited and any arrows of causation connecting two organisms must produce small incremental changes that are highly probable on the basis of the Darwinian selection mechanism. The more intermediates that are missing from this picture and the more handwaving and just-so story-telling to describe the arrows of causation, the more problematic the evolutionary explanation.
In the case of an IC system S comprised of components {S(1), S(2), ..., S(r)} and arranged in some irreducibly complex configuration C, we need a sequence of supersystems T[1] --> T[2] --> ... --> T[n] where each T[i] consists of one or more functional biological systems. Thus T[i] = {T[i](1), ... T[i](k)} (k depends on i and is at least 1) and each system T[i](j) consists of m components {T[i](j)(1), ... T[i](j)(m)} (m depends on i and j) and is arranged in some configuration C[i](j) (not necessarily irreducibly complex). In the sequence T[1] --> T[2] --> ... --> T[n], T[n] = {T[n](1)} and T[n](1) = S, the system in question. Under the assumption that S evolved by Darwinian evolution, there must be a supersystem T[1] in which the components of S are either absent or targeted in completely different systems for different functions. Such a T[1] needs to be the starting point if S is properly to be ascribed to a (macro)evolutionary process. Each arrow in this picture should represent a small incremental change that is highly probable on the basis of the Darwinian selection mechanism. In most instances it will be at the level of a single component T[i](j)(k) being slightly modified and (re)targeted to a component T[i+1](j')(k') of system T[i+1](j') (thus T[i] --> T[i+1] would signify the change T[i](j)(k) --> T[i+1](j')(k')).
In the best circumstance, each such T[i] would be explicitly exhibited down to the T[i](j)(k) level along with all the configurations C[i](j); moreover, any arrows of causation connecting two supersystems must produce small incremental changes that are highly probable on the basis of the Darwinian selection mechanism. These changes will operate at the level of individual system components and the system functions induced by their configurations. The more intermediates that are missing from this picture (whether whole systems, components, or configurations) and the more handwaving and just-so story-telling to describe the arrows of causation, the more problematic the evolutionary explanation.
Thus, when you write, "the reconstructed origin of the immune system is quite detailed, and getting more so all of the time," all you've actually done is found a few T[i](j)(k)s and even fewer T[i](j)s. You're not clear what the T[i]s are or the C[i](j)s. And above all, the arrows that connect and coordinate the whole process you simply sweep under the rug by appealing to natural selection -- as though natural selection were an incantation that guarantees success to the evolutionary process. For true believers like yourself, the incantation does the trick -- natural selection becomes the glue that automatically binds all the components in their proper place. Your filling in of details is like a man attempting to count to infinity -- the challenge ahead of you far exceeds any progress you've made to date or even any progress you give any indication of being able to make. You keep slapping down pieces of the puzzle without any justification for having anywhere near all the pieces or even a representative sample, much less that the causal powers you invoke are capable of putting the pieces together. No matter how many leaks Darwin's Titanic springs, you'll blithely keep asserting, "Steady as she goes." And down she will.
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Martin F. Poenie
Member
Member # 10
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posted 18. September 2002 04:22
Hi Rafe
To answer your point, I am not neutral on the issue of whether I think we will find precursors to proteins used in the immune system. I think we will. But it is also is possible we will not find some simply because of the literature on ORFans and detection problems. Also it is estimated that the human genome contains 50 -200 bacterial genes. One of my original contentions was that combinatorial immunity was not simply derivative of innate immunity – something remarkably new happened.
None of this has any bearing on my notion of design. The notion of IC never has really figured into my own personal thinking about design. So you ask me to defend Behe or not and my feeling is the Mike is defending the idea of design out of his notion of how it it is implemented and the whole underpinnings of his line of thought I think are different than mine. Thus I simply do not want to go there.
What is really unfortunate is that the whole environment for discussing these things is so caustic and for me, very distasteful. You say that ID can predict anything, I often feel the same way about Darwinism. Basically Darwinism is whatever happens (or happened) – with the help of hindsight. That is because, as I said before, by definition, any possible way to alter the genome falls under the rubric of random mutation and natural selection.
I see the various ways of altering the genome as a toolbox. Perhaps to draw an analogy, that would make the issue clearer, take the origin of life. There we have a toolbox that consists of chemistry and chemical reactions. And now, we dissect the chemical reactions of a living cell down and we conclude that it is nothing but ordinary chemistry. There is in fact no chemical reaction for which we cannot find numerous examples in other places. In a way that is what is going on with the evolution of the immune system. We are finding this part or that part and seeing these parts preexisted here or there. We stumble on a few surprises - parts we did not expect – but even those parts did not magically materialize. The parallel I am trying to draw is that dissecting the immune system or any other system is following the same sort of pattern as the chemistry of life did earlier. And when we succeed, which I presume in large part we will, where will we be? Having convincingly shown that the chemistry of cells is ordinary organic chemistry, have we solved the problem of how life appeared? And if to our satisfaction we find parts – precursors to the immune system – and reactions that can transform the genetic material, will that explain why they seem to suddenly come together in the combinatorial immune system in sharks?
That is, in any case, how I think about the issue.
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rafe gutman
Member
Member # 134
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posted 18. September 2002 07:45
quote:
by dr. dembski to yersinia:
You state that previously I claimed that the dots couldn't exist because they wouldn't be functional. Please show me in Michael Behe's writings or my own where we deny that IC systems can be made up of subsystems that can be functional in their own right.
michael behe's original definition of irreducible complexity:
quote:
a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease function...
An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional
(emphasis mine)
then there's dr. dembski's definition:
quote:
A system performing a given basic function is irreducibly complex if it includes a set of well-matched, mutually interacting, non-arbitrarily individuated parts such that each part in the set is indispensable to maintaining the system's basic, and therefore original, function. The set of these indispensable parts is known as the irreducible core of the system
(emphasis mine)
if my quoting is out of context, then show me where you or dr. behe have acknowledged that subsets IC components could be functional. there's also the issue of your "calculation" for the evolution of the bacterial flagella, which assumes (among other things), that all the components would have to come together at once in order for it to have any selectable function. that seems to me to "deny that IC systems can be made up of subsystems that can be functional in their own right"
in regards to paul nelson's request for a description of an IC system's evolution, i believe i have provided a simple one for the complement system. i'll repost it in case you didn't notice it:
quote:
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.
admittedly, i left out a lot of details, but if you want more, you'll first have to propose a model for the origin of an IC system through intelligent design in at least as much detail as i presented. that shouldn't be too hard, it's only 8 sentences.
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William A. Dembski
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posted 18. September 2002 09:01
Rafe,
I wrote, "Please show me in Michael Behe's writings or my own where we deny that IC systems can be made up of subsystems that can be functional in their own right." Both Behe and I have always defined IC with reference to the basic function of the system in question (if we've not said it explicitly -- and I have in NFL -- then a charitable reading would have granted that -- neither Behe nor I are that stupid). We therefore left open the possibility of subsystems having function in their own right. You and Yersinia charge us with a denial. The quotes you give indicate no such thing.
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.
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Deanne M. Taylor
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Member # 274
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posted 18. September 2002 09:11
Mr. Dembski writes:
quote:
In the case of an IC system S comprised of components {S(1), S(2), ..., S(r)} and arranged in some irreducibly complex configuration C, we need a sequence of supersystems T[1] --> T[2] --> ... --> T[n] where each T[i] consists of one or more functional
biological systems.
What you are saying here, in the case of a system "S" that exhibits irreducible complexity, comprised of several interacting components, and arranged in some configuration "C", we need a sequence of events to generate every sequential progenitor of that final system.
The beginnings of this argument may seem to be trivial, but please bear with me.
Suppose any complex system "S" is posited which is assumed to be IC, and pieces of that complex system are knocked out with wet-lab experimental techniques. The organism continues to function, therefore that piece that was knocked out can be assumed to not be part of the irreducibly complex system, "S", so isn't amenable to study.
Reducing this even further (and I'll spare the PubMed citations for those who may be bored with a list from the legitimate publication record) we find that the bane, currently, in functional genomics is how many genes are NOT required for the survival of an organism.
That is, a phenomenon has been observed in which biologists, eager to find out the function of a protein in an organism, will remove it from the organism by knocking it out of the gene, only to find that it has minimal or no effect on the ability of that organism to survive. That is, the organism goes on to reproduce and function, sometimes frustratingly as if nothing happened to it, at all. Pharmaceutical companies often find this very frustrating, slows down the discovery process and adds to the total cost of discovery.
It's a real problem.
Conversely, it's interesting that many genes have more than one function in more than one networked system, so for instance, knocking out what is understood to be a gene coding a hormone related to milk production in humans also functions as a member of a pathway that includes cell growth and survival independent of the milk-production pathway (see for instance http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12128285&dopt=Abstract
In the case of the "silent" knock-outs, it may be that a gene that is knocked out in one system may contribute to an "irreducibly complex" system in another partition of the animal, though that isn't a observed as a majority and most of the silent knock-outs grow up from embryonic state in a perfectly normal sequence of events.
That dual function aside for a moment, let us continue with considering the consequence of genes that, although they are certainly part of a pathway, are not obviously part of irreducibly
complex systems.
Work done on protein-protein interaction networks (such as DIP (database of interacting proteins) and several others) has shown that this power-law distribution of protein-protein associations and contacts means that there are a minority of protein interaction nodes that actually show any kind of hierarchical importance.
If you draw these protein-protein interaction maps, you find that they are scale-invariant. That is, the interaction map looks more like an airline flight-service map like you see in the back of those in-flight airline magazines, with a few centralized hubs and many outlier nodes (service cities) that have no additional connections outside of the hub connection) rather than some kind of highway map, where everything is connected. This property is called "scale invariance."
Scale invariance means that any small part of the network map will have the same properties of the greater part of the network map. That is, the properties of the network are invariant no matter how close or how far away you peer at the network. Small pieces of the network resemble the larger network as a whole. (Some might associate that quality with fractal behavior.. it's not too far off, but it's a little different and another topic).
Thanks for reading so far. I have to include this background for future statements.
The nodes that are the most connected to all other nodes are the hubs, which will behave as if they're IC because if you knock them out, it's like knocking out a major airline's hub. Service to all those outlier cities goes kaput. The network fails. End of story.
But if you knock out an outlier city, the network functions on, unimpeded, not even noticing that the outlier has gone away, as it lies on the very edge of the network, and removing that connection means little to the success of the network. This is a mathematical probability as well as biological . See, for example, treatises on graph theory applied to biological networks.
That protein networks exhibit this quality is something that has been measured for quite some time in the laboratory. The behavior of biological systems when one tries to knock out random players has been published and documented, and I'll spare you the citations. I'm sure you know how to do PubMed searches.
There have been some questions as to the amount of scale-free behavior in these protein interaction networks due to fuzzy experimental methods that over-predict protein-protein interactions (promiscuous interactions, yeast two-hybrid in particular)...which is actually error in the negative AGAINST scale-free networks since the error would err against scale-free properties, not support them, and even given the error of promiscuous association, the networks still showed scale-free behavior.
To improve on these observations, certain groups have improved on experimental techniques, such as a group at CuraGen Corporation who have found a method to study protein-protein interaction networks and clean up yeast-two-hybrid predictions using another experimental method which supports the true data while discarding the false, promiscuous data. They've applied it to protein interaction networks in the fruit fly, D. melanogaster to get a tighter measure of scale-invariance in the protein-protein interaction network. The power-law, scale-invariant properties of protein-protein interaction networks is accepted on evidence; the finer details, of exactly what the magnitude of that scale-free network dimension is, is currently being studied by groups all over the country.
So, protein-protein interaction networks, which make up the bulk of metabolic systems (for instance)are scale-invariant. This is an interesting and important point. It explains why biologists, when attempting knock-out experiments on randomly chosen genes have such little success in generating change in the organism. Any one specific mutation that knocks out any one particular gene is more likely to knock out
an outlier than a hub!
Most of the time, since most of the pathways go to outlying nodes, they're hitting an outlier, not a centralized node. If you close your eyes and randomly point to an airline flight path map, there's a better chance (often a much better chance if the airline has few nodes) that you'll hit the service city and not the hub. (I'll cave in and yield at least one group doing lovely studies, if not a specific citation, here...Barabasi's group at Notre Dame has worked on scale-invariant maps dealing with protein-protein interaction networks, for instance.)
Therefore, this is a good reason why so many parts of an organism's system do not show IC, and why the IC argument thus far has relied on specific examples, such as ATP synthetase, to build an argument of irreducible complexity. ATP sythetase is one such "centralized hub". Since ATP furnishes a cell with energy, the mechanism that makes this energy is central to *every* process within a cell. It is no surprise that ATP synthetase should have a central, and seemingly
IC embodiment within the cell. (I might point out that this is not a "just so" story, for the record).
These networks do not look as if they were orchestrated to as much as they appear to have been added to over time, as the bulk of the pathways seem to lie in the "outlier" category.
Which brings us to the question of evolution. If one was to mimic evolution on any scale, starting from one particular ancestral system or pathway, and add to it slapdash by gene duplication, innovation, and pressure through competition, what kind of network would we expect to see? What kinds of qualities would the nodes in the network have? Would it be scale-invariant, where certain nodes always branch out to all directions (hub creation) and outliers later become hubs of their own?
It's an interesting question. I believe some groups have already worked on that, especially Adami's paper on the evolution of complex networks.
That ATP sythetase in the Darwinian version would evolve out as a "hub"...if not THE hub, of a unicellular organism as the organism grows in complexity isn't in question, here. Evolutionists would point out that it would be a natural consequence of its central role in energy production.
But it would be more useful to say that thus far, there have been no arguments AGAINST biological networks' scale invariance showing up as a consequence of evolution, as this kind of network, with its additions to the network through gene duplication and drift, is pleasantly (at least to evolutionists) in line with what was expected for a complex network of interacting proteins.
Perhaps ID can furnish similar mathematical proof why design, not evolution, must include the observed scale invariance of protein networks.
quote:
Thus T[i] = {T[i](1), ... T[i](k)} (k depends on i and is at least 1) and each system T[i](j) consists of m components {T[i](j)(1), ... T[i](j)(m)} (m depends on i and j) and is arranged in some configuration C[i](j) (not necessarily irreducibly complex).
What you are requiring of evolutionary proponents, in the context of this reply, is that someone prove that a system or protein that currently exists as a hub (is IC) in a protein interaction network, was once, at some distant point, NOT a hub in a protein interaction network, or at least prove within a reasonable doubt that it arose from a simpler state to its current, complex state.
In other words, you wish evolutionists to contract the history of the network, back in time, run the movie backwards so to speak, and show how each of the components that make up the hubs of protein interactions became hubs in themselves.
You realize, of course, that evolutionary theory suggests that this process happens over evolutionary time, and although you demand proof for such a series of events (and I'm sure there has been proof offered), biologists will not be able to provide a series of mutations for you at this point, as this would require biological engineering capabilities we're only working towards, right now.
Additionally, you have the ability to retort that any sequence of events proposed for a Darwinian explanation of IC is a just-so story without evidence to back it up, and you can demand hard evidence. Rightly so! Science should demand hard evidence.
If that evidence is impossible to observe, one can also look at other avenues for that evidence. If you cannot be at the crime scene directly when the murder took place, you can instead use blood, fingerprints, DNA samples and any other kind of "smoking gun" evidence to point to the murderer.
I am about to offer you some evidence, though possibly not in the form you expected when you wrote that post, yet I will await why the smoking-gun evidence is not sufficient to show how systems that appear IC appeared out of a logical sequence of events. As you probably guess, it has to do with scale invariance.
Mr Dembski asks the following:
quote:
In the sequence T[1] --> T[2] --> ... --> T[n], T[n] = {T[n](1)} and T[n](1) = S, the system in question. Under the assumption that S evolved by Darwinian evolution, there must be a supersystem T[1] in which the components of S are either absent or targeted in completely different systems for different functions.
Leaving aside that there have been experimentally observed, multiple functions for the same protein in different tissues and in different states of organismal development, we should instead examine the observed qualities of biological networks in the context this challenge...
quote:
Such a T[1] needs to be the starting point if S is properly to be ascribed to a (macro)evolutionary process. Each arrow in this
picture should represent a small incremental change that is highly probable on the basis of the Darwinian selection mechanism.
The fact that biological networks yield scale-invariant behavior and physical qualities suggests that protein functions were added
sequentially through evolutionary process.
The QUALITY of the network, the very essence of the biological network, speaks to the very same mechanism you are demanding proof of. Comparisons of genomes and these physical networks between organisms have, thus far, supported scale invariance of these complex networks and an increase in complexity of these networks over evolutionary time. See the Adami paper, for instance.
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.
Think of old European or Arabic cities that have no DELIBERATE engineering design but instead are forced to grew up out of necessity for greater populations and space constraints, and how
they show evidence of new additions on old cores. One should not assume such a haphazard design grew up out of deliberate planning, but grew out of a logical progression of demand, innovation, and pruning... in genetic comparison, that would be demand, gene innovation/duplication, and drift.
Just as a geologist can track a lava flow through satellite analysis up the side of a volcano to the caldera, a mathematical biologist can create a simple mathematical model of observed gene duplication and mutational drift and end up with a scale-invariant network on his computer.
I would suggest that proponents of ID build computational, mathematical models which prove that the Darwinian model of gene duplication, innovations from duplications and chimeras, mutation, and drift cannot adequately explain the observed scale invariance in biological networks.
Perhaps ID can also propose alternatives to the theory that evolutionary processes have resulted in this measured scale-free behavior. What else could account for this haphazard, infrequent-hub kind of network? This would be a great place for ID to begin publishing in peer-reviewed journals, where rigorous mathematical models are usually viewed with favor.
I hope to see a direct application to the question of how IC addresses scale-invariant networks which actually show a minimium of IC themselves, and how ID stands to gain more from the evidence of scale-invariance in biological functional networks rather than evolutionary theory.
quote:
In most instances it will be at the level of a single component T[i](j)(k) being slightly modified and (re)targeted to a component T[i+1](j')(k') of system T[i+1](j') (thus T[i] --> T[i+1] would signify the change T[i](j)(k) --> T[i+1](j')(k')).
Leaving aside your indices for a moment, what you're saying above (for the index-challenged) is that: "in most instances it will be at the level of a single component, part of an existing cluster of components, being slightly modified and retargeted to an "improved" or modified component of the network, thus this redeployment would signify an incremental change."
I argue scale-free invariance in networks is the smoking-gun evidence for exactly what you're asking for. The qualities of extant biological networks are an end result of the very process of adaptation and convergence to a static hub, as evolutionary hubs are of necessity not able to change as quickly as their outliers (due to the sheer pressure to function in exactly the capacity they have been forced to assume). And NOT surprisingly, we see these hubs, these examples of irreducible compelexity, CONSERVED through the lineage of organismal development as proposed by evolutionary theory.
Can ID come up with an example of an complete, multi-component IC system that has shown up suddenly, unconserved, in a single organism that does not show descent or lineage in either direction?
There are many ways to approach this question, as given above.
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.
[ 18 September 2002, 09:46: Message edited by: Deanne M. Taylor ]
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Paul A. Nelson
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posted 18. September 2002 09:53
Rafe,
I did notice this:
quote:
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.
After 20+ years in the evolutionary literature, however, I've also learned how to read these scenarios. In particular, I've learned to watch for phrases like these:
"the system evolved it's own serine protease"
later, receptors appeared
the complement proteins evolved the ability to induce local inflammation
the complement system evolved a cytolytic ability (lysis)
Yes, "receptors appeared" -- just like that.
This is storytelling.
[ 18 September 2002, 09:54: Message edited by: Paul A. Nelson ]
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William A. Dembski
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posted 18. September 2002 11:31
Deanne,
Interesting post and some interesting possibilities for ID research that you raise. 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. 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.
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.
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? 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.
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?
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? Where's the causal specificity? It's all fine and well to model an evolutionary process computationally and get hierarchical systems exhibiting scale invariance. 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.
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.
I'm afraid I won't be able to do anything on this thread till the weekend.
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yersinia
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posted 18. September 2002 11:47
Wow, way more than I can address this morning.
Last one first:
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.
(How can one literature-bomb if there is no literature, as Behe said? I guess Behe's literature claims have been proven wrong)
As for an "in my own words" scenario, if you want me to re-type Matt Inlay's entire article in my own words into ISCID, I suppose I could do that, but (a) it would take many pages and (b) what's the point when the durn thing was referenced for your consideration in my very first post? That's the reason people write articles, so that every individual doesn't have to recreate the wheel him/herself. The focus on little ol' me makes it look like Nelson and Dembski are avoiding the issue.
The one thing implicit in Inlay's article and which I decided to expound on a little further is the continual selection pressure for improved immunity. The origin of the immune system is not a case like the evolution of human hands, where
function of the limb changed from swimming, then bottom-walking, then terrestrial walking, then climbing, then tool-use. In the case of the immune system the basic pressures remain the same all the way back to when immune systems began to develop near the origin of multicellularity.
The basic selection pressures for diversity and control are roughly constant and given that basis, then if the various mutation hypotheses described in Inlay's article improve function then that's basically all that is needed in terms of a NS model. The origin of the immune system is
a massive case of specialization with no change of function (at the system level; individual parts can change function as they get coopted into the system), and so the basic selection pressures are quite simple (rather like the evolution of the eye in that respect).
yersinia
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yersinia
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posted 18. September 2002 12:22
Briefly,
Dembski has just required omniscience on the part of scientists if they are to convince him that something like the immune system evolved. Plain-old hypothesis testing, successfully employed in the case of evolutionary immunology as even Peonie and Gene probably acknowledge and as documented to anyone who follows the references I have posted, has been left by the wayside.
Dembski of course does not apply his own standards to himself, evidently he thinks that:
no immune system --ID--> immune system
...is a sufficiently detailed explanation, unless and until Dembski's ridiculous and unscientific standards are met:
quote:
Your filling in of details is like a man attempting to count to infinity -- the challenge ahead of you far exceeds any progress you've made to date or even any progress you give any indication of being able to make.
Counting to infinity is of course impossible, but on his own analogy this is pretty much what Dembski demands even for events that occurred 500 million years ago.
As for literature, Dembski has made similarly wrong claims just like Behe. To pick one at random from NFL:
quote:
...the Darwinian community has been utterly stymied in explaining the emergence of irreducibly complex systems once the complexity of these systems becomes palpable. [p. 286]
This statement is utterly indefensible in the case of the immune system -- for how was I able to "literature-bomb" (and sorry if that annoys people, but the existence of literature is the key question in this thread) unless the literature in fact exists? Based on their previous comments in the thread not even those more sympathetic towards ID like Peonie and Gene will defend the characterization "utterly stymied" in this case.
As for who is being dogmatic and a "true believer", Dembski has just demonstrated that only omniscience would suffice to demonstrate the evolution of IC to him, that hundreds of articles and passed tests, and hundreds of *known* "puzzle-pieces" (not just a few, Dr. Dembski) can all be flicked aside unless this standard is met, and in someone's own words on a bulletin board no less.
To put this in perspective, a brief history of Dembski's arguments goes something like this:
- Complex-specified information cannot be produced by natural processes.
(What about cumulative selection of small bits of information?)
- Behe's irreducible complexity precludes cumulative selection because the intermediates would be nonfunctional
(What about all of these functional intermediates?)
- It's not enough to have functional intermediates, they have to be connected with detailed, testable models
(What about these hundreds of articles, books, and scientists in the field of evolutionary immunology?)
- Not detailed enough, Dembski requires infinite knowledge which no scientist can ever attain even in principle.
...and yet, after this continual retreat in position, Dembski has the chutzpa to write that he won't hold his own hypothesis to the same standards, or even a much lower standard such as, say, giving us some vague idea of who the designer is, without which one has no basis with which to test the hypothesis. And until such infinite knowledge is reached, Dembski will continue to advocate that his idea is better than doing actual scientific research:
quote:
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.
...sounds like a pretty clear admission of a "science-stopper" to me.
yersinia
PS: Unfortunately I have to work like everyone else, so will be out until tonight at least although much more could be said.
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andyg
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posted 18. September 2002 14:30
Quote from Bill 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."
This seems to me to be a very odd position to take. Bill seems to be saying that the onus is on the biologists to describe in minute detail every step in the evolution of a biochemical system - ideally documenting every DNA mutation that led to such changes - despite the absence of a biochemical fossil record. ID proponents, on the other hand, can dispense with such grunt work, because if a supernatural designer is responsible for the biochemical system in question, then "it makes no sense to try to ape your method of connecting the dots". This seems a tad unfair and rather lazy on the part of the ID camp, since they see no need to work out how the thing was designed in the first place. It also serves to shut down research rather effectively - if one concludes something was designed, then Bill seems to be saying that nothing further needs to be done (other than to pass on the conclusions to eager young minds).
If ID is not a mechanistic theory, then how can scientists make use of it? Is Bill really proposing that an ID research program should be devoted exclusively to labeling an object as being intelligently designed and then moving on to the next one?
I'm sure I won't be the first to point this out, but I doubt that Bill - or anyone else for that matter - will be able to demonstrate every genealogical step connecting them to their great-great-great-great-great-great-great-great-great-great-great-great grandparents. What does this say about our ancestry? Is the Titanic of my family tree sinking fast?
AndyG
[ 18 September 2002, 14:49: Message edited by: andyg ]
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rafe gutman
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posted 18. September 2002 19:37
dr. poenie,
i think i'm beginning to understand where you're coming from on this. i see now that your view of the status of evolutionary immunology is very much in tune with the scientific community's. your skepticism of the evidence is justified, and not just naysaying. if i understand you correctly, where we differ is in how we interpret the "big picture". richard dawkins and i could look at the exact same evidence, with the same understanding of it, and he would see it as evidence of atheism, whereas i would not. so even though you and i might make the same predictions for future findings, we'd draw different conclusions from them. i would agree that darwinism might be indistinguishable from a particular kind of intelligent design (something very similar to theistic evolution), and that it's not fair to assume one is somehow better than the other. i think though, that that distinction is outside the realm of science.
i'm sorry that these kinds of discussions always end up being so caustic. the politics often get in the way of meaningful dialogue. i'll leave you out of this from now on. i did have one last question for you though. what would you do differently? that is, if you could change how immune system origins were studied, what would you do? do you think that these issues are being approached by the scientific community in the best possible manner?
thanks
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Mike Gene
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posted 18. September 2002 21:11
Nic,
The formulation of some kind of "relative likelihood reasoning" sounds interesting, but my main point dealt with the tension created by using both the "hallmark" approach and the "parsimony" approach. It would seem to me that attempts to converge these different methods into a single approach merely end up weakening both. For example, if you were to find sufficient evolutionary hallmarks for biotic feature X, the "hallmarks" end up as nothing more than window dressing given that you already believed X evolved on the basis of parsimony. But if you don't find any hallmarks for biotic feature Y, the appeal to parsimony ends up looking like a dive down the escape hatch (to rescue the pre-existing belief that Y evolved). Put simply, by bringing parsimony into the picture, your "hallmarks" end up looking more like apologetic devices than investigative tools. Personally, I'd jettison the "parsimony" appeals, as they tend to collapse into a philosophical argument and merely undercut your hallmarks.
This problem is then amplified when some of the qualifications as part of your "relative likelihood reasoning" are put into play. For example:
quote:
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
Is this yet another apologetic move or a true investigative concern? It's hard to tell. If it is the latter, it would seem to me that non-teleologists should rigorously define some type of temporal evidential threshold, where we would not expect to find any evidence for evolution prior to this threshold. Then, appeals to ancient events would have some teeth. As it stands, the "it's too old" argument comes across as more of an excuse that gets applied in an "escape hatch" manner (creating now two escape hatches). But is the "it's too old" argument truly valid? Does it always apply? For example, which is older - the origin of mitochondria or the origin of Broca's speech center, avian lungs, and the bat's wing? It would seem to me that the evolutionary origin of the latter three, while much more recent than the origin of mitochondria, are less well "evidenced." Or, if we turn to the flagellum itself, recall that Ken Miller and many others argue the evolutionary origin of the Krebs cycle is well-evidenced. Yet the Krebs is found in both archaea and eubacteria (unlike eubacterial-specific flagellum we discuss), clearly indicating it to be older than the bacterial flagellum (from the traditional viewpoint, that is). If you can find evidence for the evolutionary origin of the Krebs, complaining that the evolutionary origin of the flagellum was too old clearly comes across as a rationalization and excuse.
Perhaps my perceptions are flawed here, but this is how this all ends up looking from where I sit:
You think the Krebs Cycle evolved and there is evidence of this evolution.
The Krebs Cycle is older than the bacterial flagellum.
We can't expect to find evidence for the evolutionary origin of the flagellum because it is too old.
Ah, but we have evidence for the evolutionary origin of the flagellum (i.e., ExbB-to be addressed soon).
Ah, but if we didn't have this evidence, we'd have to conclude the flagellum evolved because the immune system evolved.
Like I said before, I'll try to deal with your hallmark for the flagellum. In the meantime, it would be nice to see you explain why it is the capabilities of chance alone are very very limited.
[ 18 September 2002, 21:12: Message edited by: Mike Gene ]
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rafe gutman
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posted 18. September 2002 21:37
quote:
by dr. dembski:
Both Behe and I have always defined IC with reference to the basic function of the system in question (if we've not said it explicitly -- and I have in NFL -- then a charitable reading would have granted that -- neither Behe nor I are that stupid). We therefore left open the possibility of subsystems having function in their own right. You and Yersinia charge us with a denial. The quotes you give indicate no such thing.
then how do you explain the word "original" here?
"A system performing a given basic function is irreducibly complex if it includes a set of well-matched, mutually interacting, non-arbitrarily individuated parts such that each part in the set is indispensable to maintaining the system's basic, and therefore original, function."
more quotes from NFL:
quote:
a flagellum without its full complement of protein parts does not function at all. Behe therefore concludes that if the Darwinian mechanism is going to produce the flagellum, it will have to do so in one generation. (page 251)
quote:
To achieve an irreducibly complex system, the Darwinian mechanism has but two options. First, it can try to achieve the system in one fell swoop. But if an irreducibly complex system's core consists of numerous and diverse parts, that option is decisively precluded. The only other option for the Darwinian mechanism then is to try to achieve the system gradually by exploiting functional intermediates. But this option can only work so long as the system admits substantial simplifications. The second condition [that the irreducible core of the system is at the minimal level of complexity needed to perform its function] blocks this other option. Let me stress that there is no false dilemma here-it is not as though there are other options that I have conveniently ignored but that the Darwinian mechanism has at its disposal. (page 287)
again, if all three of these quotes are out of context, then it shouldn't be difficult to produce a quote from NFL where you acknowledge this fact. i'm not saying it doesn't exist (since you acknowledge that fact here), but i would like to see a quote. also, since you do accept that fact, then do you admit that your last quote above is wrong?
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