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Author
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Topic: Organisms using GAs vs. Organisms being built by GAs
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charlie d.
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Member # 159
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posted 20. March 2003 10:54
Mesk's is an excellent question, and goes to the core of modern immunological theory. Let me see what I can do to answer quickly right now, and I may get back on it later when I have more time.
In the past, it was long held that discrimination of self from non-self was crucial to the logic underlying immune system function (note that the problem however preceded the appearance of immune systems as we know them, and is already essential to the development of multicellularity, for instance).
In the innate immune system, recognition of foreign antigens is based on recognition of molecular determinants and patterns that are peculiar to pathogens (certain sugars, lipopolysaccharides, etc) and not synthesized at all by higher organisms. In this case, any mutation that changes specificity of a receptor to a "self" determinant will be eliminated by natural selection. This is what yersinia referenced to, and I think it’s pretty straightforward, though not very relevant to the question of adaptive immune system evolution.
In the case of rearranging receptors, diversity is somatically generated, and if this is extensive enough, it's almost unavoidable that some antigen receptors will recognize self molecules. However, is this necessarily bad? There are several lines of evidence that suggest this is not the case, primarily that all of us express significant levels of autoantibodies in our basic circulating repertoire (the “natural” antibodies I talked about before), even in the absence of any autoimmune symptoms. Even more surprisingly, if you genetically eliminate these low-affinity, polyspecific, self-reactive IgM antibodies from a mouse, the paradoxical result is a propensity to autoimmunity, and not the opposite. It seems thus that low affinity self-reactive antibodies may actually help clear cellular debris generated normally by cell death, while in the absence of rapid clearance, real immune responses may kick in, generating diseases causing, high affinity autoantibodies.
So what about self/non-self discrimination? It is now generally thought that things are more complex than that, and that the immune system does not simply detect any foreign substance, but needs to detect them within the appropriate context, intended as other signals indicating tissue damage, necrosis, inflammation, etc. In the absence of such signals, immune responses in fact are not efficiently activated.
Going back to the early evolution of the adaptive immune system, thus, I would imagine that the first rearranging antigen receptors were of relatively limited variability and low affinity (such as we still find in lower vertebrates and in our own natural antibodies), and that a certain level of basal self-reactivity, far from being a problem, might well have been part of their usefulness.
I can add to this later, if anybody is interested; let me know.
Here is a good review article regarding this and other issues that were discussed above.
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gedanken
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Member # 594
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posted 20. March 2003 18:20
So Mesk,
You seem to be saying that this is clearly not a case of "You either have it or you don't."
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Mesk
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Member # 630
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posted 20. March 2003 18:28
Rex and nic raise some interesting points, but IMO do not get to the heart of the matter. As charlie notes, self-reactivity of the innate immune system (that is, by antigen receptors with fixed specificity) is likely to be eliminated by natural selection against any mutations in either receptors or self molecules which resulted in self-reactivity. This selective response is not really relevant to the type of mechanisms required to prevent auto-immunity in organisms with immune diversity.
Charlie's response is more like what I was looking for. The notion that self-reactive antibodies may actually be beneficial to an organism is a fascinating idea, and one I had not encountered before. The review article charlie cited suggests a related idea (which I think charlie is also perhaps hinting at) - that the earliest precursors of modern antibodies were actually receptors for endogenous molecules rather than pathogen-associated factors.
So let me put forward a scenario for comments:
A proto-lymphocyte in some primitive organism possesses a receptor which functions in the clearance of normal cellular debris. It binds to a ligand molecule which is expressed fairly ubiquitously on the surface of endogenous cells, and the cell which expresses it floats around the primitive circulatory system clearing (probably by phagocytosis) any cells or membrane remnants which have drifted into blood vessels. Obviously these cells need to be more numerous when cellular debris is more common, so they have signalling mechanisms which trigger their proliferation is response to ligand-binding.
The transposon insertion mechanism outlined in detail in previous posts occurs in the gene encoding this receptor. As a result, the proto-lymphocyte expresses RAG1/RAG2 transposases during the normal transcriptional activation of the receptor gene; these enzymes snip themselves out of the gene, leaving genetic debris behind which alters the coding region of the gene. In a small number of cells this results in the ability to bind other cellular debris; those cells which are able to bind debris are triggered to proliferate, resulting in clonal expansion of successful debris-clearing cells. Since this process increases the potential repertoire of debris molecules which the cells can clear, this provides a benefit to the organism and is thus favoured by natural selection.
At this point there arises the issue of unwanted self-specificity. Any cell which bound to, say, an erythrocyte surface marker would be strongly expanded due to the abundance of potential targets. It is not hard to see that large numbers of cells roaming the blood vessels engulfing red blood cells would be a rather unfortunate outcome for the organism in question. However, there is one possible solution: let's postulate that the initial ligand of the receptor was expressed ubiquitously, even on RBCs and endothelial cells. This ubiquity would have been advantageous as it would have allowed the phagocytic cells to clear dead RBCs and andothelial cells, as well as any other type of cellular debris. To prevent serious tissue damage, however, there must have been a mechanism by which attack of live cells was prevented - probably a surface marker on live RBCs and endothelium which rapidly degraded after cell death, thus suppressing the phagocytosis of useful, healthy cells. This mechanism would also have been effective in preventing auto-immune attack after the receptor recombination mechanism had been introduced.
After this point, of course, there is the question of how this clearance system evolved into a system for responding to external pathogens, but due to lack of time I'll have to leave that for later. Any comments at this stage?
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Mesk
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Member # 630
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posted 20. March 2003 19:46
gedanken,
Sorry, I posted the above message before your post appeared on my browser.
If you're referring to the adaptive immune system (?) - then you're quite correct. It seems to me that there is clearly a continuum between organisms with relatively simple innate immune systems and organisms with more complex adaptive immune systems, along the following axes (and no doubt others I haven't thought of):
1. Degree of antigen receptor diversity (from a few genome-encoded, relatively non-variable receptors; to a larger number of receptors with higher allelic and haplotypic diversity; to receptors with the ability to recombine in somatic cells to generate increased diversity; to receptors with the diverse and complex diversity- and affinity-generating mechanisms seen in modern vertebrates);
2. Degree of ability to differentiate between self and non-self;
3. Degree of regulatory efficiency with respect to expression of immune molecules in situations of pathogen invasion, rather than constitutive activation;
4. Degree of affinity of receptor molecules for target antigens (e.g. the affinity maturation process, presumably a relative latecomer in vertebrate immune system evolution (?), which greatly refines the affinity of specific antibodies for particular ligands);
5. etc., etc.
What really interests me is (a) the extent to which plausible evolutionary scenarios can be devised for the various steps in the evolution of the immune system, and (b) the extent to which these scenarios can be tested using contemporary sources of evidence. The scenario I suggested above represents one possible evolutionary trajectory for the early history of the adaptive immune system, which (very tentatively) explains how massive self-directed immune assault could have been side-stepped. I invite comments from anyone about whether such a scenario is plausible, consistent with the available evidence (e.g. does the clearance system I postulated, including suppressor molecules on healthy cells which prevent misdirected clearance, exist in any form in modern organisms? I know some parallels might be drawn to the complement system, but need to think more carefully about that before I speculate), and empirically testable?
I think this sort of discussion is far more useful for the furthering of the evolution/ID debate than any amount of hand-waving about sterile concepts like IC. The question is not whether the immune system is IC (whatever that happens to mean at that particular moment in time), but whether the immune system evolved via currently understood mechanisms. That's what this entire thread is really about, but a lot of time has been spent discussing irrelevancies such as IC (a nebulous concept at best, which IMO has already been shown to be quite meaningless in the context of whether or not something could have evolved) and correcting Nelson's rather limited understanding of the immune system. I think more constructive discussion could be achieved by focusing the thread on more practical issues.
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gedanken
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Member # 594
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posted 21. March 2003 11:29
Hi, Mesk, I’m sure that you are exactly right. In fact I and others may have been somewhat forgetting the topic of this thread. But I intend to press ahead in the A sequence of tests for IC thread with understanding the logic behind IC -- I’m not a biologist and can’t contribute at all to the biological side of this issue, but I am interested in the GA side from a logical and “search” viewpoint.
Alonso said:
quote:
I am defending Behe's assertion that the VDJ recombinase/antigen receptor is IC.
By itself this indeed makes the discussion get away from the topic of this thread. Because without clarifying which definition of IC is being “defended” and what if any definitions of IC implies for GAs, we don’t have any relevance to what a GA could do (in any of the variants of the topic here). And as what you say, we have direct observational evidence to tie historical or current-day occurrences in nature to GA models. I want to understand (in that thread) what the logical implications of various definitions of IC are, and we can’t do that unless the people who are interested in IC tell me just what IC really means.
If we reach any understandings in that thread that have any implications for GAs, then I’ll report back. Thanks
[ 21. March 2003, 11:32: Message edited by: gedanken ]
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charlie d.
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Member # 159
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posted 21. March 2003 11:43
Mesk:
I think much of what you propose makes sense, but it's far to speculative at this stage. Our knowledge of immunology in cartilagineous fish is very limited, though it's gaining ground, and until we know exactly how their adaptive immune system works, it's hard to propose real, testable models. Just developing all the necessary molecular and cellular reagents for these studies (stuff that took 20+ years of work from thousands of scientists for mammals) is a massive headache.
That said, your idea of an immune inhibitory receptor on normal cells might be not so far off, though perhaps in a slightly different way from how you proposed it.
Our immune system has developed sophisticated checks and balances to ensure prevention of widespread autoimmunity. One of these many mechanisms is based on the expression on activated lymphocytes of "death receptors", whose ligation by specific ligands induces rapid apoptosis. To make a very complex story simple, in the presence of certain signals (eg, inflammatory mediators), or in organs that are "immune privileged" (i.e. that can escape normal self/non-self recognition mechnaisms, such as the eye, brain and gonads), normal cells can turn on expression of the death receptor ligands. Thus, should any lymphocyte recognize them with their antigen receptor and become activated, they would immediately commit suicide because their death receptors would become engaged by the ligands on the target cells. In this way, "bystander" cells at sites of infection and inflammation can be spared destruction, and potential autoreactive lymphocytes are eliminated before their activation runs out of control.
Importantly, from an evolutionary perspective, homologs of the same molecules and pathways involved in "death receptor" signalling in mammalians exist in drosophila (and were recently found to be involved in the modulation of innate immune responses). Thus, at least some of the precursors of the control mechanisms that are important for the prevention of autoimmunity in vertebrates were already present in invertebrates.
[ 21. March 2003, 11:48: Message edited by: charlie d. ]
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Nel
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Member # 614
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posted 05. April 2003 17:10
My apologies for my prolonged absence. Crowds and traffic caused by Operation Atlas in NYC is frustrating me to no end, it took some time to get used to. I'm going to go in chronological order here in terms of replies, in this and other threads that I was participating in. I'm going to try not to be away for so long in the future. Hopefully everyone I was having a conversation with is still participating on this board.
Ged,
With respect to IC systems, I wrote:
quote:
It is simply false that all cases of biological complexity are a matter of degree. In fact, this is the point about bringing up IC systems. You see, with IC systems you don't have "degrees". You either have it or you don't.
This is a little off topic for this thread, but it is relevant in that Darwinian evolution suffers the same problems with the flagellum as it does with aquired immunity. You say that there are degrees of selectability in that if you decrease the complexity of the flagellum you may have alternate functions that are selectable. However, as I have stated in the Evolving Inventions and in others there are not only unselectable steps leading from suspected precursors to the bacterial flagellum, but co-options events in and of themselves involve to many random chance events
even if you do get alternative functions along the way. In the case of the bacterial flagellum, you don't have a motile system, there are cases where bacteria cannot survive unless they do brave the brownian storm with a molecular machine like the bacterial flagellum. There are cases where it might not need one. But of course, the question is: what is the origin of the bacterial flagellum? Whether one can survive without one or not is irrelevant to this question. The question is , can Darwinian evolution do it. I think it is unlikely that this natural process can without intelligent intervention. is really not a gradualistic pathway, it rather invokes 10+ co-option events all due to chance as natural selection was pruning the system for the function that already exist. Another example is that the system in question, the type III secretory system they point to, post-dates the bacterial flagellum.
As if that weren't enough they also ignore the fact that the various subsystems within machines like bacterial flagellum are also IC.
What do we find in nature instead? Do we find the blind cobbling together of different functions using different parts, from wiggly things, to a somewhat functional flagellum, to the efficient, precise, fine-tuned, bacterial flagellum? Or do we find a core 20 parts that is extremely resistant to the clumsly cobbling of natural selection?
As I said in the Sequence Tests for IC thread, which I will get back to shortly, we have to start with an M ring which only has a flagellum specific function. Then we have to follow up with a C ring which is just as flagellum specific. Outside the flagellum, it has no function. Thats a few unselectable steps right there. And then you have the problem of the 6 part export machine. There is no evidence that any subset of this export machine carries out alternative function. So thats quite a few unselectable steps right there. Then you would obviously want to add FliE since it's a great proto-filament, but FliE has no obvious role outside the flagellum either and T3SS don't need FliE. Thats another unselectable step. Then you have the rod, which is three components that are likely functionally indivisible, so adding each additional component of the rod adds more unselectable steps.
This is also relevant to aquired immunity, but I will get into that in later replies in this thread.
With respect to a biological example, you quote Musgrave:
quote:
It would not be the first time that a secretory system was co-opted into motility, as the cyanobacteria have co-opted a carbohydrate export system to produce gliding motion.
This underscores just how difficult it is to get a bidirectional motor. For example, we don't see any eubacteria with Type III proteins doing it by protein secretion using a gliding mechanism. And we don't see any cyanobacteria with flagella. Furthermore, this is not reducing a system's components and getting a carbohydrate export machine. These critters simply move by using the export machine.
Again, these are not arguments from ignorance. But rather, arguments from scientific data. The assertion that a protein export machine evolved into the bacterial flagellum is contradicted by this data, since we are now converging to the thought that the protein export machine mentioned by Musgrave post-dates the bacterial flagellum. We see that it is IC, in that there is no direct Darwinian pathway to the flagellum since you cannot reduce it to one part. We see that co-option events are unlikely (as Orr stated, like seeing multi-component machines suddenly working with multi-component machines with different functions), and clearly unselectable steps. The argument from ignorance actually comes from asserting that some time in the future we will find a physical precursor and the intermediate steps needed to evolve a flagellum.
Having it or not having the function is not irrelevant. It is quite relevant in that function is dependant in how the components interact and not only in having those components. Any Darwinian evolutionary story must acknowlege the "either you have it or you don't".
With respect to my response to Yersinia, I wrote:
quote:
Yersinia, you misinterpreted my posts here. I am defending Behe's assertion that the VDJ recombinase/antigen receptor is IC. This is correct, you can't have one without the other and still get antibody diversity. The IC nature of the VDJ recombinase/antigen receptor is all or nothing.
To which you ask me to relate this to a particualr definition of IC. As I stated in my previous post, take your pick. All definitions of IC are functionally equivalent in that when you tell a design story or evolutionary story about it, you get the same results. As I will show in your thread shortly, your sequence of tests are irrelevant in this regard.
[ 05. April 2003, 17:11: Message edited by: Nelson_Alonso ]
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yersinia
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Member # 324
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posted 05. April 2003 17:40
Hey Nelson,
quote:
To which you ask me to relate this to a particualr definition of IC. As I stated in my previous post, take your pick. All definitions of IC are functionally equivalent in that when you tell a design story or evolutionary story about it, you get the same results. As I will show in your thread shortly, your sequence of tests are irrelevant in this regard.
...I think you are confusing me with gedanken here. However I would be very impressed to see that you show that all definitions of IC are functionally equivalent.
I still don't see how you can argue that recombining antigen receptors are IC when nonrecombining antigen receptors can still bind antigen at physiologically important levels in organisms. If you define function sufficiently arbitrarily then you can call it IC, but you appear to have no justification for defining function so narrowly.
Regarding flagellum evolution I recommend that you start another thread to discuss that, this one is plenty long already...
Thanks, yersinia
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Nel
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Member # 614
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posted 05. April 2003 18:21
Francis,
You ask:
quote:
Do you see IC as a way to falsify Darwinism or as a way to identify systems which may have had alternative and even perhaps non-Darwinian pathways?
I see it as both (although I am merely a fetus when it comes to Design theory and I am not an IC expert, so buyer beware). Darwinists and Design theorists are both looking at the same data, so, as a competing theory, data that contradicts Darwinian evolution opens the door for an alternative explanation whether it is ID or complexity theory or whatever.
Lateral gene transfer is indeed the complete opposite of a Darwinian pathway, which is why Darwinists were so resistant to accept it at first.
For example, James Shapiro, who was here recently, stated:
quote:
"The conventional explanation, that random changes accumulate one locus at a time, is unconvincing on both functional and probabilistic grounds."
Doolittle had to practically beg Darwinists to stop resisting LGT for obvious reasons:
quote:
Perhaps it would be easier, and in the long run more productive, to abandon the attempt to force the data that Zuckerkandl and Pauling stimulated biologists to collect into the mold provided by Darwin. If there were believable genealogies of all genes (and intragenic recombination could be ignored), one could then ask which genes have traveled together for how long in which genomes, without an obligation to marshal these data in the defense of one or another grander phylogenetic scheme for organisms. One could, as Martin (16, p. 104) has exhorted, set about discovering the "principles which must govern the distribution of genes across bacterial genomes." While retaining useful names for recognized groups (Archaea and Bacteria), one could see these as taxonomic descriptors based directly on shared genes, but only based indirectly and unpredictably on shared ancestry. As an example, one could then easily accept the fact that the cyanobacteria appear to be a very "good" taxon in the sense that many molecules support their monophyly but that they nevertheless might derive major elements of their uniquely defining photosynthetic biochemistry from different bacterial antecedents (42). As another, one might cease being surprised or upset that the obvious extensive sharing of genes between thermophilic prokaryotes makes the placement of any individual thermophile in its "true" position in the tree a highly problematic exercise (43). In other words, biologists might rejoice in and explore, rather than regret or attempt to dismiss, the creative evolutionary role of LGT.
http://cas.bellarmine.edu/tietjen/Ecology/phylogenetic_classification_and_.htm
and as Woese said, with reference to LGT:
quote:
"We cannot expect to explain cellular evolution if we stay locked in the classical Darwinian mode of thinking,"
http://www.news.uiuc.edu/scitips/02/0617evoltion.html
A Darwinian pathway is characterized as step by step, small, selectively advantageous changes, not the transfer of wholesale machines from one organism to another. This is important with respect to aquired immunity. I will get into your discussion of Rag genes in my reply to Yersinia. Whether this happens by bacterial sex is irrelevant. My statement that you quote above illustrates that a design event can be distinguished from a Darwinian evolutionary event by the same means that lateral gene transfer can be distinguished from mutation.
Suffice it to say for now, that lateral gene transfer events, especially when it comes to aquired immunity, are consisted with an IC-to-ID inference, in that we must get all the components "all at once" or we run into red queen type problems, as Behe said, a system that is "not sufficient to make a difference".
[ 05. April 2003, 19:01: Message edited by: Nelson_Alonso ]
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Frances
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posted 05. April 2003 18:40
Nelson
quote:
I see it as both (although I am merely a fetus when it comes to Design theory and I am not an IC expert, so buyer beware). Darwinists and Design theorists are both looking at the same data, so, as a competing theory, data that contradicts Darwinian evolution opens the door for an alternative explanation whether it is ID or complexity theory or whatever.
But my problem with this is that merely showing data that may contradict Darwinian evolution does not help us establish Intelligent Design. In fact unless ID movement proposes a scientific theory of ID, ID seems to be limited to doing what science already does.
Nelson:
quote:
Lateral gene transfer is indeed the complete opposite of a Darwinian pathway, which is why Darwinists were so resistant to accept it at first.
Are you sure that you are correctly representing the resistance to LGT?
You quote Shapiro "The conventional explanation, that random changes accumulate one locus at a time, is unconvincing on both functional and probabilistic grounds." but that neither addresses LGT nor Darwinian pathways.
You then claim again without much supporting evidence that "Doolittle had to practically beg Darwinists to stop resisting LGT for obvious reasons"
In your quote I neither see examples of begging nor do I understand what you consider to be these 'obvious reasons'?
Could you perhaps elaborate?
You then quote "A Darwinian pathway is characterized as step by step, small, selectively advantageous changes, not the transfer of wholesale machines from one organism to another. "
You seem to be unfamiliar with the fact that you are the product of exactly this, the transfer of wholesale machines from both your father AND your mother to you. I hope that you are not suggesting that Darwinism proposes only mutations as source for variation? You may find a useful introduction
to biology and the concept of genetic variation
Genetic variation is increased by such mechanisms as
Mutation:
Recombination: Each chromosome in our sperm or egg cells is a mixture of genes from our mother and our father. Recombination can be thought of as gene shuffling. Most organisms have linear chromosomes and their genes lie at specific location (loci) along them
Gene Flow
Thus your statement quote:
My statement that you quote above illustrates that a design event can be distinguished from a Darwinian evolutionary event by the same means that lateral gene transfer can be distinguished from mutation.
seems to ignorance of or show unfamiliarity with (Neo)-Darwinian theory.
Finally you make a claim which remains fully unsupported by any factual evidence "Suffice it to say for now, that lateral gene transfer events, especially when it comes to aquired immunity, are consisted with an IC-to-ID inference, in that we must get all the components "all at once" or we run into red queen type problems, as Behe said, a system that is "not sufficient to make a difference". "
Btw what would be inconsistent with an IC-to-ID inference? And surely we should not make the mistake to claim without much evidence that there is a red-queen type problem. In fact given that IC systems are NOT reliable indicators of ID I wonder how you made this leap? Btw how do you conclude from the observation that lateral gene transfer occurs naturally that ID is somehow involved?
More from Doolittle to show his perspectives on LGT
quote:
Lateral (also known as horizontal) gene transfer (LGT) is gene exchange across species boundaries, and is a hot topic in some circles. Microbial genomicists and phylogeneticists in particular become more excited about it with each new prokaryotic genome sequence that reaches completion. No one had anticipated that prokaryotic genomes would be so extensively mosaic, so obviously pieced together by the assembly of genes from so many different antecedents, in some never-ending game of molecular Lego.
The genomicists are generally happy about LGT. The acquisition of foreign genes and gene clusters can explain some of the striking differences in the properties of bacterial species (or strains within species) that by other criteria are almost identical. Large (>20%) differences in genetic make-up between pathogenic and benign strains of the same species (Escherichia coli O157:H7 and K12, for instance) can best be understood with models that invoke evolutionarily rapid gene acquisition (by LGT) and loss. But phylogeneticists are less pleased. They want to use gene sequences to reconstruct evolutionary trees for species on the assumption of 'vertical' gene transmission between generations, but if genes can switch species, these trees become webs — much messier. So when LGT has been inferred from comparative data only, they often somewhat petulantly ask: "What's the mechanism?"
[ 05. April 2003, 18:46: Message edited by: Frances ]
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Nel
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posted 05. April 2003 18:54
Nic,
Ged was quoting one of my replies to you. I did not confuse you with Ged.
Let me briefly respond to your post with regard to IC and antigen receptors here, but I will fully reply to your longer post in this thread which I did not yet get to.
With respect to showing IC definitions are functionally equivalent, I have done this several times already in the Sequence of Tests thread, Evolving Inventions thread, and over at the List of IC systems Thread where I compared the precise language of Dembski's definition with Behe's original definition. For example, you can see Behe talk about an IC core with respect to the blood clotting cascade. He didn't mention any of the other factors, but only a few. I really don't see a difference between any of the definitions.
You are once again completely off the mark with respect to my argument in this thread. I did not claim that antibodies are IC. And to be quite blunt, saying that antibodies are not IC because generic receptors can bind to foreign substances makes no sense to me. Something is IC if you remove several components and the thing doesn't work anymore. I guess it would be a good idea to re-state my argument since , a cursory reading of replies to my posts thus far, shows similar errors.
Behe stated that antibodies that bind to a particular epitope would be useless , or in his words, "not sufficient to make a difference". Inlay attempted to counter this argument by saying that innate receptors with single specificities are basically antibodies. Thus Behe is wrong, claims Inlay, we see organisms with few antibodies getting by just fine. But Inlay is wrong, the receptors he mentioned are generic binders. Behe's point still stands. I think this is a simple point to understand. Inlay's argument here critically depends on these receptors having single specificities, thats why he stated it this way. Otherwise the analogy to antibodies is quite irrelevant to Behe's point about IC and this system. With respect to this system, it is IC. And even the literature shows this.
And the literature shows that the data is consistent with IC, as Dr. Peonie wrote:
quote:
The similarity of RAG1 to bacterial transposases, the absence of introns in the RAG genes and their abrupt appearance in sharks has led to the suggestion that these jumped into the genome as a lateral gene transfer event. If so this is a remarkable story – that two different genes jumped into the germs cells of an agnathan, integrate into an Ig molecule and then generate the diversity of antibody and TcR molecules. At essentially the same time we get the MHC genes (see below) and probably the jaw and thymus to boot.
This is what is referred to as the "Big Bang" of aquired immunity:
quote:
In jawed fish and all "higher" vertebrates, adaptive immunity is possible because of what I like to think of as the immunological "Big Bang," which occurred in some ancestor of the jawed fish.
Janeway: Immunobiology, 2001
Your post is a critic's smorgasbord. You make many false statements in your post that I will reply to shortly but here's a taste. You say:
quote:
Behe argued that non-rearranging receptors would be useless, creating a problem for the published evolutionary scenario.
Behe stated nothing of the sort. Behe stated that antibodies (which have distinct specificities) are useless to an organism or "not sufficient to make a difference". Where does Behe say that innate receptors are useless? He never did.
P.S. I mean no offense, but, at least when you reply to me, do you really have to quote over 80% of the article you are referencing? I'd rather you discuss the article and quote the relevant passages that support your summary.
[ 05. April 2003, 19:05: Message edited by: Nelson_Alonso ]
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gedanken
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Member # 594
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posted 05. April 2003 19:16
Alonso said:
quote:
In the case of the bacterial flagellum, you don't have a motile system, there are cases where bacteria cannot survive unless they do brave the brownian storm with a molecular machine like the bacterial flagellum. There are cases where it might not need one. But of course, the question is: what is the origin of the bacterial flagellum? Whether one can survive without one or not is irrelevant to this question. The question is , can Darwinian evolution do it. I think it is unlikely that this natural process can without intelligent intervention. is really not a gradualistic pathway, it rather invokes 10+ co-option events all due to chance as natural selection was pruning the system for the function that already exist. Another example is that the system in question, the type III secretory system they point to, post-dates the bacterial flagellum.
I would like to consider a scenario (hypothesized) in which life actually develops according to evolutionary theory of descent with modification. And in this hypothesized case, the flagellum actually develops with gradualistic pathways. This may not exactly be a “scientific” scenario, because science may not assume what it wants to demonstrate. But for my purposes, I want to assume this (and indeed recognize that the results may be somewhat “circular” as Jonathan Wells would claim).
Now let’s also hypothesize that the available observable evidence from fossil or other historic remains is very sketchy. So there could be many intermediates, according to this scenario, which are not available for our observation.
Now in this hypothesis, we start with an organism that has a secretory system with some but not all of the components of the flagellum. (And the components may not function exactly as they do in the flagellum, just approximately.) Then descendents occur with “descent with modification” operations wherein they are slightly different.
(Now remember that I am not a biologist, so this must necessarily be a very sketchy description, and that real biologists may wish to differ with my approach. I am just presenting this so you can see my reasoning process from my view quite distant from a knowledgeable biologist, and is based more on the generic steps approach of what sort of steps could possibly result in what we see.)
We now ask the question, what might we see in the current day with this scenario. Remember that we have hypothesized that information is very sketchy and much of the fossil or other historical evidence may be missing, so the absence of visible present-day evidence is not surprising in our scenario.
Now I want to emphasize that this scenario presentation may not be “scientific” because we have not made any sort of declaration of any aspect that could be distinguished by observation of nature. So this is not empirical in the sense of true science -- and indeed has circularly assumed the result to be described.
The point is that I don’t see any of the difficulties for a physical system in this scenario.
For example, suppose the primitive ancestor did not have “motility” as generated by the flagellum. Then indeed, it may have limited environments in which it could survive. Indeed “there are cases where bacteria cannot survive unless they do brave the Brownian storm with a molecular machine like the bacterial flagellum. There are cases where it might not need one.” In my hypothesized case is one “where it might not need one.” The environment, limited though it may be, somehow provides the necessary support for the life of the limited organism.
(We might test for the possibility of such organisms existing by asking real biologists to describe any observed organisms, possibly similar to the organisms that have a secretory system which was posited as a possible ancestor, and ask if these organisms that were posited as possible ancestors actually lived in some environment. Was there some environment in which the organism that was posited by biologists as a potential precursor to the one with a flagellum one which actually lived in some environment? With a positive answer, then we know that such organisms would apparently not require the advantages of motility conferred by the flagellum. Please note that I am not assuming that the post-dated “type III” secretory system organism is the one that is assumed to predate and lead to the organism with the flagellum, rather that some ancestor with some sort of secretory system like that one is hypothesized. In our asking whether the ancestor could have actually lived in some environment, it might be interesting to ask if an organism with a “type III” secretory system can live in some environment, with whatever particular adaptations for “motility” that organism has -- and in fact also ask what requirements for “motility” have been observed in that case.)
Now in the sequence I am hypothesizing, I don’t quite see where there is difficulty in having a sequence of 10+ co-option events. If one can have one co-option event, and then another co-option event, and we observe co-option events happening in present day small changes in bacteria, why is there a difficulty in having 10+ co-option events? Of course that the particular set of co-option events would happen if we “replayed the tape” would have to multiply out the probabilities of such events happening in exactly that way -- if it were even possible to calculate such probabilities. But we must recognize that we might have had a different set of 10+ co-option events if we replayed the tape, it is not particularly relevant to me if the aggregate probability of all 10+ together is small, the question I would be interested in is whether there are likely such co-option events leading to some sort of changes. The particular changes, that lead to the flagellum are just ones that happened in this particular “playing of the tape” of evolution. Other passes through the same period starting with the same initial conditions might have produced different outcomes -- but this is not particularly relevant to me as we observe this particular outcome at present.
Now as I have said, my “scenario” is not presented in a scientific manner, since we have made no distinctions that could be made by direct observation to try to differentiate that scenario from others. But the reason for considering it is to consider the “explanatory filter”. Remember that to be meaningful to the “explanatory filter” we must “sweep the field clean” of possible physical explanations. It is not sufficient to simply lack knowledge of which particular physical explanation could have been the actual origin of the bacterial flagellum. For the EF to be applicable, the field must be “swept clean” and the existence of a plausible scenario clearly demonstrates that has not occurred.
I think it is worth re-emphasizing the issue of the 10+ co-option events. I have made no assumption that any of those would be “unselected” co-option events. I have not seen any explanation that denies that co-option events needed are “unselected”, as they may individually provide some slight benefit in some environment. That a particular sequence occurs may be unlikely, just as a particular set of 10 die tosses in a row may be unlikely. We all know that is irrelevant. What is relevant is whether there are possible scenarios for each of the 10 die tosses, or for each of the 10+ co-option events. The descriptions I read from biologists lead me to believe that individual co-option events are reasonably expected. And that there were reasonable precursors to the organism with the flagellum. The field has not been “swept clean”.
The issue of “degree” is very important. A small change could increase motility. I’ve seen descriptions of how limited motility could be achieved with aspects of the “sceretory” system in place, without the entire flagellum operating. This could provide a “selected” step for a slight change in a direction toward the flagellum.
I hope that Alonso and other readers will understand why I find statements like “I think it is unlikely that this natural process can without intelligent intervention” to be unsupported. The lack of knowledge of specifics of the flagellum development do not imply such difficulty. No reasonable case has been made why there are not selectable steps that could result in the flagellum.
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Nel
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posted 05. April 2003 19:33
Francis,
With respect to ID, this is going a little off-topic but, evidence that contradicts Darwinian evolution can also support intelligent design. There is absolutely no reason why it couldn't. Because what contradicts Darwinian evolution is exactly what is inaccessable to it's mechanism, but showing that the biological feature is accessable to an intelligence with foresight supports intelligent design.
Darwinian theory has similar arguments. For example, Darwin himself, and many other Darwinists after him, used sub-optimal design not only to argue against Paley's watchmaker, but also to support natural selection & random mutation.
I am extremely sure that I am correctly representing LGT. Shapiro's quote here is referring to how the Darwinian way of evolving organisms, step by selectable step, from simple to complex, is the complete opposite of LGT. For example, since this way of evolving is unlikely, says Shapiro, we have to start looking to things like, as the article in biomed that I am quoting from (registration required)goes on to say:
quote:
"The very biochemical tools that we now use in laboratories are evolved to modulate local nucleotide variation, to rearrange genomic DNA sequences, and to acquire functional DNA sequences from the environment through horizontal
gene transfer. Shapiro pointed out that we are not the first genetic engineers."
With respect to my quote of Doolittle I gave much supporting evidence in the form of a full quote by Doolittle, here is what I am referring to:
quote:
Perhaps it would be easier, and in the long run more productive, to abandon the attempt to force the data that Zuckerkandl and Pauling stimulated biologists to collect into the mold provided by Darwin.
quote:
In other words, biologists might rejoice in and explore, rather than regret or attempt to dismiss, the creative evolutionary role of LGT.
etc.
I wrote:
quote:
A Darwinian pathway is characterized as step by step, small, selectively advantageous changes, not the transfer of wholesale machines from one organism to another.
The transfer of wholesale machines from parent to child is not horizontal gene transfer. This has nothing to do with variation, we are talking about the origin of systems, that travel wholesale rather than evolve step by selectable steps, such as photosynthesis and aquired immunity.
The factual evidence for my statement:
quote:
"Suffice it to say for now, that lateral gene transfer events, especially when it comes to aquired immunity, are consisted with an IC-to-ID inference, in that we must get all the components "all at once" or we run into red queen type problems, as Behe said, a system that is "not sufficient to make a difference". "
is supported by my reference to the literature:
quote:
In jawed fish and all "higher" vertebrates, adaptive immunity is possible because of what I like to think of as the immunological "Big Bang," which occurred in some ancestor of the jawed fish.
Janeway: Immunobiology, 2001
There is a red queen type problem in that I discussed in previous posts. Please respond to that argument specifically (pun intedended). IC systems are indeed reliable indicators of ID, but I don't understand why you brought this point in so abruptly. With respect to lateral gene transfer, the origin of those genes that travel wholesale and then get assembles by rearrangement is more like complex computer software, which still leaves open the origin of those genes. ID nicely predicts this, Darwinism does not. The abrupt appearance of these machines by LGT points to a mechanism used by the intelligent designer.
You quote Doolittle for what seems to me no reason whatsoever.
Unfortunately, thats all the time I have for tonight, but I'll be back tomorrow for the rest of the replies. I promise no long absence for a while, if you replied to me, I'll get to you.(not that anyone cares ![[Wink]](wink.gif) )
[ 05. April 2003, 19:41: Message edited by: Nelson_Alonso ]
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gedanken
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posted 05. April 2003 19:47
Alonso said specifically in message to me (and having involved a discussion with Yersinia in the past):
quote:
quote:
Yersinia, you misinterpreted my posts here. I am defending Behe's assertion that the VDJ recombinase/antigen receptor is IC. This is correct, you can't have one without the other and still get antibody diversity. The IC nature of the VDJ recombinase/antigen receptor is all or nothing.
To which you ask me to relate this to a particualr definition of IC. As I stated in my previous post, take your pick. All definitions of IC are functionally equivalent in that when you tell a design story or evolutionary story about it, you get the same results. As I will show in your thread shortly, your sequence of tests are irrelevant in this regard.
The reason I ask is that I don’t believe that a particular definition of IC has been demonstrated. The definitions may or may not be relevant in the sense that “a design story” might “get the same results”. To me that is irrelevant, since the issue for me in the “sequence of tests” thread is whether there is a difficulty for evolution -- not whether “design” (especially an unembodied designer) could create the occurrence. To check for a “difficulty for evolution” we first must examine the concepts of IC themselves. If you cannot relate the particular case in question to a particular definition of IC, how can you claim that a case is “IC”? You might claim that you can’t understand how the organism could have evolved -- and to that I suggest leaving that task to those who can imagine such pathways and then checking if they are plausible and if there is any empirical evidence to support them.
Give the specific assertion, “I am defending Behe's assertion that the VDJ recombinase/antigen receptor is IC”-- give us the labeled and named definition for IC and its specific named test. (The tests for IC in the “sequence of tests” thread all have numbered names so one can identify it very specifically so there is no confusion with other tests or definitions that may have been used at some other time or place.) Take us through the specific steps of the given test -- show that it meets the definition of “IC”! (Then if you want to show further implications, do that too, but first show the meeting of the test.
But I in fact don’t believe that any particular definition has been met, certainly not any definition that has been vetted in the “sequence of tests” thread. I believe that because simple questions of what definitions mean to those who study IC haven’t been answered. Definitions so far simply allow for all sorts of co-option events to occur while fitting under the specifics of tests given for the definitions. If you believe this is wrong, then supply specific tests, demonstrate how they actually test for the wording of a given definitions, and then specify in detail which test is being used here. Then we can examine it in detail to see if the logic is sound.
That thread is not about specifics like flagella, nor is it about “design”. Rather it is about logical aspects of definitions -- what are the definitions, how can they be clarified, and how can they be tested for in general terms (not a place to argue specific cases).
[ 05. April 2003, 20:00: Message edited by: gedanken ]
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Nel
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posted 05. April 2003 19:47
Let me make some insights here into Ged's latest reply.
He writes:
quote:
I hope that Alonso and other readers will understand why I find statements like “I think it is unlikely that this natural process can without intelligent intervention” to be unsupported. The lack of knowledge of specifics of the flagellum development do not imply such difficulty. No reasonable case has been made why there are not selectable steps that could result in the flagellum.
What this paragraph seems to be saying is that the default position of the Darwinist is true no matter what the evidence says. For example, Ged accepts Darwinian evolution as true a priori . So although Ged doesn't know how the flagellum could have evolved, or doesn't have any explanation for why there are unselectable steps from the C ring to FliE (for example), he accepts Darwinism as true. To that I must question what exactly his point for being in an ID brainstorms message board when the data that supports IC and thus ID (the fact that there are unselectable steps,the Type III system post-dating the flaglelum for starters) is ignored and Ged is forced to appeal to "future explanations". I would recommend ARN for this type of Darwinan apologetics. For example, I saw absolutely no response to the amount of unselectable steps I pointed out in my response to Ged. Again, more later.
One more question before I go regarding demonstrating IC,
Ged, can you show me the function of the flagellum (motility) reduced to a single component?
[ 05. April 2003, 19:57: Message edited by: Nelson_Alonso ]
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