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Author Topic:   How do we know its irreducible?
Primordial Egg
Inactive Member


Message 1 of 15 (24570)
11-27-2002 8:35 AM


This is following on from a previous thread in which myself an Ahmad are discussing Behe's notion of irreducible complexity.

My attempted "impartial" summary of the discussion goes like:

I try to assert that to demonstrate IC, and hence falsify evolution, one must show that it is impossible for apparent IC systems to have come about through evolutionary processes.
Ahmad maintains that the burden of proof is on science to demonstrate how IC systems came about through gradual processes. He's also given me a few examples of what he considers to be IC systems (bombardier beetles, cillia) as well as briefly mentioning a few others. (Ahmad - hope this is fair )

Ahmad,

Lets backtrack to my original post to you:

I said:

quote:
Consider the following statements:

1) it is demonstrably impossible for X to produce Y
2) I cannot see how X could produce Y
3) it is conceivable that X has produced Y, but the process has not been determined yet.
4) X has been conclusively shown to produce Y

Now I would paraphrase your position as being (2), wheras your standard biologist would argue (3) (or (4)!) when it comes to irreducibly complex systems.

To overturn a pardigm, you generally have to do more than insist upon (2), you have to show that (1) must be the case.


To which you responded:

quote:
Secondly, (1) is exactly the case here. According to ToE, systems have evolved from simple to complex by natural selection and random mutations gradually but sometimes in irregular leaps (punctuated equilibria). If that is the case with a system, it is not irreducibly complex; in fact, it CANNOT be irreducibly complex since it evolved according to Behe's defintion. An IC system needs all its parts to effectively function such as if, even, one of the parts is missing, the system will cease to function. Therefore, an IC system, by definition, is unevolvable... unless proven otherwise. Surely, if a system is IC, it must have had ALL its parts from the very beginning of its existence (aka creation).

Firstly, lets just simplify definitions just for the purpose of this argument, to avoid confusion. I know it doesn't quite meet with Behe's definition, but lets just say that an IC system is one that cannot have come about through gradual change, which I think is the same as what you were getting at above. The challenge for us is to then to determine whether or not IC systems exist.

To do this, you have to show that it is impossible for the system to have arisen through gradual change. If I cannot provide an evolutionary pathway, then we have only succeeded in showing at most (2)I cannot see how X could produce Y, which is no falsification of evolution. Would you agree?

Now, there are many possible routes to get from X to Y, via Z for example. Any claims of impossibility must also take different routes into account, as long as the time periods involved are not too great.

If we then look closer at your cillia example, I'm looking here for the point at which you declare that for it to be brought about by gradual change is impossible.

quote:
For without one of these components, the system simply will not function. We can't evolve a cilium by starting with microtubules alone, because the microtubules will be fixed and rigid-not much good for moving around. Adding the flexible linker bridges to the system will not do any good either-there is still no motor and the cilia still will not bend. If we have microtubules and the walker arms (the motors) but no flexible linker arms, the microtubules will keep on sliding past each other till they float away from each other and are lost.

The first thing I note about this is that you are (implicitly) claiming that each separate component does not have a function in its own right. If you are claiming this, this is a pretty bold claim. If not then I don't see how you can claim IC.

It doesn't seem to me that you've considered all potential pathways here. Its pretty obvious that you haven't. Could the organism have evolved features which became redundant and then evolved into apparent IC? You don't discuss this. Until you do, its still an argument from incredulity I'm afraid.

quote:
All consist of a very complex system of interacting parts which cannot be simplified while maintaining functionality

Does Behe give a mousetrap as an example of an IC system as well?

quote:
Evolution simply cannot produce complex structures in a single generation as would be required for the formation of irreducibly complex systems

You haven't demonstrated this. You simply believe it.

quote:
To imagine that a chance set of mutations would produce all 200 proteins required for cilia function in a single generation stretches the imagination beyond the breaking point

Agreed. If this is what you believe the naturalistic explanation of the cilia's evolution to be then no wonder you are incredulous.

quote:
And yet, producing one or a few of these proteins at a time, in standard Darwinian fashion, would convey no survival advantage because those few proteins would have no function

Its that word "function" again. By function, do you mean "selective advantage"? How do YOU know what confers selective advantage?

To help you out, this paper discusses the potential routes Darwinian evolution can take. I'll list them out here:


  • Serial direct Darwinian evolution
  • Parallel direct Darwinian evolution
  • Elimination of functional redundancy
  • Adoption from a different function (joining of two or more non-irreducibly complex structures of functionally indivisible components or supply of an existing irreducibly complex structure of functionally indivisible components

You have to show how any structure you claim (note: positive claim) to be IC cannot have arisen through any of the means above. Thats why I can't see how you'd do it.

PE

PS This wasn't going to be in the thrust of my argument so grateful if you'd treat as an aside (maybe respond separately):

About Isaak on bombardier beetles:

quote:
He fails to mention the step-by-step evolution of the inhibitor and anti-inhibitor that the beetle possesses without which it will blow itself up to an oblivion!!

Which inhibitors / anti-inhibitors? Why do you think that without these the beetle would blow itself up?

------------------
It's good to have an open mind, but not so open that your brains
fall out. - Bertrand Russell


Replies to this message:
 Message 4 by Ahmad, posted 11-29-2002 1:23 PM Primordial Egg has not yet responded

  
Nic Tamzek
Inactive Member


Message 2 of 15 (24884)
11-28-2002 11:35 PM


Regarding the origin of eukaryotic cilia/flagella, as well as bacterial flagella and archaeal flagella, you may find this page helpful:

http://www.wikipedia.org/wiki/Evolution_of_flagella

I wrote it up at Wikipedia kinda to try it out and to get the info out there, but it really should be turned into a t.o. FAQ.

Ian Musgrave has also updated his page:
http://www.health.adelaide.edu.au/Pharm/Musgrave/essays/flagella.htm
(note that this is a new link also)

The Thornhill and Ussery article is available in web form here:
http://www.cbs.dtu.dk/staff/dave/JTB.html

nic


Replies to this message:
 Message 3 by Primordial Egg, posted 11-29-2002 5:47 AM Nic Tamzek has not yet responded

  
Primordial Egg
Inactive Member


Message 3 of 15 (24900)
11-29-2002 5:47 AM
Reply to: Message 2 by Nic Tamzek
11-28-2002 11:35 PM


Nic,

Thanks for the links. Might need a translation tho'

PE

------------------
It's good to have an open mind, but not so open that your brains
fall out. - Bertrand Russell


This message is a reply to:
 Message 2 by Nic Tamzek, posted 11-28-2002 11:35 PM Nic Tamzek has not yet responded

  
Ahmad
Inactive Member


Message 4 of 15 (24944)
11-29-2002 1:23 PM
Reply to: Message 1 by Primordial Egg
11-27-2002 8:35 AM


quote:
Firstly, lets just simplify definitions just for the purpose of this argument, to avoid confusion. I know it doesn't quite meet with Behe's definition, but lets just say that an IC system is one that cannot have come about through gradual change, which I think is the same as what you were getting at above. The challenge for us is to then to determine whether or not IC systems exist.

Right.

quote:
To do this, you have to show that it is impossible for the system to have arisen through gradual change. If I cannot provide an evolutionary pathway, then we have only succeeded in showing at most (2)I cannot see how X could produce Y, which is no falsification of evolution. Would you agree?

Agreed.

quote:
Now, there are many possible routes to get from X to Y, via Z for example. Any claims of impossibility must also take different routes into account, as long as the time periods involved are not too great.

Now keep in mind that the system is irreducibly complex (IC) and I don't think I need to remind you its definition. Therefore, say Y is IC and you want to show that it evolved from X. You, not only have to outline the evolutionary pathway (i.e Z), but also outline the function of the system when it was X and provide evidence that via Z it became Y. Your explanation must be consistent with the ToE. On my part, I will then use your explanation to outline the fallacies (if there are any) and demonstrate how the proposed evolutionary pathway is invalid for X to become Y and why evolution of Y is impossible.

quote:
The first thing I note about this is that you are (implicitly) claiming that each separate component does not have a function in its own right. If you are claiming this, this is a pretty bold claim. If not then I don't see how you can claim IC.

I see you misunderstand the very definition of IC. In such a system each component separately has no value unless all the components work together. Coordination is the keyword here. All parts of the system must maintain coordination and work as a whole to keep the system functional. Looking it other way, if, even, one of the components cease to function, the entire system breaks down. In this case, each component is highly valuable. No, I am not contradicting myself... but this is what an IC system really is.

quote:
It doesn't seem to me that you've considered all potential pathways here. Its pretty obvious that you haven't. Could the organism have evolved features which became redundant and then evolved into apparent IC? You don't discuss this. Until you do, its still an argument from incredulity I'm afraid.

Ok then, you give me the possible, potentional pathways and the redundant features, and I'll tell you why its impossible. Ofcourse, this does not dismiss the possibility of the existence of evolutionary pathways,i.e, if you can show one. Lets take my aforementioned example of the cilia here. Give me the possible potential evolutionary pathway by which the cilia evolved and I'll respond. Fair enough?

quote:
Does Behe give a mousetrap as an example of an IC system as well?

Yes he does. Why do you ask? I can use that as an example of a non-biological irreducibly complex system... if you want me to.

quote:
Ahmad: Evolution simply cannot produce complex structures in a single generation as would be required for the formation of irreducibly complex systems

PE: You haven't demonstrated this. You simply believe it.


Alright, you tell me how evolution explains the emergence of IC systems. As far as I know, the difficulty for Darwinian theory is that 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. Behe even demonstrated this by many biological and non-biological examples. A mouse-trap for instance. It has five parts that are absolutely necessary for the mousetrap to function. Take any one of these parts away and the mousetrap can no longer catch mice. You can't build a mousetrap by Darwinian natural selection. Let's say you have a factory that produces all five parts of a mousetrap but uses them for different purposes. Over the years as the production lines change, leftover parts of no-longer-made contraptions are put aside on shelves in a storage room. One summer, the factory is overrun with mice. If someone were to put his mind to it, he might run by the storage room and begin to play around with these leftover parts and just might construct a mousetrap. But those pieces, left to themselves, are never going to spontaneously self-assemble into a mousetrap. A hammer-like part may accidentally fall from its box into a box of springs, but it's useless until all five parts are assembled so they can function together. Nature would select against the continued production of the miscellaneous parts if they are not producing an immediate benefit to the organism.

Michael Behe simply claims that we have learned that several of the molecular machines in the cell are just as irreducibly complex as a mousetrap and, therefore, just as unable to be constructed by natural selection.

quote:
Agreed. If this is what you believe the naturalistic explanation of the cilia's evolution to be then no wonder you are incredulous.

Ok... you tell me the naturalistic explanation of the cilia. Enlighten me.

quote:
Its that word "function" again. By function, do you mean "selective advantage"? How do YOU know what confers selective advantage?

By function I mean, coordination of various components simultaneously for the effective functionality of a system. How do you determine "selective advantage"? Natural or Conscious?

quote:
To help you out, this paper discusses the potential routes Darwinian evolution can take. I'll list them out here:

I did discuss this with mark. Nonetheless, I will use Mike Gene's response for this paper.

quote:
Serial direct Darwinian evolution

To begin with, this pathway according to the authors, can generate complicated structures, but not irreducibly complex structures. So we can see that IC helps to rule out certain evolutionary pathways. This is also very significant in that the most persuasive examples of random mutation and natural selection (RM&NS) entail serial direct Darwinian evolution. The traditional examples of Darwin's finches (and their beaks), giraffe necks, elephant trunks, darkening wings in moths are all examples of serial direct Darwinian evolution. Thus, this means that evidence for this type of evolution is not evidence that IC can/did evolve via the blind watchmaker mechanism (BWM).

quote:
Parallel direct Darwinian evolution

"This means approximately synchronous changes in more than one component, so that modification to other components always occurs before the total modification to any one component has become significant." But they also say, [b][i]"Parallel direct Darwinian evolution can generate irreducibly complex structures, but not irreducibly complex structures of functionally indivisible components, and this is the valid conclusion to draw from Behe's thesis.[/b][/i]

Thus, once again, we can see that when we are dealing with IC molecular machines (which are composed of functionally indivisible parts), the various examples of Darwinian evolution cited by Dawkins et al.(and used by the authors) are irrelevant. None of it amounts to evidence that Behe's IC examples evolved by the BWM.

quote:
Elimination of functional redundancy

Now this pathway is quite interesting. ToE states systems evolved from simple >> complex. Yet this pathway assumes the opposite. Thus, if simple beginnings are needed to "come into existence by chance," the complicated beginning, assumed by this pathway, may be too complicated to "come into existence by chance." In other words, this pathway does not eliminate the design inference behind IC, but instead, suggests that IC is an indirect indicator of an originally designed state.

Nevertheless, what we need is evidence that the initial state was more complicated than the IC state. For example, are we talking about flagellum that were originally composed of 60 parts? Where is the evidence for such a claim? It is an interesting thought, but without evidence, we can't take it beyond the realm of philosophy.

quote:
Adoption from a different function (joining of two or more non-irreducibly complex structures of functionally indivisible components or supply of an existing irreducibly complex structure of functionally indivisible components

They begin with an example:

"For example, scale-feather intermediates would offer no aerodynamic advantage, but one can hypothesise a sequence from scales to primitive but airworthy feathers in which each step offers an increased advantage as insulation. Their use for proto-flight motility would therefore only begin after this sequence. Recently discovered fossil evidence suggests that feather evolution did indeed follow such a sequence, with proto-feathers, composed of the same proteins as feathers, in Sinosauropteryx (Chen et al., 1998; Padian, 1999), probably marginally airworthy feathers in the non-flying Caudipteryx and Protarchaeopteryx (Ji et al., 1998), and feathers in the flying Archaeopteryx (Padian, 1998). The proto-feathers and feathers probably also possessed functions in display, camouflage, recognition, etc., and it is possible that the actual sequence was more complicated than the above hypothetical one, with evolution at some stages being driven primarily by selection for such functions (Padian & Chiappe, 1998). However, the proto-feathers in Sinosauropteryx were so thickly distributed that they almost certainly did function as insulation (Padian, 1999)."

Now this example is faulty for a number of reasons:

1. The so-called feathers in Sinosauropteryx were nothing but "frayed collagenous fibers beneath the skin." (Anne Gibbons. 1997. Plucking the feathered dinosaur)

2. There is absolutely no evidence that Caudipteryx and Protarchaeopteryx are "scale-feather" intermediates.

3. Protofeathers are nothing but "theoretical construct". (Olson 1999)

4. This is not a clear example of generating IC and this whole topic ignores Behe's points on pp. 40-41. The fact that various proteins can share domains doesn't really support adoption from a different function, as there is no reason to think a designer would ensure that each and every part of a system is truly unique. For example, that both a lawnmower and automobile have spark plugs is not evidence that one motor was co-opted to form another by random changes and selection.

The only clear examples, in in my opinion (according to Gene), of adoption from a different function are as follows:

1. Antifreeze glycoprotein in the blood of Antarctic notothenioid fishes, which enables them to survive in icy seas, is considered to have evolved from a functionally unrelated pancreatic trypsinogen-like protease, and the recent discovery of chimeric genes which encode both the protease and an antifreeze glycoprotein polyprotein strongly supports this theory (Cheng & Chen, 1999).

2. Crystallins (proteins with refractive functions in the eye lens) are closely related or identical to stress-protective proteins in non-ocular tissues (eg. Drosophila a-crystallins and small heat-shock proteins are homologous).

But note that in both cases, these proteins don't function as well-matched components in an IC system. Thus, while sometimes a protein might adopt a different function since it is not constrained to interact with multiple partners, an IC component is unlikely to arise in this fashion because it is constrained to interact with multiple partners.

Since the adoption from a different function explanation relies heavily on pure chance, it is unlikely to be a general solution to IC. In fact, as Behe notes, the more complex the system, the less likely that this pathway is what generated IC (since it relies more heavily on converging independent, random events).

Gene provides other counter-examples where adoption from a different function is not possible. For example, imagine a mutation occurred in a bacterium that disabled dnaJ. IC predicts this would be lethal and selection would prevent this organism from altering the gene pool. But if adoption from a different function is common, the mutation need not be lethal and a new chaperone machine would evolve around the protein substituting for the lost component. Why, then, do we not see this occuring?

When we look to eubacteria, the three chaperone components are universal. They are found in gm+ and gm- bacteria, thermophiles (Thermotoga and Aquifex), spirochetes, Deinococcus, Campylobacter, cyanobacteria, Neisseria, and even Mycoplasma. Again, this is most likely due to the fact that this chaperone machine is IC (IC predicts functional constraint) and other proteins cannot substitute through adoption from a different function. This is where this pathway collapses.

If adoption from a different function was a common IC generator, why do we not see permutations in Archaea, where a laterally transferred dnaK gene would find helpers in the archaeal cytoplasm and evolve a new chaperone machine? And all of this is significant because the chaperone machine is a very simple example of IC having only three parts.

In summary, the adoption from a different function explanation is unlikely to be a general solution to IC as it relies too heavily on pure chance as an explanation for apparent design. We thus need independent evidence that this explanation validly applies in any system in question, especially in light of the fact that examples of this pathway do not lend themselves easily to explaining the origin of IC. Furthermore, if we don't see evidence of permutations that run through out the entire IC system, there is good reason to dismiss this explanation.

quote:
You have to show how any structure you claim (note: positive claim) to be IC cannot have arisen through any of the means above. Thats why I can't see how you'd do it.

Thats easy. I outlined some of the fallacies of the mechanism of the proposed pathways. Now to explain why an IC system could not have arisen from any of the four evolutionary pathways as outlined above. I'll take the bacterial flagella as my example here. Lets list out the four pathways first:

1. Serial direct Darwinian evolution.
2. Parallel direct Darwinian evolution
3. Elimination of functional redundancy
4. Adoption from a different function

Since the flagella is irreducibly complex and functionally indivisible molecular machine, we can predict that it couldn't have evolved by pathways (1) and (2), the reasons of which I already outlined with quotes from the authors. Now (3) which predicts that the flagella evolved from something more complex than flagella in the present stage. This pathway is as interesting to Mike as it is to me. Now say the flagella was originally composed of 60 parts just to produce the motion of cilia instead of the 30 parts. Where is the evidence? We are claiming that the flagella is irreducibly complex and functionally indivisible; so if the evolutionists apply (3), they do need to show the evidence. In other words, for (3) the burden of proof lies on the evolutionists... not us. Therefore, number (3) pathway cannot be applied to the evolutionary pathway for the IC of flagella. Now evolutionary pathway (4) which relies heavily on chance. A functioning flagellum requires about 30 gene products (components). So what does (4) pathway predict? That prior to the existence of the flagellum, these 30 gene products (or their duplicates) all existed doing something else. Then, they just happened to all fit together by chance to create a flagellum. And afterwards, the other 30 or so hypothetical functions of these original gene products disappeared. For it is chance that determines whether the 30-or-so gene products just happen to come together to form a functioning flagellum, as selection was pruning these gene products in accord with 30-or-so different functions. Thus, the (4) evolutionary pathway is really a return to using chance as an explanation for apparent design, and just as it was not convincing in pre-Darwinian days, it is not convincing today. Thus, pathway (4) blown off. There is no absolutely no evidence that pathway (4) could have resulted in the emergence of flagella and it is highly very unlikely.

quote:
Which inhibitors / anti-inhibitors? Why do you think that without these the beetle would blow itself up?

I will reply to this later. Insha Allah (if God willing), day after tomorrow

Regards,
Ahmad


This message is a reply to:
 Message 1 by Primordial Egg, posted 11-27-2002 8:35 AM Primordial Egg has not yet responded

Replies to this message:
 Message 5 by mark24, posted 11-29-2002 2:21 PM Ahmad has not yet responded

  
mark24
Member (Idle past 3242 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 5 of 15 (24951)
11-29-2002 2:21 PM
Reply to: Message 4 by Ahmad
11-29-2002 1:23 PM


Ahmad,

www.evcforum.net/cgi-bin/dm.cgi?action=page&f=5&t=141&p=3 -->www.evcforum.net/cgi-bin/dm.cgi?action=page&f=5&t=141&p=3">http://www.evcforum.net/cgi-bin/dm.cgi?action=page&f=5&t=141&p=3

On a similar subject.....

Thanks,

Mark

------------------
Occam's razor is not for shaving with.


This message is a reply to:
 Message 4 by Ahmad, posted 11-29-2002 1:23 PM Ahmad has not yet responded

    
Nic Tamzek
Inactive Member


Message 6 of 15 (24963)
11-29-2002 3:42 PM


Hi Ahmad,

What if I told you that Mike Gene:

1) Has admitted that IC is, at least in some cases, readily accessible to Darwinian evolution -- e.g., the case of the PCP degradation pathway?

2) And that he similarly accepts, or at least doesn't dispute, the evolution of some very complex and (according to Behe) IC systems, like blood-clotting and the immune system?

Kinda takes the wind out of the IC argument, doesn't it?

nic


Replies to this message:
 Message 8 by Ahmad, posted 11-30-2002 8:55 AM Nic Tamzek has responded

  
Nic Tamzek
Inactive Member


Message 7 of 15 (24964)
11-29-2002 3:45 PM


PS: If you want to see a large number of IDists getting pasted on the immune system question, check out this thread at ISCID:

Organisms using GAs vs. Organisms being built by GAs
http://www.iscid.org/ubb/ultimatebb.php?ubb=get_topic;f=6;t=000152

And, if the immune system can evolve naturally, why should we be impressed by the flagellum?

nic


  
Ahmad
Inactive Member


Message 8 of 15 (25027)
11-30-2002 8:55 AM
Reply to: Message 6 by Nic Tamzek
11-29-2002 3:42 PM


quote:
1) Has admitted that IC is, at least in some cases, readily accessible to Darwinian evolution -- e.g., the case of the PCP degradation pathway?

Incorrect. Darwinian evolution merely deals with (1) and (2) pathway, i.e, Serial Direct and Parallel direct evolution both of which, as the authors say, cannot give rise to irreducibly complex and functionally indivisble molecular machines. The PCP degradation pathway is an example of a metabolic pathway. If you have read his works, do you forget the important distinction he gives between an IC machines and the IC nature of metabolic pathways? There is a huge difference between molecular machines like the ribosome or flagellum and the PCP degradation pathway. What you want to prove by calling it Gene's admission is bizarre.

quote:
2) And that he similarly accepts, or at least doesn't dispute, the evolution of some very complex and (according to Behe) IC systems, like blood-clotting and the immune system?

Hmm... now I need some sites for that. Show me where Gene says so. Just curious.. so that at least I can read his whole article.

Regards,
Ahmad


This message is a reply to:
 Message 6 by Nic Tamzek, posted 11-29-2002 3:42 PM Nic Tamzek has responded

Replies to this message:
 Message 10 by Nic Tamzek, posted 11-30-2002 11:38 AM Ahmad has responded

  
Nic Tamzek
Inactive Member


Message 10 of 15 (25040)
11-30-2002 11:38 AM
Reply to: Message 8 by Ahmad
11-30-2002 8:55 AM


quote:
Originally posted by Ahmad:
Incorrect. Darwinian evolution merely deals with (1) and (2) pathway, i.e, Serial Direct and Parallel direct evolution both of which, as the authors say, cannot give rise to irreducibly complex and functionally indivisble molecular machines. The PCP degradation pathway is an example of a metabolic pathway. If you have read his works, do you forget the important distinction he gives between an IC machines and the IC nature of metabolic pathways?

Like I said, he thinks IC can evolve. Behe was wrong. He then sets up a sub-category of IC which he thinks is impossible/very improbable to evolve, called IC machines. But this is clearly a retreat from Behe's position.

The PCP degradation has three required parts. Non-degradors only have two. Yet it evolved anyhow, and quite recently (PCP is an artifical pesticide).

Read that ISCID thread, I think that Mike Gene may have given us his position on the immune system again in the thread. He certainly didn't defend Behe, Dembski, Nelson et al., even though he is probably the person who knows more about it that any of them.

nic


This message is a reply to:
 Message 8 by Ahmad, posted 11-30-2002 8:55 AM Ahmad has responded

Replies to this message:
 Message 11 by Ahmad, posted 12-01-2002 6:50 AM Nic Tamzek has not yet responded

  
Ahmad
Inactive Member


Message 11 of 15 (25117)
12-01-2002 6:50 AM
Reply to: Message 10 by Nic Tamzek
11-30-2002 11:38 AM


quote:
Like I said, he thinks IC can evolve. Behe was wrong.

Now where does Behe state the non-evolvability of metabolic pathways that are IC? His main arguments focuses around the examples of IC molecular machines which are very distinct, in function and nature, from metabolic pathways. So where exactly does Behe get it wrong, I wonder.

quote:
He then sets up a sub-category of IC which he thinks is impossible/very improbable to evolve, called IC machines. But this is clearly a retreat from Behe's position.

How is it a retreat? Behe merely outlines the several problems with traditional explanations for the origin of metabolic pathways. He makes no such claim of that metabolic pathways can't evolve for him to be wrong. Gene elaborates it further.

quote:
The PCP degradation has three required parts. Non-degradors only have two. Yet it evolved anyhow, and quite recently (PCP is an artifical pesticide).

Interesting. What I got from Gene's webpage has this to say:

"What all of this means is that any evidence for the evolution of metabolic pathways does not translate as evidence for the evolution of IC machines. This is especially true if dealing with a sluggish pathway, composed of three enzymes, all borrowed from other pre-existing pathways, as with the PCP degradation pathway. There is a huge difference between molecular machines like the ribosome or flagellum and the PCP degradation pathway."

And I am interested in knowking more about how this PCP is used as an insecticide as you claim. Any links?

quote:
Read that ISCID thread, I think that Mike Gene may have given us his position on the immune system again in the thread. He certainly didn't defend Behe, Dembski, Nelson et al., even though he is probably the person who knows more about it that any of them.

How do you know how much he knows? Whatever it is, just because he didn't defend them does not at all favor your claim about him. I'll try to email him and hear it from the horse's mouth.

Regards,
Ahmad


This message is a reply to:
 Message 10 by Nic Tamzek, posted 11-30-2002 11:38 AM Nic Tamzek has not yet responded

  
Nic Tamzek
Inactive Member


Message 12 of 15 (25178)
12-01-2002 8:43 PM


Ahmad,

quote:

quote:
--------------------------------------------------------------------------------
Like I said, he thinks IC can evolve. Behe was wrong.
--------------------------------------------------------------------------------

Now where does Behe state the non-evolvability of metabolic pathways that are IC?


IC is IC, isn't it? Anything with multiple parts required can't (according to Behe) function without those multiple parts, therefore (according to Behe) the function cannot be reached gradually because you need all the parts. I don't see how being a metabolic pathway makes any difference, if it's an IC metabolic pathway.

Some metabolic pathways have only one required part (at least hypothetically) -- e.g., the AMP biosynthesis pathway is Behe's example in chapter 7 (p. 140 starting) -- and are therefore not technically IC according to Behe: "[t]hey do not necessarily require several parts to function" (p. 142). But some metabolic pathways (particularly that break down toxins through several toxic intermediate steps, e.g. the PCP degradation pathway) do require several parts to function and are therefore IC. But they can evolve anyway, apparently well within human lifetimes.

quote:

His main arguments focuses around the examples of IC molecular machines which are very distinct, in function and nature, from metabolic pathways. So where exactly does Behe get it wrong, I wonder.

How is the blood clotting cascade so radically distinct from a metabolic pathway?

And of course, Behe includes the lactose metabolism pathway as IC -- note that it's a metabolic pathway -- as proven by the vociferous debate that Behe and Ken Miller had over it. Behe has since mentioned lactose metabolism in many speeches. At other times, to be sure, Behe has claimed that metabolic pathways aren't IC, but this seems to be an argument of convenience for him and he uses it only when confronted with evidence that this or that metabolic pathway has evolved.

quote:

quote:
--------------------------------------------------------------------------------
He then sets up a sub-category of IC which he thinks is impossible/very improbable to evolve, called IC machines. But this is clearly a retreat from Behe's position.
--------------------------------------------------------------------------------

How is it a retreat? Behe merely outlines the several problems with traditional explanations for the origin of metabolic pathways. He makes no such claim of that metabolic pathways can't evolve for him to be wrong. Gene elaborates it further.


No, Gene appears to concede the evolution of IC metabolic pathways -- as shown by the PCP degradation example, which has three required enzymes. This is different than Behe, who says basically IC = can't evolve (or IC = wildly unlikely to evolve, a pointless distinction often tediously insisted on by IDists).

quote:

quote:
--------------------------------------------------------------------------------
The PCP degradation has three required parts. Non-degradors only have two. Yet it evolved anyhow, and quite recently (PCP is an artifical pesticide).
--------------------------------------------------------------------------------

Interesting. What I got from Gene's webpage has this to say:

"What all of this means is that any evidence for the evolution of metabolic pathways does not translate as evidence for the evolution of IC machines. This is especially true if dealing with a sluggish pathway, composed of three enzymes, all borrowed from other pre-existing pathways, as with the PCP degradation pathway. There is a huge difference between molecular machines like the ribosome or flagellum and the PCP degradation pathway."


Mike Gene says there's a huge difference between the PCP degradation pathway and the flagellum etc., but then the PCP degradation pathway has had (at most) only about 60 years to evolve, as PCP was introduced as an artificial pesticide only in 1939 IIRC. It probably took rather less time than that, given that really only a few mutations were required (the key mutation was simply regulation). The point that the pathway makes is that "multiple parts required" is no barrier *at all* to evolution. Numerous similar examples, e.g. atrazine degradation, experimental studies of the evolution of multipart metabolic pathways in the lab, etc., support the point.

To back up: the main argument against IC is change-of-function, i.e. cooption. As you've been reading Mike Gene, you know that his response to this argument is (1) to concede that it works in certain cases but that (2) it is an appeal to chance and is therefore a very unlikely explanation.

But he admits that the PCP degradation pathway, with 3 required parts, was assembled from enzymes with other original functions! (One of them is quite a radical switch, too) And if we look at evolution in general, we see that change-of-function is a ubiquitous event, not radically unlikely at all. Essentially every gene origin event is a cooption-of-function event. Your hands were not always functioning as tool-using hands, but in your ancestors were climbing hands, before that feet, and before that fins.

Here is some of the documentation backing up the above:
Topic: Co-option/change of function, literature citations on its long-recognized importance in evolution

The Origin of "Information" (new genes especially) via natural causes, Refuting a key ID claim (refs, webpages)

quote:
And I am interested in knowking more about how this PCP is used as an insecticide as you claim. Any links?

On the evolution of PCP degradation:

quote:

Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.

Trends Biochem Sci 2000 Jun;25(6):261-5

Copley SD.

Dept of Chemistry and Biochemistry and Cooperative Institute for Research in Environmental Studies, University of Colorado at Boulder, Boulder, CO 80309, USA. copley@cires.colorado.edu

The pathway for degradation of the xenobiotic pesticide pentachlorophenol in Sphingomonas chlorophenolica probably evolved in the past few decades by the recruitment of enzymes from two other catabolic pathways. The first and third enzymes in the pathway, pentachlorophenol hydroxylase and 2,6-dichlorohydroquinone dioxygenase, may have originated from enzymes in a pathway for degradation of a naturally occurring chlorinated phenol. The second enzyme, a reductive dehalogenase, may have evolved from a maleylacetoacetate isomerase normally involved in degradation of tyrosine. This apparently recently assembled pathway does not function very well: pentachlorophenol hydroxylase is quite slow, and tetrachlorohydroquinone dehalogenase is subject to severe substrate inhibition.

[On the key step of the origin of PcpC, the central step in the origin of PCP degradation]

Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol.

Biochemistry 2000 May 9;39(18):5303-11

Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD.

Department of Molecular, Cellular and Developmental Biology and Cooperative Institute for Research in Environmental Sciences, University of Colorado at Boulder, Campus Box 216, Boulder, Colorado 80309-0216, USA.

Tetrachlorohydroquinone dehalogenase catalyzes the replacement of chlorine atoms on tetrachlorohydroquinone and trichlorohydroquinone with hydrogen atoms during the biodegradation of pentachlorophenol by Sphingomonas chlorophenolica. The sequence of the active site region of tetrachlorohydroquinone dehalogenase is very similar to those of the corresponding regions of maleylacetoacetate isomerases, enzymes that catalyze the glutathione-dependent isomerization of a cis double bond in maleylacetoacetate to the trans configuration during the catabolism of phenylalanine and tyrosine. Furthermore, tetrachlorohydroquinone dehalogenase catalyzes the isomerization of maleylacetone (an analogue of maleylacetoacetate) at a rate nearly comparable to that of a bona fide bacterial maleylacetoacetate isomerase. Since maleylacetoacetate isomerase is involved in a common and presumably ancient pathway for catabolism of tyrosine, while tetrachlorohydroquinone dehalogenase catalyzes a more specialized reaction, it is likely that tetrachlorohydroquinone dehalogenase arose from a maleylacetoacetate isomerase. The substrates and overall transformations involved in the dehalogenation and isomerization reactions are strikingly different. This enzyme provides a remarkable example of Nature's ability to recruit an enzyme with a useful structural scaffold and elaborate upon its basic catalytic capabilities to generate a catalyst for a newly needed reaction.

[atrazine degradation, a similar case]
Melamine deaminase and atrazine chlorohydrolase: 98 percent identical but functionally different.

J Bacteriol 2001 Apr;183(8):2405-10

Seffernick JL, de Souza ML, Sadowsky MJ, Wackett LP.

Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, St. Paul, Minnesota 55108, USA.

The gene encoding melamine deaminase (TriA) from Pseudomonas sp. strain NRRL B-12227 was identified, cloned into Escherichia coli, sequenced, and expressed for in vitro study of enzyme activity. Melamine deaminase displaced two of the three amino groups from melamine, producing ammeline and ammelide as sequential products. The first deamination reaction occurred more than 10 times faster than the second. Ammelide did not inhibit the first or second deamination reaction, suggesting that the lower rate of ammeline hydrolysis was due to differential substrate turnover rather than product inhibition. Remarkably, melamine deaminase is 98% identical to the enzyme atrazine chlorohydrolase (AtzA) from Pseudomonas sp. strain ADP. Each enzyme consists of 475 amino acids and differs by only 9 amino acids. AtzA was shown to exclusively catalyze dehalogenation of halo-substituted triazine ring compounds and had no activity with melamine and ammeline. Similarly, melamine deaminase had no detectable activity with the halo-triazine substrates. Melamine deaminase was active in deamination of a substrate that was structurally identical to atrazine, except for the substitution of an amino group for the chlorine atom. Moreover, melamine deaminase and AtzA are found in bacteria that grow on melamine and atrazine compounds, respectively. These data strongly suggest that the 9 amino acid differences between melamine deaminase and AtzA represent a short evolutionary pathway connecting enzymes catalyzing physiologically relevant deamination and dehalogenation reactions, respectively.


quote:

quote:
--------------------------------------------------------------------------------
Read that ISCID thread, I think that Mike Gene may have given us his position on the immune system again in the thread. He certainly didn't defend Behe, Dembski, Nelson et al., even though he is probably the person who knows more about it that any of them.
--------------------------------------------------------------------------------

How do you know how much he knows? Whatever it is, just because he didn't defend them does not at all favor your claim about him. I'll try to email him and hear it from the horse's mouth.

Regards,
Ahmad


I've had a number of online debates with Mike Gene, so everything I say about what he thinks is simply my interpretation based on that experience. You are free to ask him yourself. Unfortunately I don't keep a database of Mike Gene quotes on tab.

I am, however, sure he knows a lot -- in fact, he knows enough to know that (despite being tremendously complex and IC according to Behe) there is plenty of evidence and a thick stack of peer-reviewed literature indicating that the immune system did, in fact, originate via evolution. This, too, undermines Behe, Nelson, Dembski, et al.

My opinion is that arguments for ID based on biological complexity are rather badly undermined once the evolution of horrendously complex things like the vertebrate immune system is conceded.

Mike Gene thinks that the idea is still salvagable. He is written a lot on why but I for one still don't "get it". If you have better luck, please explain it to us...

Thanks, nic

[This message has been edited by Nic Tamzek, 12-01-2002]


Replies to this message:
 Message 14 by Nic Tamzek, posted 12-01-2002 9:53 PM Nic Tamzek has not yet responded
 Message 15 by Ahmad, posted 12-04-2002 2:24 PM Nic Tamzek has not yet responded

  
Nic Tamzek
Inactive Member


Message 14 of 15 (25188)
12-01-2002 9:53 PM
Reply to: Message 12 by Nic Tamzek
12-01-2002 8:43 PM


One more on atrazine degradation; this article is handily free online here:

http://jb.asm.org/cgi/content/full/180/1/152

quote:

AtzC Is a New Member of the Amidohydrolase Protein Superfamily and Is Homologous to Other Atrazine-Metabolizing Enzymes

J Bacteriol. 1998 January; 180 (1): 152158

Michael J. Sadowsky,1,2,3,4* Zhaokun Tong,1,4 Mervyn de Souza,3,4,5 and Lawrence P. Wackett3,4,5

Pseudomonas sp. strain ADP metabolizes atrazine to cyanuric acid via three plasmid-encoded enzymes, AtzA, AtzB, and AtzC. The first enzyme, AtzA, catalyzes the hydrolytic dechlorination of atrazine, yielding hydroxyatrazine. The second enzyme, AtzB, catalyzes hydroxyatrazine deamidation, yielding N-isopropylammelide. In this study, the third gene in the atrazine catabolic pathway, atzC, was cloned from a Pseudomonas sp. strain ADP cosmid library as a 25-kb EcoRI DNA fragment in Escherichia coli. The atzC gene was further delimited by functional analysis following transposon Tn5 mutagenesis and subcloned as a 2.0-kb EcoRI-AvaI fragment. An E. coli strain containing this DNA fragment expressed N-isopropylammelide isopropylamino hydrolase activity, metabolizing N-isopropylammelide stoichiometrically to cyanuric acid and N-isopropylamine. The 2.0-kb DNA fragment was sequenced and found to contain a single open reading frame of 1,209 nucleotides, encoding a protein of 403 amino acids. AtzC showed modest sequence identity of 29 and 25%, respectively, to cytosine deaminase and dihydroorotase, both members of an amidohydrolase protein superfamily. The sequence of AtzC was compared to that of E. coli cytosine deaminase in the regions containing the five ligands to the catalytically important metal for the protein. Pairwise comparison of the 35 amino acids showed 61% sequence identity and 85% sequence similarity. AtzC is thus assigned to the amidohydrolase protein family that includes cytosine deaminase, urease, adenine deaminase, and phosphotriester hydrolase. Similar sequence comparisons of the most highly conserved regions indicated that the AtzA and AtzB proteins also belong to the same amidohydrolase family. Overall, the data suggest that AtzA, AtzB, and AtzC diverged from a common ancestor and, by random events, have been reconstituted onto an atrazine catabolic plasmid.


nic

[This message has been edited by Nic Tamzek, 12-01-2002]


This message is a reply to:
 Message 12 by Nic Tamzek, posted 12-01-2002 8:43 PM Nic Tamzek has not yet responded

  
Ahmad
Inactive Member


Message 15 of 15 (25453)
12-04-2002 2:24 PM
Reply to: Message 12 by Nic Tamzek
12-01-2002 8:43 PM


Nic Tamzek,

quote:
IC is IC, isn't it? Anything with multiple parts required can't (according to Behe) function without those multiple parts, therefore (according to Behe) the function cannot be reached gradually because you need all the parts. I don't see how being a metabolic pathway makes any difference, if it's an IC metabolic pathway.

But there is a difference. Behe never makes any such claim of the unevolvability of metabolic pathways. There is a difference and Gene outlines it beautifully:

"I would like to introduce an important distinction concerning the IC nature of molecular machines when compared to the IC nature of metabolic pathways. The IC nature of the two differ in that the former depend on direct, specific contacts between components while the latter do not.

A molecular machine functions when energy (usually in the form of ATP binding/hydrolysis) enters the complex through a specific input portal. This energy input then triggers a cascade of unidirectional, conformational changes among the parts. Using our symbolic conventions above, think of A changing shape to induce a shape change in B, which induces a shape change in C, which induces a shape change in D, which then elicits the functional output. The parts require a series of direct contacts to convey the energy/information/mechanical flow that brings about the function. Removing any part interrupts this flow and renders the entire complex functionless, such that all the non-affected gene products are now without function.

A metabolic pathway functions differently. In this case, protein A reacts with an original substrate to produce product 1. Product 1 is then converted into product 2 by protein B. Protein C then converts product 2 into product 3. And finally, protein D converts product 3 into product 4. We then define the appearance of product 4 from the original substrate as the function (F). One could reasonably interpret this as IC as proteins A,B,C and D are needed to convert the original substrate into product 4. Yet such a pathway could evolve because various metabolic pathways are typically interlocked through their substrates/products. That is, product 2 may bind to protein C (for conversion into product 3), but product 2 may also react with several other proteins and thus be useful elsewhere. Since metabolic pathways produce products that can exist apart from any particular pathway, it is easier for the proteins in a pathway to exist apart from any particular function.

To appreciate just how different this is from an IC machine, consider the following. As mentioned above, you can isolate each individual component on the bacterial flagellum and fill test tubes with those individual parts. Most of the parts will not do anything in that test tube, except for the input portal which binds ATP. In contrast, you can take any protein from a metabolic pathway and fill a test tube with it and it will do something significant - catalyze a specific chemical reaction. In other words, the components of a pathway are not F-dependent; they will perform their subfunction apart from F. In contrast, most parts of a molecular machine are F-dependent and will not perform their subfunction apart from F.

This means that a metabolic pathway may be poised to evolve (as we might expect from ID). Using nothing more than simple chemical rules and selection pressures, various components of metabolic pathways may realign themselves to carry out new functions. Since the proteins of any pathway interact through the intermediaries of their substrates and products, and these can exist independently of the proteins, readjustments are plausible, especially when aided by gene duplication. The parts of a molecular machine, however, are not interacting through independent intermediaries, but through direct physical contact. And this places much more stringent constraints on the system."

quote:
Some metabolic pathways have only one required part (at least hypothetically) -- e.g., the AMP biosynthesis pathway is Behe's example in chapter 7 (p. 140 starting) -- and are therefore not technically IC according to Behe: "[t]hey do not necessarily require several parts to function" (p. 142). But some metabolic pathways (particularly that break down toxins through several toxic intermediate steps, e.g. the PCP degradation pathway) do require several parts to function and are therefore IC. But they can evolve anyway, apparently well within human lifetimes.

But there is a difference as outlined by Gene. Behe
even ACKNOWLEDGES such pathways may have evolved (see DBB 151 ff.)

quote:
How is the blood clotting cascade so radically distinct from a metabolic pathway?

Well metabolic pathways are not irreducibly complex as Behe stated on page 150-151 of his book. Thus metabolic pathways simply aren’t in the same category as the blood clotting cascade. There is a difference.

quote:
And of course, Behe includes the lactose metabolism pathway as IC -- note that it's a metabolic pathway -- as proven by the vociferous debate that Behe and Ken Miller had over it. Behe has since mentioned lactose metabolism in many speeches. At other times, to be sure, Behe has claimed that metabolic pathways aren't IC, but this seems to be an argument of convenience for him and he uses it only when confronted with evidence that this or that metabolic pathway has evolved.

Incorrect. It is actually Ken Miller who claimed that the lactose system was irreducibly complex. Why did he say that? Because he claimed to have shown the evolution of the lactose system, right in the laboratory using Hall's work, to an irreducibly complex system. Behe disproved him here.

quote:
No, Gene appears to concede the evolution of IC metabolic pathways -- as shown by the PCP degradation example, which has three required enzymes. This is different than Behe, who says basically IC = can't evolve (or IC = wildly unlikely to evolve, a pointless distinction often tediously insisted on by IDists).

Show me where in DBB does Behe explicity claim that IC metabolic pathways can't evolve. You can't, 'cause he does not make any such claim. In response to Miller, Behe says:

"I clearly stated in Darwin’s Black Box metabolic pathways are not irreducibly complex (Behe 1996, pp. 141-142; 150-151), because components can be gradually added to a previous pathway."

quote:
Mike Gene says there's a huge difference between the PCP degradation pathway and the flagellum etc., but then the PCP degradation pathway has had (at most) only about 60 years to evolve, as PCP was introduced as an artificial pesticide only in 1939 IIRC. It probably took rather less time than that, given that really only a few mutations were required (the key mutation was simply regulation). The point that the pathway makes is that "multiple parts required" is no barrier *at all* to evolution. Numerous similar examples, e.g. atrazine degradation, experimental studies of the evolution of multipart metabolic pathways in the lab, etc., support the point.

Irrelevant. Read again. There is a distinct difference IC molecular machines and the IC nature of metabolic pathways. Molecular machine's assembly-dependant nature makes it different from metabolons.

quote:
To back up: the main argument against IC is change-of-function, i.e. cooption. As you've been reading Mike Gene, you know that his response to this argument is (1) to concede that it works in certain cases but that (2) it is an appeal to chance and is therefore a very unlikely explanation.

But he admits that the PCP degradation pathway, with 3 required parts, was assembled from enzymes with other original functions! (One of them is quite a radical switch, too) And if we look at evolution in general, we see that change-of-function is a ubiquitous event, not radically unlikely at all. Essentially every gene origin event is a cooption-of-function event. Your hands were not always functioning as tool-using hands, but in your ancestors were climbing hands, before that feet, and before that fins.


You are wrong on two premises:

1. If you had fully read Gene's explanation, you would have not failed to notice the glaring distinction between the possibility of co-option hypothesis in a molecular machine and in a metabolic pathway. Metabolic pathways produce products that can exist apart from any particular pathway, so it is easier for the proteins in a pathway to exist apart from any particular function. An analogy is also given to understand this very vital point and I pasted it above. he components of the metabolic pathway are not F-dependent; they will perform their subfunction apart from F. In contrast, most parts of a molecular machine are F-dependent and will not perform their subfunction apart from F. F stands for "Function". He makes it very clear that using nothing more than simple chemical rules and selection pressures, various components of metabolic pathways may realign themselves to carry out new functions. Since the proteins of any pathway interact through the intermediaries of their substrates and products, and these can exist independently of the proteins, readjustments are plausible, especially when aided by gene duplication. This does not exist in the case of molecular machines. The parts of a molecular machine, however, are not interacting through independent intermediaries, but through direct physical contact. And this places much more stringent constraints on the system.

2. Co-Option hypothesis, as Gene stated, is entirely dependent on chance and thus highly unlikely. You say that almost all gene origins is done by the co-option hypothesis. Give me some examples.

Let me review your websites now:

1. Co-option/change of function, Citations of this in the literature

The (presumably yours) first post discusses about the origin of feathers. You say:

" I was struck by this passage from Maynard Smith's The Theory of Evolution. It almost sounds like it was written to respond to Behe, except that it was written in 1958 (I think; I have the 1993 Canto edition which is the fourth edition):"

Similar assumtions were also made by Thornhill and Ussery in their classification of darwinian pathways. But it is not clear this is an example of generating IC and this whole topic ignores Behe's points on pp. 40-41. The fact that various proteins can share domains doesn't really support adoption from a different function, as there is no reason to think a designer would ensure that each and every part of a system is truly unique. For example, that both a lawnmower and automobile have spark plugs is not evidence that one motor was co-opted to form another by random changes and selection.

To quote Smith:

"In this case the difficulty disappears once it is realized that during the early stages of the evolution of feathers, the latter were probably of selective advantage because they conserved heat, and only later did they become functional in flight."

The so-called ‘feathers’ of reptiles were likely frayed collagen fibres.

It’s also most unlikely that flight feathers would evolve for heat insulation first, because natural selection for heat insulation would tend to remove any complexity, because a hairlike structure is much better for insulation. In fact, flightless birds have feathers superficially similar to hair, and in some cases this can be explained by loss of information for the complexity of flight feathers.

In your next post, you quote darwin as saying:

"We should be extremely cautious in concluding that an organ could not have been formed by transitional gradations of some kind. Numerous cases could be given amongst the lower animals of the same organ performing at the same time wholly distinct functions;"

Darwin, himself, was confounded on the lack of transitional species... let alone their organs. Therefore in his book The Origin of Species he wrote the following in the chapter "Difficulties of the Theory":

"…Why, if species have descended from other species by fine gradations, do we not everywhere see innumerable transitional forms? Why is not all nature in confusion, instead of the species being, as we see them, well defined?… But, as by this theory innumerable transitional forms must have existed, why do we not find them embedded in countless numbers in the crust of the earth?… But in the intermediate region, having intermediate conditions of life, why do we not now find closely-linking intermediate varieties? This difficulty for a long time quite confounded me." (page 179)

Your fourth post deals with an increase in genetic information with a resultant increase in complexity. The article cites two ways of doing so:

1. Exon-Shuffling

This mechanism merely produces genetic and phenotypical variety, in an organized way by producing new exon combinations and thus greater genetic diversification. It does not play any role in the "origin of genetic information" as you claim, because it does not add any new genetic information in the first place but recombines existing gene sequences to provide variety.

2. Gene Duplication

This predicts a number of duplicated genes with specialized functions. One question to ask here is to develop the specialized functions, the duplicated genes still had to evolve structural changes. What drove the changes? In all likelihood, a number of specializations would have had to develop simultaneously to have any value. An additional concern here is the high probability of the evolving genes messing up the original system. This is very likely with an abundance of structurally similar gene products. If one of these gene products becomes nonfunctional, it could get in the way of the function of original gene product. This phenomena is readily observed today. For instance, the chemotherapy drug methotrexate looks like the B-vitamin folacin, but does not work like it. The drug will compete with the real vitamin for binding to functional sites, but will not actually function. This action kills cancer cells.

Another problem with gene duplication is that it doesn't account for all, or even most, of the complexity in many systems. For example, the complexities of oxygen transport involve many genes which are not structurally similar. This is obvious when one considers anemia, a breakdown in oxygen transport.

Overall, like exon shuffling, gene duplication does not add any new genetic information and for it to provide complexity.. is highly unlikely. At the articles conclusion, the authors say:

"However our results provide another indication that biological evolution works like a tinkerer, "who does not know exactly what he is going to produce, but uses whatever he finds around him whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a `bricoleur' who uses everything at his disposal to produce some kind of workable object".

Now where does it explain the "origin" of the string, fragments of wood, or old carboards?? And do they consider the high improbability that these three structures will, naturally, combine together to form a well-built string boats?? Seems very unlikely... unless a supernatural force is added to the scenario, i.e, "creation".

2. The Origin of "Information" (new genes especially) via natural causes, Refuting a key ID claim (refs, webpages)

Well to begin with, Johnson stood unrefuted. The examples you gave show nothing of the "creation" of genetic information just as Johnson predicts. Let me begin by quoting Musgrave again to prove my point:

"My second favorite example is the Sdic gene, where the annexin and dynenin intermediate chain genes were duplicated in tandem, then the intervening sequences deleted to form a single new gene, (the Sperm specific dynenin intermediate chain gene Sdic). The good thing about this example is that a previously non-coding part of the sequence became the protein coding sequence, and the protein coding sequence has a non-coding role." (Emphasis mine)

Where is this so-called "creation" of genetic information that you have been talking about? All I see is the deletion of intervening sequences of intermediates to form a gene. This deletion is loss of information... not the other way round. There is no increase in specified complexity either. And note... this is a "selective sweep" which is the directional selection of genes that already existed rather than creation of novel genes.

The second example is given by theyeti about the creation of jingwei gene in Drosophilia by exon recombination. Once again.. no new genetic information is added but new genetic recombinations are expressed. Speaking of the efforts to change the fruit fly's genes, Lester and Bohlin make the following statement:

"But this sort of reshuffling is not likely to result in major evolutionary change. It simply recognizes what already exists. Even with new mutations, it will not likely lead to new original metabolic functions and new protein molecules." (Lester LP, Bohlin RG. 1984. The natural limits to biological change. Grand Rapids, MI: Zondervan Publishing House, p 69.)

"It simply recognizes what already exists." This is an important statement. The new Jingwei gene was produced by shuffling or recombining preexisting genes. Nothing new has been created; only new genetic (exon) combinations have been expressed!

The same explanation also goes for the sphinx gene in Drosophilia except that this is an "unusual" retroposition process, as the authors claim. They give three hypothesis for the origin of the sphinx gene.. all of which require the retroposition and thus nothing new is created.

AFGB is produced by the "the recruitment and iteration of a small region spanning the boundary between the first intron and second exon of the trypsinogen gene (Fig. 1). This newborn segment was expanded and then iteratively duplicated (perhaps by replication slippage or unequal crossing-over) to produce 41 tandemly repeated segments."

A simple case of intron-exon recombination from the existing existing trypsinogen gene. No genetic information is created, once again but genetic recombinations expressed.

Evolution needs swags of new information, if a microbe really did change into a man over several billion years. The additional new information would take nearly a thousand books of 500 pages each to print the sequence. Random changes cannot account for a page, or even a sentence, of this, let alone accounting for all of it. You have an incredible faith!

quote:
On the evolution of PCP degradation:

Interesting pages. I'll go through them in detail when I have the time. You still haven't showed where Behe claims the unevolvability of metabolic pathways.

quote:
My opinion is that arguments for ID based on biological complexity are rather badly undermined once the evolution of horrendously complex things like the vertebrate immune system is conceded.

Mike Gene thinks that the idea is still salvagable. He is written a lot on why but I for one still don't "get it". If you have better luck, please explain it to us...


Yes the immune system us highly complex... yet the idea of its evolution is hardly convincing. I know very little about it and Insha Allah (if God willing) will find out more from my library. Sorry for the long response...

Regards,
Ahmad


This message is a reply to:
 Message 12 by Nic Tamzek, posted 12-01-2002 8:43 PM Nic Tamzek has not yet responded

  
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