Irreducible Complexity

[Administrator2]

THE GALATIAN

The point of the email was not that the components of the flagellum existed in another form in simpler structures of the cell.

Rather, it points out that the combination of proteins found in the flagellum is not irreducibly complex. So the Type III Secretory "syringe" that has the components of the flagellum that can be adapted to motion rather than movement to inject molecules into another cell.

The reason that this sort of motility evolved in bacteria seems clear. The Reynolds number a measure of viscosity related to turbulent flow, is about 1X10^7 for a bacterium, while it is about 1X10^-4 for a sperm cell. Even waving cilia would be inefficient for a bacterium.

Rotation is a more sensible approach when viscosity is to the point that it doesn't matter much how one orients the paddle on a return stroke.

Keeping in mind that there is essentially no inertia for a bacterium in water, due to the low Reynolds number, it's clear that any motion by a structure of the cell would impart a useful unbalanced force on the cell.

Carrier proteins, large protein molecules involved in active transport, work by rotating in the cell membrane. They are powered by the same processes that make the syringe/flagellum assemblies go, but they are much simpler. Nevertheless, they do impart a moment on the cell when they turn, as a portion of the protein is normally protruding from the cell membrane.

The simplest form of locomotion for a cell would then be an active transport molecule that had lost a specific site, and turned freely. Again, because of the viscosity at this scale, even a very short "flagellum" would provide a usable moment. The Type III Secretory Apparatus is on the cell membrane, protruding out into the environment. It moves at the base, because it is used to protrude and expel cell material. But it also has the important elements of a flagellum. It provides a moment when it does move, (because of the low Reynolds number, there is little inertia, so efficiency is not the issue) and it is made of many of the same proteins of the more complex flagellum.

One could object, saying that these have two different "purposes". But the history of evolution has always been not of the appearance of completely new features, but of the reworking of old features to new uses. And here we have an obvious candidate in the form of a moving structure on the surface of the cell that has many of the features of a flagellum.

There's a lot of interesting work to be done here. But it becomes very clear that even the simplest bacterial flagellum is not the simplest form of motility structure possible, and there are a number of possible ways for it to evolve.

[ June 07, 2002, 09:39 AM: Message edited by: Administrator ]

 

[Administrator2]

JOHN PAUL

Time to bring the water to the horse.

By now we all should be well aware that Behe’s book, Darwin’s Black Box, is a challenge to scientists to objectively demonstrate how apparent IC biochemical systems arose via purely natural processes and to get that work published in peer-reviewed journals. You don’t have to take my word for it all you have to do is to read the book.

Just below what Helen posted from the book, also on page 72:

The general professional literature on the bacterial flagellum is about as rich as the literature on the cilium, with thousands of papers published on the subject over the years. That isn’t surprising; the flagellum is a fascinating biophysical system, and flagellated bacteria are medically important. Yet, here again, thew evolutionary literature is totally missing. Even though we are told that all biology must be sen through the lens of evolution, no scientist has ever published a model to account for the gradual evolution of this extraordinary molecular machine.

So what is Behe talking about when he speaks of irreducible complexity?

From page 39 of Darwin’s Black Box

Darwin knew that his theory of gradual evolution by natural selection carried a heavy burden:

”If it could be demonstrated that any complex organ existed which could not have been formed by numerous, successive, slight modifications, my theory would break down.”

It is safe to say that most scientific skepticism about Darwinism in the past century has centered on this requirement. From Mivart’s concern over the incipient stages of new structures to Margulis’s dismissal of gradual evolution, critics of Darwin have suspected that his critereon of failure had been met. But how can we be confident? What type of biological system could not be formed by “numerous, successive, slight modifications”?

Well, for starters, a system that is irreducibly complex. By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively stop functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving 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. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution. Since natural selection can only choose systems that are already working, then if a biological system cannot be produced gradually it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act on.

(bold added)

John Paul:
In the Galatian’s example, the structure had a function as that 10-part (protein) piece (which appears to go against Behe’s definition). As I stated in my earlier post we now have to figure out how that 10-protein structure came together in the first place. Is it IC? Then we have to figure out, seeing that this 10-protein structure has a function, what happens to the organism once that function has been removed because of the mutational accumulation that is required for that 10-protein structure to become part of the flagellum. Once that is accomplished we have to figure out where the other parts (proteins) of the flagellum came from and what put all the parts together so that the flagellum would form and function as it does.

More from Behe on IC (Darwin’s Black Box posted earlier in this thread):

Might there be an as-yet-undiscovered natural process that would explain biochemical complexity? No one would be foolish enough to categorically deny the possibility. Nonetheless, we can say that if there is such a process, no one has a clue how it would work. Further, it would go against all human experience, like postulating that a natural process might explain computers. Concluding that no such process exists is as scientifically sound as concluding that mental telepathy is not possible, or that the Loch Ness monster doesn't exist. In the face of massive evidence we do have for biochemical design, ignoring that evidence in the name of a phantom process would be to play the role of the detectives who ignore an elephant.*

*Same elephant mentioned in the article below:

http://www.creationequation.com/Archives/TheBiologist.htm

John Paul:
Here’s another difference between Creationists and evolutionists:

Evolutionists say the apparent design in living organisms is illusory and the apparent sequence of fossils is real and needs to be explained.

Creationists say the apparent design in living organisms is real and needs to be explained and the apparent sequence of fossils is illusory.

How can we be sure of the design in living organisms?

Again, Behe from Darwin’s Black Box:

Our ability to be confident of the design of the cilium or intracellular transport rests on the same principles to be confident of the design of anything: the ordering of separate components to achieve an identifiable function that depends sharply on the components.

 

[Administrator2]

HELEN

Galatian, I'm glad you agree with God's design regarding the flagellum. However your agreement does not mean it evolved. Nor does it mean that proteins somehow switched jobs and that the governing mechanisms in the cell allowed this. I'm sure you know that proteins in the cell are recycled continually for most kinds of cells in most areas. Extra proteins are a useless waste and are dissassembled and the amino acids used again for another protein. The cell of any organism will not produce a new form or function that we have seen. Your example of a changed metabolic pathway is the only example you have and it had to replace one that was disturbed by intelligent designing scientists. The fact that it had a perfectly good metabolic pathway in the first place and also had the ability to replace it when artificially disturbed says nothing about the emergence of a NEW function and form, such as a flagella.

In the meantime, the point of Behe, again, is that any irreducibly complex structure or function cannot function in that way or be what it is unless it is ALL there from the start. Part of a flagellum doesn't work. Part of a blood clotting cascade is a killer without the rest, etc.

 

[Administrator2]

THE GALATIAN:

By now we all should be well aware that Behe’s book, Darwin’s Black Box, is a challenge to scientists to objectively demonstrate how apparent IC biochemical systems arose via purely natural processes and to get that work published in peer-reviewed journals.

That's just what Hall's work on E. coli demonstrated.

"Evolution on a Petri Dish : The evolved B-galactosidase system as a model for studying acquisitive evolution in the lab", Barry G Hall, Evolutionary Biology (1982) #15, pg 85-150.

Mutation produced an entirely new way of utilizing a food source, and then made it irreducibly complex by adding a regulator. Now the system can't work unless both are present. Since Behe declared that to be irreducible complexity, we now have undeniable evidence that IC evolves.

The general professional literature on the bacterial flagellum is about as rich as the literature on the cilium, with thousands of papers published on the subject over the years. That isn’t surprising; the flagellum is a fascinating biophysical system, and flagellated bacteria are medically important. Yet, here again, thew evolutionary literature is totally missing.

A quick look found these:
(a quote from the report, not the abstract)

In the absence of flagella, the cell surface of Synechococcus sp. WH8113 must generate thrust. Theoretical work suggests that a cyanobacterium could swim at the observed speeds by oscillating its surface in the manner of a traveling wave [6,13]. Whereas motility is powered by an ion-motive force across the cell membrane [17] and the protein SwmA that is required for propulsion is associated with the outer membrane [3], the traveling wave must be formed at the very exterior of the cell body, outside the crystalline surface layer. Since the spicules contact the cell and outer membranes and protrude into the surrounding medium, they could be utilized to transmit motions in the cell membrane or outer membrane into the surrounding medium. If motors concealed in the cell membrane or outer membrane are capable of contracting and expanding in a regular manner (perhaps in analogy to the motor protein embedded in the basolateral membrane of cochlear outer hair cells that contract and expand to set the length of the cells [5]), these oscillations would be transduced into a rowing motion of the spicules. In this case, the crystalline surface layer could serve as oarlocks for the spicules, converting smaller motions at the bases of spicules into larger motions at the tips.

Envelope structure of Synechococcus sp. WH8113, a nonflagellated swimming cyanobacterium
Aravinthan DT. Samuel, Jennifer D. Petersen, and Thomas S. ReeseBMC Microbiol. 2001; 1(1): 4

A simpler form of motion, using a primitve "motor", and a simpler protein complex from the cell wall.

The fliD gene encoding the flagellar cap protein (FliD) of Clostridium difficile was studied in 46 isolates belonging to serogroups A, B, C, D, F, G, H, I, K, X, and S3, including 30 flagellated strains and 16 nonflagellated strains. In all but three isolates, amplification by PCR and reverse transcription-PCR demonstrated that the fliD gene is present and transcribed in both flagellated and nonflagellated strains. PCR-restriction fragment length polymorphism (RFLP) analysis of amplified fliD gene products revealed interstrain homogeneity, with one of two major patterns (a and b) found in all but one of the strains, which had pattern c. A polyclonal monospecific antiserum raised to the recombinant FliD protein reacted in immunoblots with crude flagellar preparations from 28 of 30 flagellated strains but did not recognize FliD from nonflagellated strains. The fliD genes from five strains representative of the three different RFLP groups were sequenced, and sequencing revealed 100% identity between the strains with the same pattern and 88% identity among strains with different patterns. Our results show that even though FliD is a structure exposed to the outer environment, the flagellar cap protein is very well conserved, and this high degree of conservation suggests that it has a very specific function in attachment to cell or mucus receptors.

Molecular Characterization of fliD Gene Encoding Flagellar Cap and Its Expression among Clostridium difficile Isolates from Different Serogroups
Albert Tasteyre, Tuomo Karjalainen, Véronique Avesani, Michel Delmée, Anne Collignon, Pierre Bourlioux, and Marie-Claude BarcJ Clin Microbiol. 2001 March; 39(3): 11781183

Again, we see other functions for these units, consistent with the evolution of flagella. Here's an interesting one that shows flagella as having an structural function as well as motility:

Bacterial shape usually is dictated by the peptidoglycan layer of the cell wall. In this paper, we show that the morphology of the Lyme disease spirochete Borrelia burgdorferi is the result of a complex interaction between the cell cylinder and the internal periplasmic flagella. B. burgdorferi has a bundle of 7–11 helically shaped periplasmic flagella attached at each end of the cell cylinder and has a flat-wave cell morphology. Backward moving, propagating waves enable these bacteria to swim in both low viscosity media and highly viscous gel-like media. Using targeted mutagenesis, we inactivated the gene encoding the major periplasmic flagellar filament protein FlaB. The resulting flaB mutants not only were nonmotile, but were rod-shaped. Western blot analysis indicated that FlaB was no longer synthesized, and electron microscopy revealed that the mutants were completely deficient in periplasmic flagella. Wild-type cells poisoned with the protonophore carbonyl cyanide-m-chlorophenylhydrazone retained their flat-wave morphology, indicating that the periplasmic flagella do not need to be energized for the cell to maintain this shape. Our results indicate that the periplasmic flagella of B. burgdorferi have a skeletal function. These organelles dynamically interact with the rod-shaped cell cylinder to enable the cell to swim, and to confer in part its flat-wave morphology.

Borrelia burgdorferi periplasmic flagella have both skeletal and motility functions
Mohammed Abdul Motaleb, Linda Corum, James L. Bono, Abdallah F. Elias, Patricia Rosa, D. Scott Samuels, and Nyles W. Charon
Proc. Natl. Acad. Sci. USA. 2000 September 26; 97(20): 1089910904 ; published online before print September 19, 2000.

Since evolution works by reworking old structures to new uses, this finding is a very interesting breakthrough.

It is safe to say that most scientific skepticism about Darwinism in the past century has centered on this requirement. From Mivart’s concern over the incipient stages of new structures to Margulis’s dismissal of gradual evolution, critics of Darwin have suspected that his critereon of failure had been met. But how can we be confident? What type of biological system could not be formed by “numerous, successive, slight modifications”? Well, for starters, a system that is irreducibly complex.

No, Hall's study put an end to that idea. Irreducible Complexity is quite easily evolved.

By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively stop functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving 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.

This one is a stunner. Here one has declared a priori, that anything capable of evolving cannot, by definition, be irreducibly complex. But then, this is nothing but an attempt to deny evolution by definition. As you have seen, irreducibly complex (in the sense that all components must be present for the system to work) featurse do evolve, and rather readily.
And such a definition is impossible to use, since one must prove a negative, i.e. demonstrate that it could not have evolved.

John Paul:

In the Galatian’s example, the structure had a function as that 10-part (protein) piece (which appears to go against Behe’s definition).

As I stated in my earlier post we now have to figure out how that 10-protein structure came together in the first place. Is it IC?

A good question, in more ways than one. Now we know that the typical bacterial flagellum has antecedents, we ask next, "How about the Type III Secretory Apparatus?". And if we can show a simpler antecedent for that, we can keep backing up, presumably to the time when the four forces decoupled and made chemistry possible. To what end?

It's to prove a negative. But science is not in the business of doing that. Nor is religion, as far as I know.

 

[Administrator2]

THE GALATIAN

Helen:
Galatian, I'm glad you agree with God's design regarding the flagellum.

Of course, as we have discussed before, I believe it is insulting God to suggest that He "designs" like a limited creature. I am, however, continually impressed by the way He created nature to evolve such things.

However your agreement does not mean it evolved.

Of course not. It is, rather, the evidence that counts. The fact that we find a simpler structure in the cell, with the same proteins, demonstrates that the flagellum is not irreducibly complex after all. Of course, we also have to specify which flagellum, since there are several different ones, of differing levels of complexity. It also turns out that bacterial flagella still function as secretory structures, and this works, even in the absence of most parts of the flagellum.

http://minyos.its.rmit.edu.au/~e21092/flagella.htm

Nor does it mean that proteins somehow switched jobs and that the governing mechanisms in the cell allowed this.

Check the link above. There is evidence for just that happening.

I'm sure you know that proteins in the cell are recycled continually for most kinds of cells in most areas. Extra proteins are a useless waste and are dissassembled and the amino acids used again for another protein. The cell of any organism will not produce a new form or function that we have seen.

We certainly have seen numerous examples of that happening. One of the most remarkable is that several genera of bacteria have evolved enzymes capable of digesting nylon oligomers.

http://www.nmsr.org/nylon.htm

Your example of a changed metabolic pathway is the only example you have and it had to replace one that was disturbed by intelligent designing scientists.

That's the nature of evolution; it is indifferent to how the environment actually got changed. But the response is entirely by the sorting of mutations by natural selection. And if you note the example linked above, you'll see that new information, in the form of a frame shift that created a gene to digest nylon oligomeres (moderate-sized nylon polymer) did exactly that.

The fact that it had a perfectly good metabolic pathway in the first place and also had the ability to replace it when artificially disturbed says nothing about the emergence of a NEW function and form, such as a flagella.

See above. There are many other examples. Most of the new genes for antibiotic resistance are like this. In some cases, the precise nature of the mutation is known.

In the meantime, the point of Behe, again, is that any irreducibly complex structure or function cannot function in that way or be what it is unless it is ALL there from the start.

That's what Hall's experiment refuted. The new metabolic pathway is irreducibly complex, because it cannot function without both components present. Yet it evolved by stepwise accumulation of mutations.

Part of a flagellum doesn't work.

Actually, that's not quite true, either. All of them work as secretory structures, even if the other parts are missing. And even the motility function isn't irreducibly complex in most bacteria.

Part of a blood clotting cascade is a killer without the rest, etc.

But since we have observed that irreducible complexity evolves, it doesn't really say anything about evolution. After all, part of the enzyme system in Hall's bacteria won't work either. Yet it evolved.

 

[Administrator2]

JOHN PAUL

It is now obvious that the galatian hasn’t read Behe’s book Darwin’s Black Box, nor has he read Behe’s responses to his critics which I linked to in the 3rd post of this thread and has been posted since February 24th of this year. This is no way to conduct a debate. In order to debate properly you have to know what it is you are debating against. In this case it is irreducible complexity. If you are going to argue against Behe you have to know what his position is. That would mean reading his material that pertains to this topic. Reading other material by Behe might give you more insight into his position.

Here is the .pdf file of Behe’s responses to his critics. In it he rebuts Miller’s claim (notice it isn’t Hall’s claim) that Hall’s experiment(s) show that irreducibly complex systems can evolve and have been shown to do so.

http://www.iscid.org/papers/Behe_ReplyToCritics_121201.pdf

From the 3rd post of this thread:

John Paul:
(snip ATP stuff)

If you want to discuss IC it would be a good idea to read Behe’s “Darwin’s Black Box”. At least read this:

Michael J. Behe: A Response to Critics of Darwin's Black Box

http://www.iscid.org/ubb/ultimatebb.php?ubb=get_topic&f=10&t=000010

I like this from Nelson Alonso in a reply to Behe’s article,
[qoute]Describing this device, Science News makes it clear that it is not like a machine, it is one.

Nelson’s reply discusses ATP synthase. He ends it with this,
“Like the many IC systems Behe discusses, there seems to be nothing in the literature about the Darwinian evolution of the ATP synthase.”

 

[Administrator2]

THE GALATIAN

John Paul: Nelson’s reply discusses ATP synthase. He ends it with this,
“Like the many IC systems Behe discusses, there seems to be nothing in the literature about the Darwinian evolution of the ATP synthase.”

Actually, that's wrong. Here's one.

Proc. Natl. Acad. Sci. USA. 2001 August 14; 98 (17): 98539858
DNA/DNA hybridization to microarrays reveals gene-specific differences between closely related microbial genomes .
E. Murray, D. Lies, G. Li, K. Nealson, J. Zhou, and J. M. Tiedje
ABSTRACT:
DNA microarrays constructed with full length ORFs from Shewanella oneidensis, MR-1, were hybridized with genomic DNA from nine other Shewanella species and Escherichia coli K-12. This approach enabled visualization of relationships between organisms by comparing individual ORF hybridizations to 164 genes and is further amenable to high-density high-throughput analyses of complete microbial genomes. Conserved genes (arcA and ATP synthase) were identified among all species investigated. The mtr operon, which is involved in iron reduction, was poorly conserved among other known metal-reducing Shewanella species. Results were most informative for closely related organisms with small subunit rRNA sequence similarities greater than 93% and gyrB sequence similarities greater than 80%. At this level of relatedness, the similarity between hybridization profiles was strongly correlated with sequence divergence in the gyrB gene. Results revealed that two strains of S. oneidensis (MR-1 and DLM7) were nearly identical, with only 3% of the ORFs hybridizing poorly, in contrast to hybridizations with Shewanella putrefaciens, formerly considered to be the same species as MR-1, in which 63% of the ORFs hybridized poorly (log ratios below -0.75). Genomic hybridizations showed that genes in operons had consistent levels of hybridization across an operon in comparison to a randomly sampled data set, suggesting that similar applications will be informative for identification of horizontally acquired genes. The full value of microbial genomic hybridizations lies in providing the ability to understand and display specific differences between closely related organisms providing a window into understanding microheterogeneity, bacterial speciation, and taxonomic relationships.

I found about 30 different articles on the evolution of ATP, in which the evolution of enzymes for ATP was also discussed. The oldest was published twelve years ago.

[ June 11, 2002, 09:27 AM: Message edited by: Administrator ]

 

[Administrator2]

HELEN
Galatian, Hall’s work, as described in Evolution on a Petri Dish, from the quotes you have given, and the way you describe it, involved intelligently knocking out one function, keeping the E.coli in optimal living conditions, and then seeing the function be restored via another pathway internally.

At the very least, this tells me that E.coli were designed well enough that they were able to establish alternate metabolic pathways in a pinch to keep themselves going.

Now, if you would care to explain how, in totally natural conditions, like, say, an animal’s gut, E.coli is going to have a pathway knocked out in the first place? Or be in optimal conditions to try to survive?

In short, as this seems to be the only example you have (you have been using it for about four years now), might I suggest that it is not nearly sufficient to show what it is you are wanting it to show? The E.coli is still E.coli. The change evidently did not stay among the E.coli. Both of these results are exactly what would be predicted by the various groups opposed to evolution. And that is because that is what we see continually: basic type is maintained (biological stasis), and in the wild, there is a reversion to wild type, with mutations and variations simply varying around a mean and never heading anywhere by building on top of one another to produce a new type.

And yes, there has been a great deal written about the cilia and flagellum. That is not the point. The point is that the ONLY paper even approaching the possibility of them arising evolutionarily was published the SAME year as Behe’s book, in another language in Europe! Therefore he was right in saying the scientific literature was barren of explanations for the evolutionary process. It was simply taken for granted.

Ken Miller has attempted to show how the flagellum can arise by a series of purely natural processes. His attempt uses impossible protein transfers which somehow stay through how many generations? And then as if that isn’t enough imagination, it turns out the entire scenario is simply a ‘what if’ story with no basis on scientific fact whatsoever. “Theoretical work suggests” is also not enough to show anything actually happened, only that a man can imagine it happening!

Nor is there ANY DATA showing how a more ‘primitive’ means of cellular locomotion is related to cilia or flagellum development.
Your quote involving cell shape does show one interesting point I have made a number of times, though, and that is that the genome does NOT carry all the information regarding cell replication. So a change in the genome itself (mutation) is not enough to even change the shape of your B.bufgdorferi.

Now, about “design”. The opposite is “undesigned.” Are you saying the world is not designed?

Design involves plan. Man is stuck with needing to design sequentially. God is not. This is where your straw man of God not being a designer falls flat. God is God. The plan, or design for the world and humanity did not need step by step incubation in His mind! He invented time! So He is not subject to it.

When we refer to God as the Intelligent Designer (which we do if we are Christian, although the Intelligent Designer may have another identity to someone else), we are not saying God needed to be involved in a mental step-by-step process. We are saying that the world shows evidence of design, intentional, intelligent design. We do know from Genesis that it was created via a step-by-step process, so this would also indicate a grand Design in the mind of God. Therefore it is no insult to God to credit Him with the marvelous beauty, complexity, and interrelationships we see in creation.

 

[Administrator2]

[Administrator: this includes two emails from Galatian arriving in the same group]

THE GALATIAN

Helen:

Galatian, Hall’s work, as described in Evolution on a Petri Dish, from the quotes you have given, and the way you describe it, involved intelligently knocking out one function, keeping the E.coli in optimal living conditions, and then seeing the function be restored via another pathway internally.

Well, you need to remember that Hall never actually "knocked" out anything. He merely found a mutant that had lost the ability to metabolize one particular substance. Having done that, he then simply cultured it in the usual manner, in the presence of that substance.

If he had stupidly done this, would it then count? What if that mutation was never noticed by anyone, and the new pathway evolved. How would that be different? These are certainly good issues you've brought up here, and deserve some discussion.

At the very least, this tells me that E.coli were designed well enough that they were able to establish alternate metabolic pathways in a pinch to keep themselves going.

Although (as you know), I object to the use of "design" because I think it's disrespectful to God, I'm inclined to agree with you that God certainly created living things with an ability to evolve new features in such events. We differ primarily in how far back we think God's creation incorporated such wonders.

Now, if you would care to explain how, in totally natural conditions, like, say, an animal’s gut, E.coli is going to have a pathway knocked out in the first place? Or be in optimal conditions to try to survive?

Good questions. There's really only one way to lose such a function. A mutation damages the system in such a way that it no longer functions. The reason E. Coli would survive such a mutation is that it does not depend on any one particular substrate for an energy source. Hence it would survive quite readily. What Hall did was put the bacterium in an environment with a good amount of that substrate. Hence, any bacterium gaining the ability to metabolize it again would be at a considerable advantage.

In short, as this seems to be the only example you have (you have been using it for about four years now),

I found out about it last year, I think. It's certainly a great one, though. How often do you actually get to be there when an irreducibly complex system evolves?

might I suggest that it is not nearly sufficient to show what it is you are wanting it to show? The E.coli is still E.coli.

Of course you're right; it is. The good part is that it’s an E. Coli with a new, irreducibly complex metabolic pathway.

The change evidently did not stay among the E.coli. Both of these results are exactly what would be predicted by the various groups opposed to evolution.

Heck, even evolutionists like Behe said that it was impossible. But there it is.

I'll pick up on the question of "design" as an attribute of creation later.

* * *

And yes, there has been a great deal written about the cilia and flagellum. That is not the point. The point is that the ONLY paper even approaching the possibility of them arising evolutionarily was published the SAME year as Behe’s book, in another language in Europe! Therefore he was right in saying the scientific literature was barren of explanations for the evolutionary process. It was simply taken for granted.

I think it was an understandable oversight. I'm just making the point that the literature has many papers on the evolution of cellular structures.

Ken Miller has attempted to show how the flagellum can arise by a series of purely natural processes. His attempt uses impossible protein transfers which somehow stay through how many generations? And then as if that isn’t enough imagination, it turns out the entire scenario is simply a ‘what if’ story with no basis on scientific fact whatsoever. “Theoretical work suggests” is also not enough to show anything actually happened, only that a man can imagine it happening!

The fact that we see those "flagella proteins" showing up in simpler moving structures, and that the simplest flagellum would be no more than a single molecule rotating in the cell membrane (of which there are many) is merely evidence that the flagellum could have evolved. We may never know precisely how. But what we don't know for sure is a shaky foundation.

Your quote involving cell shape does show one interesting point I have made a number of times, though, and that is that the genome does NOT carry all the information regarding cell replication.

Yes. We know, for example, that the mitochondria, chloroplasts, and other organelles have their own DNA, which is more like bacterial DNA than that of eukaryotes . So that is technically not our genome, even though the information therein is essential to the survival of almost every eukaryotic cell. It's the best evidence that eukaryotes evolved from prokayotes by endosymbiosis.

Do you have any other examples?

So a change in the genome itself (mutation) is not enough to even change the shape of your B.bufgdorferi.

It isn't, that's also true. Form in living things is an interaction between genes and the environment. Have you had time to read "On Growth and Form"? D'Arcy Thompson shows that much of the form of living things can be shown to be due to physical forces of the environment. He also shows how the complex "designs" of bee combs and termite mounds can be accomplished by very simple rules for each insect's behavior.

Now, about “design”. The opposite is “undesigned.” Are you saying the world is not designed?

Looks created to me. The reason Paley had to chose a watch in his paper asserting design, was that if he had chosen a created object, no one would conclude it was designed.

Design involves plan. Man is stuck with needing to design sequentially. God is not. This is where your straw man of God not being a designer falls flat. God is God. The plan, or design for the world and humanity did not need step by step incubation in His mind! He invented time! So He is not subject to it.

If we redefine "design" to exclude planning, then we are no longer insulting God. So, If that's how you define it, then I have no compliant. After all, we say that a man's painting is his "creation", and that probably also is an affront to the creator, unless we redefine "creation". I can see your point, but I think I'll leave "creation " for God's way, and "design" for the things creatures do.

When we refer to God as the Intelligent Designer (which we do if we are Christian, although the Intelligent Designer may have another identity to someone else), we are not saying God needed to be involved in a mental step-by-step process. We are saying that the world shows evidence of design, intentional, intelligent design. We do know from Genesis that it was created via a step-by-step process, so this would also indicate a grand Design in the mind of God.

I think any Christian, including theistic evolutionists would agree with you, if you define "design" as you have earlier. It is that "grand design" by which God created everything in one stroke, from which that "stepwise" creation came about.

Hence, you are right, I think, in asserting that God had already provided the means by which E. Coli evolved a new metabolic pathway. The very fabric of living things contains the ability to adapt to environments. I know that you don't think of it that way, but it's really just a different aspect of the same creation.

Therefore it is no insult to God to credit Him with the marvelous beauty, complexity, and interrelationships we see in creation.

On that, we can agree. It's always a challenge talking to you, Helen. But it's always a pleasure. Thanks for the input.

 

[Administrator2]

JOHN PAUL

John Paul: Nelson’s reply discusses ATP synthase. He ends it with this,
“Like the many IC systems Behe discusses, there seems to be nothing in the literature about the Darwinian evolution of the ATP synthase.”

galatian:
Actually, that's wrong. Here's one.

John Paul:
How did I know that you were going to ignore the pertinent part of the post and instead divert attention away from your unsubstantiated claims? By doing so it would appear that you are abandoning Miller’s premise that Hall’s experiments show that IC can evolve.

BTW, according to Hall we are seeing adaptive mutations in his experiments. Something the modern synthesis (or neo-Darwinism if you prefer) states can’t happen, but what Dr. Spetners non-random evolutionary hypothesis relies on.

Proc. Natl. Acad. Sci. USA. 2001 August 14; 98 (17): 9853-9858
DNA/DNA hybridization to microarrays reveals gene-specific differences between closely related microbial genomes .
E. Murray, D. Lies, G. Li, K. Nealson, J. Zhou, and J. M. Tiedje

John Paul:
The full article can be read here:

http://www.pnas.org/

Click on the Search feature.

Once there enter 171178898 in the box for the DOI:10.10733/pnas. search selection. You can also enter the authors in the appropriate boxes.

What will be clear to anyone reading this is it is not a paper on the Darwinian evolution of the ATP synthase.

One more thing to clear up- Behe’s book Darwin’s Black Box was published in 1996. From the book:

The general professional literature on the bacterial flagellum is about as rich as the literature on the cilium, with thousands of papers published on the subject over the years. That isn’t surprising; the flagellum is a fascinating biophysical system, and flagellated bacteria are medically important. Yet, here again, thew evolutionary literature is totally missing.

galatian:
A quick look found these:
(a quote from the report, not the abstract)

Envelope structure of Synechococcus sp. WH8113, a nonflagellated swimming cyanobacterium
Aravinthan DT. Samuel, Jennifer D. Petersen, and Thomas S. ReeseBMC Microbiol. 2001; 1(1): 4

Molecular Characterization of fliD Gene Encoding Flagellar Cap and Its Expression among Clostridium difficile Isolates from Different Serogroups
Albert Tasteyre, Tuomo Karjalainen, Véronique Avesani, Michel Delmée, Anne Collignon, Pierre Bourlioux, and Marie-Claude BarcJ Clin Microbiol. 2001 March; 39(3): 11781183

Borrelia burgdorferi periplasmic flagella have both skeletal and motility functions
Mohammed Abdul Motaleb, Linda Corum, James L. Bono, Abdallah F. Elias, Patricia Rosa, D. Scott Samuels, and Nyles W. Charon
Proc. Natl. Acad. Sci. USA. 2000 September 26; 97(20): 1089910904 ; published online before print September 19, 2000.

John Paul:
Now as far as I know, 2000 & 2001 are after 1996. All the galatian has done was to show that it appears scientists are taking up the challenge. That is if these articles really do discuss the evolution of the flagella. Let’s take a look:

The first article, which can be read here:

http://www.biomedcentral.com/1471-2180/1/4

The authors discuss the motile mechanism for Synechococcus sp. WH8113:

Conclusion

The envelope structure of Synechococcus sp. WH8113 provides new constraints on its motile mechanism. The spicules are well positioned to transduce energy at the cell membrane into mechanical work at the cell surface. One model is that an unidentified motor embedded in the cell membrane utilizes the spicules as oars to generate a traveling wave external to the surface layer in the manner of ciliated eukaryotes.

And finally:

Conclusions

The organelle that drives the motility of swimming cyanobacteria has not yet been identified. The spicules identified here could comprise part of the motility apparatus as they extend to both the site of energy transduction (the cell membrane) and the site of mechanical work (external to the surface layer). In any case, our elucidation of the surface structure (summarized in Fig. 5) provides new constraints on theoretical models for motility.

However flagella is mentioned:

In the absence of flagella, the cell surface of Synechococcus sp. WH8113 must generate thrust.

(bold added)

Behe’s challenge was not met by the first article.

The second article can be found here:

http://jcm.asm.org/cgi/content/full/39/3/1178

It basically says that flagellated & non-flagellated bacteria have the Genes fliC & fliD. Although similar they aren’t exact copies.

To gain insights into why certain strains are nonflagellated, we investigated the transcription of the fliD gene by detection of cap protein mRNA by RT-PCR in the nonflagellated strains. Nonflagellated strain EX560, the fliD gene of which was not amplified by PCR, was not studied. The results show that a single 1,524-bp product was obtained in all nonflagellated C. difficile strains (Fig. 2). Thus nonflagellation is not a result of the absence of transcription of the fliD gene.

(bold added)

a little more from the article:

A bacterial flagellum consists of a basal body in the membrane, the hook, and a helicoidal filament. The major structural component of the filament, the flagellin FliC, is assembled in subunits. Proteins called hook-associated proteins (HAP1, HAP2, and HAP3) are required to join the filament to the hook and to cap the distal tip of the filament. The fliD gene encodes HAP2, which functions as a capping structure at the distal end of the filament. It has been shown to have a function in mucin attachment by P. aeruginosa (1, 3), and H. pylori (18) and virulence in P. mirabilis (22).
We are interested in finding out whether flagella play a role in C. difficile intestinal attachment. Earlier studies from our laboratory have allowed characterization of the 39-kDa flagellin protein. The flagellin gene (fliC) was cloned and sequenced, and the recombinant protein was characterized (31). The diversity of the fliC gene among different isolates was studied, and it was found that the gene is present and expressed in both flagellated and nonflagellated strains (32).

And as you can see the purpose of the article was not to demonstrate how the flagella evolved, just what its possible role is in a certain scenario. It does show that there is interest in the flagella, but Behe wasn’t disputing that.

I am not so sure the last article states what the galatian thinks it does it reference to the evolution of the bacterial flagelum. To read the last article just go to the PNAS search linked to above, enter the first two author’s names as shown plus the first four words of the title and you should get the article. Or enter the DOI number 200221797 .

The link I see in the last article is that the internal periplasmic flagella (allegedly) evolved into the external motility mechanism we are discussing. However upon further investigation I found the following which pretty much wipes out any hope of this organisms’ periplasmic flagella evolving into the flagella we are discussing:

http://www.hsc.wvu.edu/micro/faculty/charon.htm

Our current focus is on Borrelia burgdorferi, which causes Lyme disease, and Serpulina hyodysenteriae, which causes swine dysentery. With respect to B. burgdorferi, we have taken two separate approaches. First, we characterized in depth their swimming behavior using light microscopy, and with high voltage electron- microscopy, their structure. We found that these organisms swim using backward propagating flat waves, much like the waves found in eukaryotic cells such as sperm. In addition, the electron microscopic analysis allowed us to determine the position of the periplasmic flagella within the cell, and the function that structures play in cell motility. The studies allowed us to develop a detailed model of how these organisms swim as a consequence of the rotation of their internal periplasmic flagella.

Our second approach has been to concentrate on the genetics of B. burgdorferi motility. We have identified and characterized most of the genes involved in motility and chemotaxis. These genes involve four clusters comprising 5 different operons; one very large operon consisted of 26 genes. Suprisingly, all the promoters from the five operons were sigma 70-like. This is in marked contrast to what is found in other bacteria. Most bacteria have a hierarchical control of flagellar synthesis involving specific factors such as sigma 28 which become active at different phases of flagellar assembly. The basis for this difference could be related to the biology of these bacterial species. Perhaps motility and chemotaxis are so vital to Borrelia burgdorferi that it has evolved a unique control mechanism for flagellar synthesis. Our future goals are to construct allelic exchange mutations in specific chemotaxis and motility genes, and to analyze the role of motility in the development of Lyme disease.

(bold added)

It can be seen these articles do not say what Galatian claims they say.

 

[Administrator2]

SCOTT PAGE

A creationist writes:

BTW, according to Hall we are seeing adaptive mutations in his experiments. Something the modern synthesis (or neo-Darwinism if you prefer) states can’t happen, but what Dr. Spetners non-random evolutionary hypothesis relies on.

Is that the same Hall that co-authored this (emphasis mine):

Genetics 2002 Mar;160(3):823-32

Predicting Evolutionary Potential. In vitro evolution accurately reproduces natural evolution of the tem beta-lactamase.

Barlow M, Hall BG.

Biology Department, University of Rochester, Rochester, New York 14627-0211.

To evaluate the validity of our in vitro evolution method as a model for natural evolutionary processes, the TEM-1 beta-lactamase gene was evolved in vitro and was selected for increased resistance to cefotaxime, cefuroxime, ceftazadime, and aztreonam, i.e., the "extended-spectrum" phenotype. The amino acid substitutions recovered in 10 independent in vitro evolvants were compared with the amino acid substitutions in the naturally occurring extended-spectrum TEM alleles. Of the nine substitutions that have arisen multiple times in naturally occurring extended-spectrum TEM alleles, seven were recovered multiple times in vitro. We take this result as evidence that our in vitro evolution technique accurately mimics natural evolution and can therefore be used to predict the results of natural evolutionary processes. Additionally, our results predict that a phenotype not yet observed among TEM beta-lactamases in nature-resistance to cefepime-is likely to arise in nature.

Or maybe this one:

: J Bacteriol 1999 Feb;181(4):1149-55

Spectra of spontaneous growth-dependent and adaptive mutations at ebgR.

Hall BG.

University of Rochester, Rochester, New York.

A comparison of the spectra of spontaneous growth-dependent and adaptive mutations in ebgR shows that both spectra are dominated by insertion sequence (IS)-mediated mutations. The difference between growth-dependent mutations (61% IS mediated) and adaptive mutations (80% IS mediated) is highly significant (P < 0.0001). In contrast, the spectra of growth-dependent and adaptive non-IS-mediated mutations do not differ from each other and therefore do not provide support for the hypothesis that adaptive and growth-dependent mutations arise by substantially different mechanisms.

As for Spetner's 'hypothesis', have any creationists been able to find any documentation at all describing anything similar to what Spetner requires in multicellular eukaryotes? That is, where are the before-and-after genetic analyses that demonstrate the changes that would be needed

 

[Administrator2]

JOHN PAUL

Does Hall’s experiment(s) involving E. coli really show that IC can evolve? According to Dr. Behe the answer is a resounding “No”!

The following can be read in its entirety at the following URLs:

http://www.iscid.org/papers/Behe_ReplyToCritics_121201.pdf

and

http://www.arn.org/docs/behe/mb_trueacidtest.htm

Dr. Behe:
When I first read this section of Miller’s book I was quite impressed by the prospect that actual experiments-not theoretical, “just-so” stories- had produced a genuine, non-trivial counterexample to irreducible complexity. After going back to read Professor Hall’s publications, however, I found that the situation was considerably different. Not only were Hall’s results not what I expected based on Miller’s description, in fact they fit most naturally within a framework of irreducible complexity and intelligent design. The same work that Miller points to as an example of Darwinian prowess I would cite as showing the limits of Darwinism and the need for design.

John Paul:
From this it is obvious that Dr. Behe really wants scientists to take up his challenge. He is as sick of “just-so” stories as the rest of us who, for good reasons, doubt the grand sweep of the ToE.

C. Adaptive Mutation

Dr. Behe:
So what did Barry Hall actually do? To study bacterial evolution in the laboratory, in the mid 1970's Hall produced a strain of E. coli in which the gene for just the beta -galactosidase of the lac operon was deleted. He later wrote:

John Paul:
If, as Behe states, Hall produced that strain with the lac operon deleted, that would be a sign of intelligent intervention (yes even if it was done stupidly). Can anyone link us to Hall’s original paper(s) so we can see if he says how this strain was produced (naturally or with his intervention)?

All of the other functions for lactose metabolism, including lactose permease and the pathways for metabolism of glucose and galactose, the products of lactose hydrolysis, remain intact, thus re-acquisition of lactose utilization requires only the evolution of a new beta -galactosidase function. (Hall 1999)

Thus, contrary to Miller’s own criterion for “a true acid test,” a multipart system was not “wiped out” - only one component of a multipart system was deleted.

John Paul:
Well maybe the deletion of that one component led to the multi-part system’s not functioning correctly (or at all) but that just shows that all the components need to be in place for that multi-part system to function correctly. IOW, if you have an apparent irreducibly complex multi-part system you have to demonstrate how each of those parts arose and then how they came together to form that multi-part system, before you can say the apparent IC of that system is illusory. As anyone can see Hall’s experiment(s) did not do this.

as Hall later wrote:

Adaptive mutations are mutations that occur in non-dividing or slowly dividing cells during prolonged non lethal selection, and that appear to be specific to the challenge of the selection in the sense that the only mutations that arise are those that provide a growth advantage to the cell. The issue of the specificity has been controversial because it violates our most basic assumptions about the randomness of mutations with respect to their effect on the cell. (Hall 1997)

Dr. Behe:
The mechanism(s) of adaptive mutation are currently unknown. While they are being sorted out, it is misleading to cite results of processes which “violate our most basic assumptions about the randomness of mutations” to argue for Darwinian evolution, as Miller does.

John Paul:
Heck I say bring on all the evidence for adaptive mutations that you can. I am sure Dr. Spetner would appreciate it. It does show how far evolutionists will go to try to refute IC, even including experiments that could show their premise of only random mutations leading to diversity to be questionable.

 

[Administrator2]

JOHN PAUL

BTW, according to Hall we are seeing adaptive mutations in his experiments. Something the modern synthesis (or neo-Darwinism if you prefer) states can’t happen, but what Dr. Spetners non-random evolutionary hypothesis relies on.

Scott page:
Is that the same Hall that co-authored this (emphasis mine):

Genetics 2002 Mar;160(3):823-32

Predicting Evolutionary Potential. In vitro evolution accurately reproduces natural evolution of the tem beta-lactamase.

Barlow M, Hall BG.

Biology Department, University of Rochester, Rochester, New York 14627-0211.

(please refer to Scott Page’s post for a clip of the above paper)

John Paul:
Most likely the same guy. No one has said adaptive (or directed) mutations are not natural. They are natural they just aren’t random. Was there a point to citing this article?

AIG discusses the article here:

http://www.answersingenesis.org/docs2002/0408lab_evolution.asp

Or maybe this one:

: J Bacteriol 1999 Feb;181(4):1149-55

Spectra of spontaneous growth-dependent and adaptive mutations at ebgR.

Hall BG.

University of Rochester, Rochester, New York.

(please refer to Scott Page’s post for a clip of the above paper)

John Paul:
Again most likely the same guy. And again the debate is random vs. non-random, not adaptive vs. growth-dependent or adaptive vs. natural.

If you are going to post stuff like this it may be a good idea to state the relevance of the material and even post the URL so we can read the whole article without having to search for it. If you are getting this stuff off the internet you are at the website anyway so just give us the link.

Scott Page:
As for Spetner's 'hypothesis', have any creationists been able to find any documentation at all describing anything similar to what Spetner requires in multicellular eukaryotes? That is, where are the before-and-after genetic analyses that demonstrate the changes that would be needed

John Paul:

From Merriam-Webster’s collegiate dictionary ( http://www.m-w.com/ ). NOTE: Definitions for all main words used (ie Hypothesis, Theory and Law) can also be found there be entering the respective word in the proper box or by going to the hypothesis definition and clicking on them.

Main Entry: hy·poth·e·sis Pronunciation: hI-'pä-th&-s&sFunction: nounInflected Form(s): plural hy·poth·e·ses /-"sEz/Etymology: Greek, from hypotithenai to put under, suppose, from hypo- + tithenai to put -- more at DODate: circa 16561 a : an assumption or concession made for the sake of argument b : an interpretation of a practical situation or condition taken as the ground for action2 : a tentative assumption made in order to draw out and test its logical or empirical consequences3 : the antecedent clause of a conditional statementsynonyms HYPOTHESIS, THEORY, LAW mean a formula derived by inference from scientific data that explains a principle operating in nature. HYPOTHESIS implies insufficient evidence to provide more than a tentative explanation <a hypothesis explaining the extinction of the dinosaurs>. THEORY implies a greater range of evidence and greater likelihood of truth <the theory of evolution>. LAW implies a statement of order and relation in nature that has been found to be invariable under the same conditions <the law of gravitation>.

Grin… If Dr. Spetner’s non-random evolutionary hypothesis had what the evolutionist asks for it would no longer be a hypothesis now would it?

However the theory of evolution is allegedly well beyond the hypothesis stage.

Have any evolutionists been able to find any documentation that random mutations can lead to the vast diversity of life from some genetically unknown single-celled organism that just happened to have the ability to self-replicate? True we know that copying errors occur, but that doesn’t mean they can lead to the grand sweep of evolution required by the ToE. We also know that other mutations occur, but that doesn’t make them random.
Do evolutionists have any evidence, besides our ignorance, that recombination, duplications/ amplifications, insertions, deletions, inversions and transpositions of genetic material are random events?