I've been spending quite a bit of time debunking ID (Intelligent Design) arguments on various other blogs. This blog is for storing some of my longer arguments. I prefer to call ID 'Imagination Deficit' as I feel that better describes it.

Thursday, December 21, 2006

The "Oh no it isn't" argument

I have noticed in one or two of my (now disabled) comments the use of what I call the "Oh no it isn't argument".

As this is the holiday season I thought I would do a little piece on this form of 'argumentation'. What does the holiday season have to do with it, I hear you ask? Well, that's because it's Panto season in the UK (where I grew up). A 'Panto' is a Pantomime - a stage show that's put on for the kids at Christmas where they can go and watch a funny version of a well known fairy tale. A common feature is the comical sidekick to the main hero - usually called Buttons - who is guaranteed to provide two traditional Pantomime moments. The first is when something scary (a bear is a favorite) is right behind Buttons, and the whole audience shouts "it's behind you!". The second - and more relevent - is when Buttons makes some outrageous statement and the whole audience shouts "Oh no it isn't!" and Buttons replies "Oh yes it is!" (or possibly the other way round!). This back and forth 'argument' can go on for some time, and is great fun for the kids.

It's not often seen outside the Panto or the school playground, and certainly not often seen in arguments around science. The proper form of an adult argument is to actually provide a counter argument with examples or evidence rather than just sitting there shouting "Oh no it isn't!".

So, to provide a good example of this kind of 'argument', let me direct you to this prime example by 'Joe G' over at 'intelligentreasoning' (ironic name).

I posted in an earlier piece a desciption of the kind of story that ID proponents call 'just-so stories'. Joe's 'intelligently reasoned' response (the profanity is all his, sorry):
OD's above explanation would NOT be labeled a 'just-so story' by ID advocates. Like everything else OD says about ID this turd was taken from his arse.
I could sit here and go "Oh yes it is!". It would be in keeping with the jollity of the Christmas season after all... ;)

However, I prefer to demostrate the way an adult 'intelligently reasons' instead. You see, I didn't pick the gene duplication example out of a hat. I picked it because it happens to be a part of a particular evolutionary hypothesis that is indeed frequently labelled a 'just-so story' by ID advocates - the evolution of the bacterial flagellum. If you don't believe me, just type the following into Google and see which hits you get:

bacterial flagellum "just so story"

The results contain most of the major pro-ID blogs. Oh look - evidence.

So this wasn't just a random example. It is exactly this kind of hypothesis that is labelled a 'just-so story' by ID advocates, indeed gene duplication is a major part of what I could call ID's "favorite" so-called evolutionary 'just-so story'.

What we actually see if we look a little closer at the hypothesis for the evolution of the bacterial flagella is a testable, falsifiable scientific hypothesis that generates predictions, and is based on well known mechanisms of evolution that themselves started off as testable, falsifiable scientific hypotheses that generated predictions.

Finally, my line of argument actually gives links to hard evidence and does not just consist of the infantile "Oh yes it is". Although I will make a prediction at this point - that this little lesson will be wasted on the (cough) 'intelligently reasoning' Joe G.

No Comment

I have disabled comments on this blog because I don't have time to moderate them and some contributors were unable to stay on topic. If you trackback to any of my entries I should have time to come and have look at what you said.

Tuesday, July 04, 2006

Just So

One things that the attackers of science (including ID advocates) frequently do is accuse scientists of constructing 'just-so stories'.

This is first of all a deeply ironic claim, given that the ID advocates either are unable to or refuse to identify any candidate for a designer. Therefore the ID 'explanation' for - well - everything is: 'an unknown intelligent designer did it using unknown methods for unspecified reasons at an unknown time'.

The above doesn't even reach the lofty heights of a 'just-so story' because there is absolutely no detail whatsoever. At least Kipling supplied some detail with his stories, even if it was entirely fanciful!

So, let's contrast this contentless, meaningless ID 'explanation' with some examples of the kinds of evolutionary narratives that the ID advocates claim are 'just-so stories', and see if we can spot any differences.

I'm going to use gene duplication as my example. I'm not going to reference any scientific journals whatsoever in this section.

'Just-so story'

A scientist while investigating a bacterial genome discovered that two genes doing apparently different tasks were almost identical in sequence, only differing by a few base pairs. This was a very interesting discovery, and the scientist decided to investigate a bit further. The first thing he did was to sit down and think about ways in which this related genes could have been produced. He came up with a few explanations, but the one he thought was the most likely was that the original gene had been copied (duplicated) in it's entirety, and then one of the copies had been changed by point mutations until was performing a different task to the original.

(The above explanation is typically labelled a 'just-so story' by ID advocates. We have some evidence. The scientist has constructed a explanation to account for it. There is no other evidence at this point that the explanation is correct. Science typically refers to these kinds of explanations as 'hypotheses', and they are acknowledged to be entirely tentative in nature.)

Having come up with a perfectly reasonable explanation for the origin of these two very similar genes what does the scientists do next? Does he drop the subject having explained it to his satisfaction and then move on to his next project? Actually he doesn't. He decides that this hypothesis needs testing to see if it actually correct. So the scientist has a think about what predictions he can make from his hypothesis, and how he can therefore design some tests for it.

If this gene duplication has occurred once, the scientist thinks it is likely that similar duplications could have occurred elsewhere in the genome. So finding other related pairs of genes ('homologs') would be additional evidence to strengthen the explanation. There may be multiple duplication events to create a 'family' of related genes, which would provide more evidence. There is a chance that having had a duplication event, one of the copies could lose it's start sequence and become 'redundant', finding these would also provide extra evidence. And of course the best evidence of all would be to have an organism with a fully sequenced genome and to have a duplication event actually happen, so when the genome is examined again later there are now two (or more) copies of a gene where before there was one.

(So the whole point of the scientific hypothesis above is that can be used to create testable predictions. This is why it is not a 'just-so story'. It's a starting place for further investigation. The hypothesis might turn out to be wrong or incomplete.)

The scientist then widens his search and looks for other closely related pairs of genes. And he finds them. And so do other scientists in other organisms. He looks for families of related genes. He finds those too. And so do other scientists. He looks for redundant genes ('pseudogenes'). And finds them. As do other scientists. Other scientists using his research as a basis observe the duplication event occuring. The gene duplication hypothesis moves from being a tentative hypothesis to being a known evolutionary mechanism with multiple strands of overlapping evidence that are fully consistent with each other.

Other scientists use the now known and familiar concept of redundant pseudogenes to form their own hypotheses. One group start with the observation that most mammals have a gene for producing vitamin C and chimps and humans do not have this gene. This group of scientists use the two known (and repeatably tested and confirmed) phenomena of common descent and redundant pseudogenes to predict that the ancestor of chimps and humans once had a functional vitamin C gene and that it has become a redundant pseudogene. They also predict that that the human and chimp redundant pseudogenes will be more closely related to each other (less small point mutations) than the chimps will be with various other ape species. They look for the redundant vitamin C pseudogene in humans and chimps. And they find them. And sequence analysis shows the close relationship exactly as predicted.

So from the first original predictive testable hypothesis we have spawned a whole raft of new experiments, repeatedly tested and confirmed the predictions of the hypothesis and used the new mechanism to drive the next round of scientific hypotheses. Just so.

The real science

Of course at the moment the above is just my condensed version of the kind of events that led to the discovery of gene duplication and redundant pseudogenes. No scientific narrative is ever complete without references to the real science.

A pubmed search on the term "gene duplication" gives more than 3000 references, some of them are below.

Gene families include the hemoglobin/myoglobin family, the immunoglobulin superfamily, the family of seven-membrane-spanning domain proteins, the G-protein family, the serine protease family and the homeobox family.

Observation of gene duplication:

Brown, C. J., K. M. Todd and R. F. Rosenzweig, 1998. Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Molecular Biology and Evolution 15(8): 931-942.

Evolution of duplicate genes:

Hughes, A. L. and R. Friedman, 2003. Parallel evolution by gene duplication in the genomes of two unicellular fungi. Genome Research 13(5): 794-799.

Lynch, M. and J. S. Conery, 2000. The evolutionary fate and consequences of duplicate genes. Science 290: 1151-1155. See also Pennisi, E., 2000. Twinned genes live life in the fast lane. Science 290: 1065-1066.

Ohta, T., 2003. Evolution by gene duplication revisited: differentiation of regulatory elements versus proteins. Genetica 118(2-3): 209-216.

Park, I.-S., C.-H. Lin and C. T. Walsh, 1996. Gain of D-alanyl-D-lactate or D-lactyl-D-alanine synthetase activities in three active-site mutants of the Escherichia coli D-alanyl-D-alanine ligase B. Biochemistry 35: 10464-10471.

Zhang, J., Y.-P. Zhang and H. F. Rosenberg, 2002. Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nature Genetics 30: 411-415. See also: Univ. of Michigan, 2002, How gene duplication helps in adapting to changing environments.

The 'missing' vitamin C gene:

Nishikimi, M., R. Fukuyama, et al. (1994) "Cloning and chromosomal mapping of the human nonfunctional gene for L-gulono-gamma-lactone oxidase, the enzyme for L-ascorbic acid biosynthesis missing in man." Journal of Biological Chemistry 269: 13685-13688.

Ohta, Y. and Nishikimi, M. (1999) "Random nucleotide substitutions in primate nonfunctional gene for L-gulano-gamma-lactone oxidiase, the missing enzyme in L-ascorbind acid biosynthesis." Biochimica et Biophysica Acta 1472: 408-411.

Some more examples of human redundant pseudogenes:

Rouquier, S., A. Blancher, et al. (2000) "The olfactory receptor gene repertoire in primates and mouse: Evidence for reduction of the functional fraction in primates." PNAS 97: 2870-2874.

Haag, F., Koch-Nolte, F. et al. (1994) "Premature stop codons inactivate the RT6 genes of the human and chimpanzee species." Journal of Molecular Biology 243: 537-546.

In conclusion

So the ID claim that evolutionary narratives are 'just-so stories' is patently, demonstrably false. Evolutionary narratives when they are first hypothesised are acknowledged to be tentative and a mere starting point for further investigation. Once the real science has been done, evolutionary narratives themselves can 'evolve' from tentative hypotheses to become tested, known and fully accepted mechanims of evolution. These mechanisms can then be used as the basis for further tentative hypotheses, in the confidence that the mechanisms themselves are well known and repeatedly demonstrated.

Let's finish by once more contrasting this with the ID position. Given that ID is merely a 'inference' of design which is baseless without any detail concerning the designer, the mechanisms of the design, the timeframe of the design or the intentions of the designer, there is literally nothing we can pull out of here in order to make predictions or perform tests. Even Kiplings fantastical Just So Stories are theoretically testable. ID can't even claim that.

Tuesday, June 20, 2006

Responding to Mike Gene

It's always a shame when someone closes an argument without allowing you to respond, as Mike Gene has done to this discussion at Telic Thoughts.

Mike seems to think I've been misrepresenting his arguments. I don't believe I have. But going round and round those claims again is not going to get us very far, so I'm going to stick to the actual claims that Mike is making for the science.

Mike said:

"Fine. You seem unaware of the context where I have been debating this issue for years, and a common argument was that the homology between the TTSS and flagellum suggested that the TTSS predated the flagellum (a point that you will ironically make below). If you think it important to distinguish between “a TTSS” and the TTSS that we observe and study, you should spell out their differences and why they are important."

Actually the point I am making is the same as the one made by Mike himself here (emphasis added by me):

"There is no evidence that anything like the type III system predated the flagellum."

Now, ignoring for a moment Mike's claim that there is no evidence, the key point in this sentence I would like to highlight is 'anything like'. To quote Mike again (same quote as above):

"If you think it important to distinguish between “a TTSS” and the TTSS that we observe and study, you should spell out their differences and why they are important."

Yes, this is vitally important. Because the claim being made by the scientists is that 'something like' the modern TTSS was involved in the evolution of the flagellum. Let's call it a simple, ancestral secretory system. So we have at least three structures we are interested in:

- a simple ancestral TTSS, which was precursor to both the flagellum and eventually the modern TTSS
- the modern flagellum which is probably a precursor to the modern TTSS
- the modern TTSS

And making a clear distinction between the known modern TTSS and the speculation of a simpler precursor system is extremely important to understanding how the evolutionary explanation works.

We revisit this exact point later on in Mike's reply, Mike quotes me as saying (emphaisis added by me here):

"Because, as is mentioned in your paper, "several proteins of the flagellum's basal body are homologous to the secretory machinery of this export system". This is evidence that something like the type III system predated the flagellum. It's not conclusive - but it's still evidence."

To which Mike replied:

"See? You want to claim that the homologies are evidence that “the type III system predated the flagellum,” yet the evolution of the TTSS from the flagellum also accounts for the homologies."

Mike has got my claim wrong. I am claiming that the homologs - certainly some of them - are evidence that something like the type III system predated the flagellum.

Mike is bundling all the homologies into one group. There are multiple homologies between the modern TTSS and the modern flagellum. Some of the homologies suggest a distant ancestor precursor secretory system which is something like the modern one. Others amonst the homologies suggest that the modern flagellum predates the modern TTSS. By overgeneralising and bundling all the homologies into one the disctinction is being lost.

So there is in fact evidence that something like the modern TTSS predates both the flagellum and the modern TTSS. This can be seen from some of the homologies between the two modern systems. Other homologies suggest the order in which the two modern systems have arisen.

"If you think it important to distinguish between “a TTSS” and the TTSS that we observe and study, you should spell out their differences and why they are important."

I hope I have at least partly answered this. Nick Matzke's entire model rests on this distinction.

This next bit is my opinion and has nothing to do with any claims MikeGene may be making (just to make it clear!).

When we are trying to piece together the evolution of a complex structure that probably occurred many millions if not billions of years ago. When we are doing this we are obviously having to hypothesise tentative models. The whole point is that - having coming up with such a hypothesis - we can now test parts of it to see if it actually works. We have a starting point for more investigation. And if - or more likely when - we find some evidence that contradicts this hypothesis (after all, it's extremely tentantive at this stage) then we will be able to revise it, come up with some new predictions from the revised hypothesis and test it again.

And this is exactly how scientific investigations work. It can be that we will never fully model all of the steps in the evolution of the flagellum to our satisfaction, which won't stop us from trying to.

Friday, June 16, 2006

Review of IC Revisited

Review of "IC Revisited"

Mike Gene from the Telic Thoughts blog has an article which revisits Behe’s concept of Irreducible Complexity, or IC. Unfortunately, Mike’s analysis contains quite a few of the conceptual errors we commonly see when ID protagonists are making their arguments. I refer to these errors:

• Presumption of specification
• Only allowing one possible explanation and not a combination of explanations
• Ignoring known mechanisms of evolution

Mike shares these fundamental errors with Dembski. In reviewing Mike’s arguments I will highlight where these errors occur, and why these errors cause his arguments to fail.

So, here we go… I have copied Mike's article out in full (some of the formatting and graphics have been lost I'm afraid), and I have inserted my comments in the relevent places. I have prefixed the start of all my comments with OD:, and they are all in green text.

Irreducible Complexity ReVisited

by Mike Gene

The concept of irreducible complexity (IC), as introduced by biochemist Mike Behe, is often cited as a phenomena with the ability to prove evolution impossible. Unfortunately, the concept of IC cannot shoulder this burden. To appreciate this, let us consider the basic proposal of IC. Behe defined it as follows:

"A single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning."

OD: I agree with the statement that IC cannot prove evolution impossible.

IC describes a system whose function is dependent on the interaction of multiple components, such that the removal of even one component results in the complete loss of function. IC can thus be represented as follows:

A + B + C + D ® F

where A,B,C, and D represent specific components (gene products) and F represents the function that is elicited by the interaction of these four parts. From this observation, it is commonly argued that that F could not possibly evolve, as F requires the presence of all four components. In other words, there would be no selective advantage of having parts A, B, and D compared to an organism having only parts A and B. Why? Because both combinations fail to elicit the function.

The basic flaw in this argument is as follows: While it is true that function F requires components A, B, C, and D to exist, it does not follow therefore that parts A,B,C, and D require function F to exist. And it is this basic flaw that has been exploited by the opponents of ID. There are three basic routes to circumvent the IC obstacle. Yet, while they exploit the inability to prove the impossible, whether they account for general explanations for the evolutionary origin of IC systems is highly doubtful. To see this, let's go back to the original IC formula, yet make one modification and discuss systems in which F is dependent on an IC state. That is, the function can only exist if multiple gene products interact with each other.

OD: This should be fun

1. Original Helping Activity (OHA) Becomes Essential

In this scenario, one envisions a component fortuitously associating with a protein complex that initially serves a non-essential, but helpful activity. But as the organism containing this modified system itself evolves, the originally helpful activity now becomes essential in this new context. Yet this explanation is fatally flawed.

OHA may be a plausible explanation for the modification of an IC system, but it fails to explain the origin of the IC system. For example, we can imagine the following modification:

A + B + C ~D ® F

where A,B, and C are essential for function F and ~D helps to make a more efficient F. D is thus not part of the IC system as F can exist without it. Then, as the organism evolves, this increased efficiency becomes essential to maintain to the newly evolved state, giving:

A + B + C + D ® F

The problem is that this scenario begins with an IC system needing A, B, and C. Thus, for OHA to explain the origin of an IC system, we would need to see the following.


A ® F


A ~B ® F

Then A + B ® F, etc.

But this explanation violates the assumption that F is dependent on an IC state. For example, consider the following molecular machines and their functions (long recognized by molecular biologists):




Translate mRNA to synthesize proteins


Propel bacterial cells

F-ATP Synthase

Convert proton/ion gradient into ATP


Replicate pre-existing DNA

The functions carried out by these machines could no more be carried out by a single gene product than an internal combustion engine could work built from only one part. This is obvious from our study of the functions carried out by these machines, as several subsystems divide up the labor and then integrate to generate the function. Thus, it is no surprise that the entire living world provides not one single example of these functions being carried out by single gene products.

OHA therefore fails completely as an explanation for the origin of IC systems. However, again it may be a useful scenario for explaining how an existing IC system can be modified over time, considering that many IC systems are species specific.

OD: I agree with the contention that OHA alone could not be responsible for the evolution of these so-called IC systems. The most important statement is the last one – OHA can indeed be very useful in helping to explain the modification of so-called IC systems, as we shall see later.

2. Elimination of Function Redundancy

In this scenario, one envisions the original functional state as being complex (involving many gene products) and thus bypasses the fatal flaw of the OHA scenario. However, the complex state originally envisioned is redundantly complex:

A + B + C + D + E + G ® F

where B/E and C/G share the same subfunction. In other words, a loss of B or C or E or G alone still allows for function F to be elicited. Thus, such a system fails the classic definition of IC as provided by Behe. The thinking then is that since B/E and C/G share redundant subfunctions, one member of each two-member family can be lost by mutation. For example, an IC system could then evolve through the loss of components E and G, yeilding:

A + B + C + D ® F.

Thus, an IC system can evolve.

This explanation, however, involves some sleight of hand. While the originally proposed 6-part system does not need all six parts, it still contains an essential IC core. That is, this system still requires a four-part interaction involving A, B/E, C/G, and D to elicit F; IC is simply embedded in the redundant complexity. It is assuming an IC state to explain the origin of IC systems, thus elimination of functional redundancy also fails to explain the origin of the IC system. Like the OHA scenario, however, it may explain how IC systems have been modified since their origin. For example, in using the above scenario, it might explain why one organism carries out function F using components A,B,G, and D and another uses A,E,C, and D, etc. After all, it is not unreasonable to suppose that some originally designed complex systems were redundantly complex. This would buffer these systems against failure and also provide an avenue to front-load evolution. Therefore, if IC harkens back to an originally redundant complexity, this does not damage the IC ® ID inference in one bit.

OD: This arugment suffers from ‘presumption of specification’. Mike’s example is that we start with:

A + B + C + D + E + G ® F

And end up with:

A + B + C + D ® F

However he neglegts the possibility that the original state could have had a different function, so:

A + B + C + D + E + G ® H

Could end up as:

A + B + C + D ® F

And, voila, we could even have produced one ‘irreducibly complex’ system with function F from another one with function H.

This is particualarly relevent to the discussions around Behe’s favorite ‘example’ of IC, the bacterial flagellum. It has been suggested in the past the the flagellum may have come from the TTSS however the latest research suggest that the TTSS (which is supposed to be IC) may well actually be a flagellum missing some parts – i.e. one purported IC system with one function has come from another with a different function.

The argument could be made: “but that’s just made the problem worse, now you have to explain the larger so-called IC predecessor with function H as well!” We’ll get on to that shortly.

3. Cooption of Alternative Function (CAF)

This explanation best exploits the logical flaw in the "IC = evolution is impossible" argument. That is, since the existence of A, B, C, and D need not be F-dependent, CAF simply proposes that A, B, C, and D did indeed exist prior to F, whereby these components performed some alternative, original function.

As such, this is really the only evolutionary explanation that has the potential to explain the origin of an IC system.

OD: I disagree with this contention. Again, more about why later.

Thus, let's take a closer look at it.

This explanation would look as follows:

A + B + C + D ® F
| | | |

where G, H, I, and F are functions that previously employed components A, B, C, and D, respectively. A, B, C, and D could be directly donated into the newly formed IC system if functions G - J become disposable. Or, a gene duplication may occur for each of the gene products, allowing the duplicates to be recruited into the newly formed IC system. Or, gene products A - D could exist and now carry out dual roles in the cell.

While such a scenario provides a working explanation for the origin of the IC system, a serious investigator will want to know if there is reason to think this scenario is relevant to the origin of any particular IC system in question (the mere ability to imagine such scenarios is not evidence that such a scenario happened). Put simply, we need evidence to think this scenario applied.

OD: Certainly.

Back in 1997, Julie Thomas posted an analysis of IC to the talk.origins newsgroup that is relevant here. Thomas describes what is needed when considering component (player) C, but keep in mind the same analysis would apply for A, B, and D:

However, in order for alternative activity to pose a serious challenge to the IC status of actual player C, several things must be demonstrated:

1. Evidence must exist that indicates the similar activity is older. Since this explanation proposes the acquisition of function F after the existence of the similar activity, alternative activity fails as an objection to IC if the similar activity post-dates function F. Put simply, the secondary activity must reflect a more ancient state and not a recent by-product of actual player C's role.

OD: You can add to that logical predecessors to the modern state. If the construction of the modern state requires (just for example) that the parts have to be secreted outside the cell in order to be constructed, then an earlier secretory system becomes a logical predecessor.

2. The similar activity should exist at biologically relevant states. This is important as in vitro evidence can be misleading. For example, if actual player C is a DNA-binding protein, but binds to RNA in the test tube under conditions that are not seen in the cell, the similar activity is biologically suspect and may simply be an artifact of the unnatural in vitro conditions.

OD: This only works if the assumption is made that the conditions in the cell have been the same as now throughout the cell’s several billion years of evolution. That is one hell of an assumption to make and thoroughly unwarranted.

3. Is the alternative activity present in the organism with the IC system in question? Similar activities, detected by in vitro tests using extracts from two very different organisms is of questionable biological relevance since the lineage of the organism with the IC system in question may have never possessed anything like the alternative activity.

OD: Only if the alternative activity is a ‘logical predecessor’ i.e. the new activity depends on it in some way. If the new activity is a complete replacement – and a more efficient one – then evolution predicts that the original activity is more likely to be lost.

4. The similar activity should not be part of another IC system. Otherwise, the argument travels in a circle. For example, single-stranded binding (ssb) proteins are involved in DNA replication and DNA recombination. If one explains away the role of ssb proteins in replication by appealing to recombination, yet explains away the role of ssb proteins in recombination by appealing to replication, we have gotten nowhere and have only the appearance of a refutation of actual player C's role in an IC system.

OD: This is wrong. See earlier example of flagellum ‘degenerating’ to TTSS with different function. While we still have to explain the evolution of the supposedly IC flagellum we now have an extremely good explanation of the evolution of the alledged IC TTSS.

Such analyses will go a long way in resolving IC claims. If the similar activity post-dates player C's role, it fails as an explanation. If it is found only in test tube assays, the explanation is severely weakened. If the similar activity is part of another IC system, the original role may be in question, but some IC role remains.

However, even if a particular system successfully overcomes these obstacles, it is not clear CAF applies. CAF makes an assumption about cell biology than is increasingly untenable, namely that the cell is basically a soup. This soupy aspect of the cell is needed for A, B, C, and D to escape their original functional states in order to fortuitously interact. Yet it is becoming increasingly clear than many machine components are assembled into the complex very quickly after being synthesized and/or targeted to specific sites of assembly. For example, it's becoming more and more clear that certain metabolic enzymes are secured in various places and interact as tightly fitting complexes that directly hand-off product/substrate. Where they are found and how they are arranged is just as important as their existence.

OD: This is taking one or two examples of assembly and extrapolating it into a generalisation that is not correct. While some components in the cell are assembled in place, most are not. And the rest of the cell is filled to bursting with proteins banging into each other millions of times every second, providing effectively endless opportunities for exactly the kind of interactions we are talking about.

This was beautifully illustrated with some mutant work in Drosophila that showed a specific glycolytic isozyme was required for flight, as the existence of another isozyme was not functional due to its mislocation. As one reviewer of this study commented, "The presence of catalytically functional proteins alone is therefore not adequate; they must be properly located."

OD: In that specific scenario, yes. Not for a great many others though. This whole line of argument also begs the question of where the ‘assembly apparatus’ came from. If there is a protein complex that gives the cell an advantage in selection, then anything that aids the construction of that complex will itself be a highly selectable trait.

Therefore, for the CAF scenario to work, the alternative function should not anchor the component-to-be-borrowed and if it does, some cellular change must be invoked to liberate it.
Yet the most basic problem with CAF is its complete reliance on chance. If we return to the originally proposed pathway above, we are asked to believe that while A, B, C, and D have long been shaped by selection to carry out their original alternative functions, a fortuitous interaction among them all would spontaneously emerge a brand new function.

OD: This is a complete misrepresentation of what the co-option explanation is all about. I will again come back to this one later, at the end of this section.

Selection might be invoked to fine-tune and improve this new function, but the bottom line remains in that raw chance is being credited for the creation of a novel function. I explained this elsewhere as follows:

"Co-option is the most commonly cited non-teleological means to generate an IC system. Yet, it is essentially a return to raw coincidence to account for apparent design. The brilliance of Darwin was to minimize the role of chance in apparent design. But once we turn to the co-option explanation, we leave this explanatory appeal behind, as chance reasserts itself into a place of prominence. For it is chance that determines whether the various gene products just happen to come together to form a new functioning system, as selection was previously pruning these gene products in accord with various different functions. If one is to invoke co-option, good supporting evidence is required."

The problem of invoking chance to explain the origin of a new function is quite serious when dealing with IC molecular machines. For these machines to work, their components are usually tightly fitted into a whole through the interactions of their complementary conformations. It would be unlikely for four various proteins, pruned by selection to carry out their original functions, just happened to have sufficient conformational complementarity to assemble into a novel machine with a novel function (which explains why no one has ever observed cooption to spawn a new molecular machine). Unless, of course, certain machines were designed to channel evolution by cooption, meaning that certain cooption events were rigged to occur. And this brings me to another problem I highlighted before:

"But the problems with co-option are deeper. Once we leave the random tweaking of a protein along a linear axis guided by selection and instead appeal the multiple coincidences entailed by different, independent proteins being shaped for various other functions that just happen to coalesce into a brand new system, the role of coincidence itself is brought into question. As I have explained elsewhere, design might also be reflected as a front-loaded state that is likely to find various anticipated solutions. In such cases, IC may serve as the springboard by which one detects design through a front-loaded original state. In other words, IC may have evolved through co-option and RM&NS, but that is not the whole story. The whole story may entail whether the original state was stacked such that a random search was likely to stumble upon a new IC state through shuffling and co-opting what was originally designed. In other words, we may have a situation where evolution was designed to spawn certain IC systems when the conditions were right."

Thus, for CAF to be truly an alternative to ID, we need to modify it as coincidental cooption of alternative functions, CCAF.

There is also the problem of universality found in many large IC cores. CCAF does not predict such universality, but instead predicts various permutations of the core as a consequence of evolving over long periods of time and co-opting any protein that just happens to work. I'll will explain this problem in more detail in another article.

Given the many problems associated with CCAF, we need some rather strong indepenent evidence to ensure that it applies to any system in question. Without such evidence, CCAF functions only to remind us that there are other possible explanations for IC apart from ID. But that's all it can offer.

OD: As promised, another look at co-option. Let’s say that we have a protein A*, that performs function Z, which is a selectable function.

A* ® Z

A chance encounter with protein B* gives a two protein complex that does Z a bit better than A* did alone.

A* + B* ® Z

Over time both A* and B* can slowly change through random mutation, and any mutations that produce a better function of Z are selected for. It may even become irreducibly complex to the point that A* can no longer do the function alone. Note that this is a simple example of ‘linear evolution’ being able to generate IC. It hasn’t generated the IC function F, but it has generated a simple IC version of function Z.

In a separate part of the cell – and possibly millions of years later - proteins D* and K have formed a similar partnership to produce function Y.

D* + K* ® Y

By chance, the gene for protein D* is duplicated and we now have two proteins D* and D** (called homologs - lots more on this later), both of which can form a complex with K. One of these – let’s say the new one – has a small mutation which means that it can now also bind with protein B*, and we have a new complex, with a whole new function X:

A* + B* + D** + K ® X

At some point (possibly millions of years later), protein C* becomes bound into the complex as well, and creates another new function, the legendary F:

A* + B* + C* + D** + K ® F

And the K part is pruned because it is not really required for function F, and it’s removal increases the fitness function of F.

A* + B* + C* + D** ® F

The remaining parts evolve slowly over time, and any improvements are accumulated until we end up with:

A + B + C + D ® F

What this examples shows is that a combination of all three possible explanations above – plus the usual small changes over time - can result in our irreducibly complex flagellum. This assumption – that it must be one explanation or another is a frequent mistake made by ID advocates. This includes Dembski with his explanatory filter which states something must be a product of chance or regularity or design and ignores that it could be a product or two or indeed all three.

Note also that the final result includes NONE of the original components in their original forms. And that groups of components can be co-opted. The evolution of new binding sites on homologs is frequently down to simple point mutations. Proteins can - and do - have multiple binding sites to other proteins.

The above argument clearly demonstrates the fallacy of only allowing one explanation for a phenomenon.

Irreducible Complexity Again

So where do we stand? IC as formulated by Behe does not prove evolution is impossible (it should be pointed out that Behe himself stated this in his book). So what is its utility to the ID theorist?

I think the primary utility of IC is that it helps bring a high resolution focus to any origin event in question. That is, while IC may not make it impossible for evolution to produce something, I think it can be likened to a rate-limiting step in a metabolic pathway. Biochemists often focus on rate-limiting steps, as these steps are the "logjams" of pathways that not only serve to dictate the ultimate speed of the pathway, but also can serve as effective points of regulation. We can think of IC as obstacles for evolution for the following reasons:

a) IC rules out the Darwinian mechanisms that have been most firmly established and observed, change along a linear axis. Consider the examples of the evolution of the giraffe neck, the finch beak, or wing color in moths. None of these examples represent the evolution of IC. A pre-existing neck is lengthened, a pre-existing beak is reshaped, and a pre-existing wing is darkened. Thus, the most intuitive examples of Darwinian selection provide no basis to infer the same explanation for the origin of IC.

OD: There’s the dreaded ‘intuition’ word again. There’s not a lot that is intuitive about evolution, especially the time scales involved. 3.5 billion years is a lot of time.

This is clearly seen from an example found in Richard Dawkins' writings. Dawkins explains how photoreceptor cells (with ninety-one layers of photon-capturing membranes) could have evolved to become more efficient at capturing photons:

"The point is that ninety-one membranes are more effective in stopping photons than ninety, ninety are more effective than eighty-nine, and so on back to one membrane, which is more effective than zero. This is the kind of thing I mean when I say there is a smooth gradient up Mount Improbable. We would be dealing with an abrupt precipice if, say, any number of membranes above forty-five was very effective while any number below forty-five was totally ineffective. Neither common sense nor the evidence leads us to suspect any such hidden discontinuities."

But Dawkins is flat-out wrong in believing there are no such hidden discontinuities, as IC provides one example. In the examples mentioned above, A does not give us 10% function, A+B does not give us 25% function, etc. Instead, removal of A or B or C or D results in complete loss of function, the abrupt precipice.

OD: This is a nice summary of the IC fallacy. We lose function F but may well gain a new function.

All of this means that Dawkins' example of adding membranes to improve photon capture rates does not apply to the origin of IC systems. The most intuitive and well documented examples of Darwinian evolution are rendered irrelevant by IC. This conclusion was also shared by biologists Thornhill and Ussery who, writing in the only paper that discusses IC in the scientific literature, observed that Darwinian evolution along such a linear axis "cannot generate irreducibly complex structures."

b) Because of a), IC critics turn to OHA, EFR, and CCAF. But as we have seen, the first two explanations don't really explain the origin of IC. For example, consider the bacterial flagellum. When you survey any bacterial species, the flagellum is usually composed of 30-40 gene products. But when you compare all bacteria, only 20-25 are universally shared. We can interpret these 20-25 as a core IC system needed for flagellar function.

OHA fails to explain this set since it would have to assume the propulsion could have been originally carried out by one gene product. But we know this is false as a beaker full of any one of these 20-25 gene products in isolation does not elicit even a trace of rotary motion. In fact, it should be increasingly clear after discussing a) that OHA ultimately boils down to a Dawkinsian explanation along a single axis (where helping activity improves the original function). This is further reason for dismissing this explanation.

EFR fails to explain the original set of 20-25 since it actually assumes an even larger initial set that included these 20-25 gene products. Furthermore, there is not the slightest scrap of evidence for thinking the original flagellum was composed of something like 75-100 proteins (a prediction of EFR).

OD: Actually the discovery that the TTSS (about 10 protein parts) is descended from the flagellum (around 50) completely invalidates this argument. There is no reason whatsoever to believe that the flagellum might NOT have had more parts in the past.

However, I should mention that both OHA and ERF may explain the differences seen in the 10-15 flagellar proteins that are not part of the IC core, as some of these proteins are widely distributed in a mosaic pattern (hinting of EFR), while others appear more species specific (hinting of OHA). The utility of OHA and EFR are found in explaining the modification of previously IC systems, not their origin.

OD: As demonstrated above, they can be a part of the explanation for the origin of supposedly IC systems.

CCAF is the only viable evolutionary explanation for the origin of the IC core, yet the rather large size of this core appears to preclude coincidence as a mechanism.

OD: Only if you speculate that all bits got together simultaneously – i.e. at one specific instant of time they spontaneously assembled themselves into a flagellum. Which of course is not what the proposed mechanism is at all. The example ABCD complex above frequently mentions the phrase ‘million of years’, which is not at all the same thing as 'at exactly the same moment'.

Furthermore, there is no evidence that the various components of the core existed prior to the flagellum.

OD: Actually there is. The parts of the flagellum have to be secreted outside the cell in order for the flagellum to be constructed. So it is logical to conclude that some kind of primitive secretory system must at least have been present in the cell, and said secretory system makes an excellent candidate for a precursor to a flagellum because it could also help in the assembly of the flagellum – the secreted parts would be in the right place to start with.

Nevertheless, this is a commonly invoked explanation in cyberspace, propped up by the finding that many components of the type III protein secretion system share similarity with flagellar components. Yet this appeal fails Thomas' tests mentioned above, given that the evidence indicates the type III system evolved from the flagellum. Thus, the core 20-25 flagellar components remain intact (not to mention that the type III system itself is quite IC and without an evolutionary explanation if we reject its flagellar origin).

OD: Which doesn’t preclude the possibility of another – probably simpler - secretory system being a precursor to both the flagellum and the TTSS.

While IC may not have proven it is impossible to evolve a flagellum (our example), it does present an obstacle to evolution that can only be overcome by coincidental cooption of alternative functions, an explanation without evidential support and plagued with problems.

OD: No it doesn’t present an obstacle, because the arguments being used are not correct.

When we consider that the flagellum is a sophisticated molecular machine, whose appearance coincides with the appearance of bacteria, ID remains a very reasonable explanation for its origin.

OD: Whether ID is a reasonable explanation for anything at all is a topic for another day.

Types of IC

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.

OD: This is a very artificial distinction. Metabolic pathways do still require physical contact, they just don’t require that the parts are touching each other at all times.

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.

OD: The orginal function may be lost, but there could still be function. Look at your own ‘TTSS from flagellum’ statement above.

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.

OD: And it’s perfectly normal to see the protein parts of the flagellum – or their homologs – being used elsewhere in the cell as well. Again, the TTSS is a shining example.

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.

OD: Same statement as above. You’re not correct.

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.

OD: There is a very well known phenomenon known as ‘gene duplication’. It’s a very common – and potentially very powerful – mutation. It happens when a piece of DNA is copied twice by accident, and if it happens when copying a working gene then there can be two working copies of the gene present in the cell. These are called homologs. Only one homologous gene is required to maintain the function described above, the other homolog is ‘free to receive’ mutations.

So the argument above is bogus – as there is no constraint whatsoever on the second homolog.

It should be noted that there are only a couple of proteins of all the ones that make up the bacterial flagellum that have NOT had homologs found for them so far. This serves to demonstrate just how common a phenomenon gene duplication is. There is stacks of evidence for gene duplication, including many experiments where gene duplication has been observed to happen.

I should mention that many metabolic pathways do involve direct communication between proteins. As a result, a product from one enzyme is directly channeled into the active site of another protein. And it appears that the physical contacts between the two proteins may form these channels, such that the product never sees the aqueous state. But such a hookup is different from the molecular machine, as these metabolons (as they are called) work in increase the efficiency of the reaction. We know this because a test tube full of freely diffusing proteins can still carry out the reaction. A molecular machine, in contrast, does not function if its components are freely diffusing about a test tube. For example, ribosomes only function after assembly has occurred. It's the assembly-dependent nature of the machine's function that makes it different from metabolons.

OD: All of which has no bearing on homologs whatsoever.

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.

OD: Only if you ignore one of the most prevalent and powerful ‘tools’ of evolution, that of gene duplication. If you take into account all the homologous proteins that are floating around in a bacterium at any particular time, then the evidence for the evolution of metabolic pathways is also extremely strong evidence for the evolution of so-called ‘IC machines’.

Nevertheless, the origin of metabolic pathways remains an interesting question. The explanations above assume the modification of pathways or the creation of new pathways that are really latent in any cell simply as a function of the potential for hooking up new sequences. But there is the thorny question of the minimal number of metabolic pathways required to sustain cellular life and the minimal number of enzymes in those pathways. This minimal set may indeed represent an IC state where the function is Life. Where did it come from?

OD: There’s a whole field of study called abiogenesis dedicated to answering these very questions. We may never know for sure, after all most of it happened billions of years ago.

Non-teleological appeals to chance to explain their origin would be quite unconvincing (Behe outlined several problems with traditional explanations for the origin of metabolic pathways). And finally, there are the metabolons. There is decent circumstantial evidence that many are quite ancient (pointing again to the sophistication of the original life forms). What if it is the case for some metabolons, especially core ones, that the efficiency brought about by channeling is indeed essential to support cellular life? An ID theorist might want to look for ways to disrupt structural contacts without affecting catalytic ability to see if such dispersal is lethal or produces a cell unlikely to survive out of the lab. If this is the case, the IC nature of metabolons may join the molecular machines as a serious problem for non-teleologists.

OD: I still haven’t spotted any serious problems yet. There is nothing about the models that have been proposed so far for the evolution of the flagellum that is even improbable. All of the mechanisms proposed have been observed happening is similar fashion in bacteria before. Most of the components of the flagellum have already had homologs found in the cell. Pretty much all of the building blocks are there. Using a primitive secretory system as a starting point is logical. There is also nothing particularly challenging about evolving a secretory system, in fact most bacteria already have two or more different varieties of secretory system. There are a number of different varieties of flagella out there as well.


Hordes of IC critics have appeared since Behe published his book. A few books, many review papers, dozens of web pages and thousands of forum messages have dissected Behe's concept in every way imaginable. Yet despite all this effort, the non-teleological payoff has been meager. They have successfully prevented IC from being used as a proof of the impossibility of evolution. But that's about as far as they have gotten.

OD: We have completely debunked Behe’s IC theory. The payoff was watching Behe admit under oath that ID is more plausible if you’re religious, and that ID is as scientific as astrology, both of which were priceless. We have also enjoyed finding out that IC is meaningless as a criticism of evolution, and is also purely a negative argument against evolution and - even if true (which it isn't) - is still not evidence for design.

Because of IC, they have lost the most powerful Darwinian mechanism (change along a single axis) and must appeal to indirect explanations, two of which likewise fail to explain the origin of IC, leaving only one mechanism which turns out to be an appeal to raw chance.

OD: Why should change along a single axis be the ‘most powerful’ mechanism? It may be the most likely, but I think it's very debatable that it is the 'most powerful'.

There is also never any appeal to ‘raw chance’ alone in evolution. Evolution is a combination of chance mechanisms (random mutation) and the exact opposite (natural selection). Natural selection is by it’s very definition a chance altering mechansim – beneficial mutations have a greater chance of being spread than deleterious ones. Evolution also requires a very large amount of time. We have over three billion years of that.

For example, because of IC analyses, we now know that the bacterial flagellum is a sophisticated molecular machine without any fingerprint of it having a Darwinian origin.

OD: Apart from all those homologs already in the cell. And the fact that the TTSS shares a number of components with the flagellum. And the fact that there is nothing in the ‘design’ of a flagellum that could not be accounted for by well known, repeatably tested evolutionary mechanisms.

Those who still insist on Darwinian explanations for the origin of such a system are drawing upon their expectations that all biotic features have a Darwinian origin. They are free to expect this, but they err in demanding others to think as they do.

OD: Those that state that evolutionary explanations for the origin of such a system are ‘unlikely’ are not drawing on the full resources available to evolution.

They are ignoring the fact that evolution can use a combination of techniques to achieve a result.

They are making a false presumption of specification by drawing a target on a wall around the arrow after it has been fired, whereas evolution doesn’t even have a target.

They are ignoring some of the most powerful evolutionary mechanisms.

And they are assigning low probability thresholds based on faulty reasoning.