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Molecular Clues of Teleology

January 12, 2012

Molecular Clues of Teleology

Previously, I mentioned a testable prediction the front-loading hypothesis makes. I said that:

Importantly, the front-loading hypothesis predicts that these homologs of protein components in important molecular machines will be more conserved in sequence identity than the average prokaryotic protein.” (Consider reading my previous post so that this post might be more intelligible.)

Well, I decided to tentatively test this prediction made by the front-loading hypothesis, using a small dataset consisting of only two important eukaryotic proteins: tubulin and actin. The former protein consists of more than one chain, so I only focused on the beta chain.

Here’s the deal:  both of these proteins are well-conserved among eukaryotes. They play a crucial role in eukaryotes, as well. Tubulin is a major component of cilia, and actin can be found in sarcomeres, an important component of muscle cells. Actin also plays a major role in the cytoskeleton.

Tubulin shares homology with a prokaryotic protein, FtsZ, while actin shares homology with the bacterial protein MreB.

To test the prediction I outlined earlier, we need to align tubulin, actin, FtsZ, and MreB amino acid sequences to determine the degree of sequence conservation for each protein.  So, I grabbed a couple of tubulin beta sequences from UniProt, one belonging to Volvox  (accession number: P11482) and the other to a frog (Q91575). When aligned (using ClustalW), there is 88.514% sequence identity shared between the two sequences. The same procedure was done for actin: a Volvox actin sequence (P20904) was aligned with a frog actin sequence (P04751). The result was 89.655% sequence identity shared between the two sequences. Clearly, both tubulin and actin are very highly conserved in sequence identity, with actin being just slightly more conserved.

What about the prokaryotic homologs of these two proteins? Are they also well-conserved, as is expected under the front-loading hypothesis, or are they no more conserved than the average prokaryotic protein?

When FtsZ sequences belonging to Escherichia coli (P0A9A6) and Caulobacter (P0CAU9) are aligned, there is 83.3% sequence similarity.  The most common degree of sequence similarity between E. coli proteins and Caulobacter proteins ranges from 51-60% sequence similarity. Thus, the fact that tubulin’s prokaryotic homolog is considerably more conserved in sequence identity than the average prokaryotic protein is exactly what we would expect under the front-loading hypothesis.

I did the same thing with actin’s prokaryotic homolog, MreB. If we align MreB sequences from E. coli (P0A9X4) and Caulobacter (Q9A821), there is 86.5% sequence similarity. Interestingly enough, the telic prediction plays out again.

But this isn’t the whole story. Recall that I also noted in my previous post that: “…the front-loading hypothesis predicts that, in general, the more highly conserved in sequence identity a protein component is in a [major eukaryotic molecular system], then the higher the degree of sequence conservation will be in its prokaryotic homolog…

And this is exactly what we find for FtsZ and MreB. In eukaryotes, actin is slightly more conserved than tubulin, suggesting that actin is just a bit more important than tubulin. Consistent with the front-loading prediction, we find that actin’s prokaryotic homolog, MreB, is more conserved than tubulin’s prokaryotic homolog, FtsZ. This correlation is expressed in the figure below.

Figure. This illustrates the observation that actin is more conserved than tubulin, and interestingly, actin’s prokaryotic homolog, MreB, is more conserved than tubulin’s prokaryotic homolog, FtsZ, which is what the front-loading hypothesis predicts. Cool!

Thus, we can see that the two predictions I made earlier, from a front-loading perspective, are tentatively confirmed, tantalizing us to explore this further with larger data sets. Since only a small dataset was used here, the predictions can only be considered very tentatively confirmed. But it’s a clue that teleology was involved in life’s history.


A front-loading prediction and molecular machines

January 9, 2012

Unfortunately, many proponents of ID are content with simply criticizing Darwinian evolution instead of focusing their energy on developing a robust, testable teleological hypothesis in biology. Thankfully, the front-loading hypothesis, an inherently telic hypothesis, is testable and it does make predictions about the biological world. So, let’s delve into one of the predictions it makes regarding molecular machines like cilia, etc.

First, a bit of context. Under the front-loading hypothesis, the earth was seeded with unicellular life in the distant past. These life forms had the genomic information necessary for shaping subsequent evolution. For example, such unicellular life forms would have had the genes necessary for the origin of metazoa. But what about the origin of molecular machines which are only found in non-prokaryotic life forms, such as cilia? Could such molecular systems have been front-loaded?


A coolish diagram of the structure of cilia. Image taken from here.

If a molecular machine has played a fairly major role in shaping evolution, then, from a front-loading perspective, it’d be a pretty safe guess to suppose that that machine was either designed into the initial cells, or it was front-loaded to exist in the future. How could something like the cilium be front-loaded? First of all, the major protein components – or homologs of these proteins – of the cilium would have to be designed into the initial cells. This would ensure that the blind watchmaker – non-teleological evolution – wouldn’t have to tinker around with genes and form a cilium from scratch, since the essential components or their homologs would be in the first cells, although they wouldn’t be functioning as a cilium: they’d probably be performing functions independent of each other.

Let’s use a simpler example. Suppose that a certain molecular machine, called X, is specific to eukaryotes. System X is composed of three basic components: A, B, and C. If a designer(s) were to front-load system X, starting with prokaryotes, homologs of components A, B, and C could be designed into the prokaryotic genome. Thus, the first life forms on earth would have had the proteins A1, B1, and C1 (the 1 at the end of each letter means that there are homologs of the components A, B, and C). However, from a rational design perspective, there is a problem. If system X is to arrive on the scene roughly a billion years after the first life forms appeared on earth, proteins A1, B1, and C1 are likely to diverge in sequence identity to such an extent that their initial sequence identity is effectively erased. This, of course, means that after this divergence, A1, B1, and C1 are extremely unlikely to be co-opted into system X, as planned, because their diverged sequence identity has totally modified their function and 3D shape, etc.

How can this problem be overcome? There’s a pretty simple solution, actually. If proteins A1, B1, and C1 are given functions such that their sequence identity is well conserved, and thus their 3D shapes, this problem is overcome.

From this simple solution that a rational designer would inevitably use, we can formulate a couple of predictions from the front-loading hypothesis:

a. Components of molecular machines/systems that are of major importance in eukaryotes will share deep homology with proteins in prokaryotes.

b. Importantly, the front-loading hypothesis predicts that these homologs of protein components in important molecular machine will be more conserved in sequence identity than the average prokaryotic protein.

c. Also, we can tentatively predict that the more essential a component is to a major molecular machine, then the greater degree of sequence conservation in its prokaryotic homolog. With this latter prediction, we can guess how important a component is to a molecular machine by the level of sequence conservation the protein shows across different taxa. Thus, the front-loading hypothesis predicts that, in general, the more highly conserved in sequence identity a protein component is in a molecular machine, then the higher the degree of sequence conservation will be in its prokaryotic homolog.

Note that non-teleological evolution does not make the last two predictions, only the first one. Thus, we can test the front-loading hypothesis on the exclusive last two predictions it makes. If these predictions are confirmed, this will be positive evidence in favor of the front-loading hypothesis.



The Bacterial Flagellum and Homology

December 25, 2011

The Bacterial Flagellum and Homology

In this brief analysis, I’m going to discuss the bacterial flagellum and the homology a number of its components share with non-flagellar proteins. The below table is a list of flagellar proteins found in the genus Salmonella, their length in terms of amino acid residues, and their homologs (if any). Protein lengths were taken from UniProt, and the data on homologs were taken from Pallen and Matzke’s 2006 paper in Nature Reviews Microbiology, “From the Origin of Species to the origin of bacterial flagella.”

Flagellar Protein Length (amino acid) Homology with non-flagellar proteins?
FlgA 219 Yes (CpaB)
FlgBCFG 138; 134; 251; 260 No; but homology with FlgBCEFGK
FlgD 232 No
FlgE 403 No; but homology with FlgBCFGK
FlgH 221 No
FlgI 367 No
FlgJ 316 No
FlgK 553 No; but homology with FlgBCEFG
FlgL 317 No; but homology with FliC
FlgM 97 No
FlgN 140 No
FlhA 692 Yes (YscV)
FlhB 383 Yes (YscU)
FlhDC 113; 192 Yes (other activators)
FlhE 130 No
FliA 239 Yes (RpoD, RpoH, RpoS)
FliB 401 No
FliC 200 Yes; homology with FlgL and EspA
FliD 467 No
FliE 104 No
FliF 579 Yes (YscJ)
FliG 331 Yes (MgtE)
FliH 235 Yes (YscL; AtpFH)
FliI 456 Yes (YscN; AtpD; Rho)
FliJ 147 Yes (YscO)
FliK 405 Yes (YscP)
FliL 155 No
FliM 334 Yes (FliN; YscQ)
FliN 137 Yes (FliM; YscQ)
FliO 125 No
FliP 245 Yes (YscR)
FliQ 89 Yes (YscS)
FliR 264 Yes (YscT)
FliS 135 No
FliT 122 No
FliZ 183 No
MotA 295 Yes (ExbB; TolQ)
MotB 309 Yes (ExbD; TolR; OmpA)

When these figures are added up, we get a total of 12,322 amino acid residues. Thus, it appears that Salmonella flagella are composed of roughly 12,322 amino acid residues. What percent of the Salmonella flagellum, in terms of amino acid residues, has absolutely no known homologs? A total of 3,195 amino acid residues belong to proteins in the flagellum that have no known homologs. This means that approximately 25.9% of the Salmonella flagellum lacks sequence homology.  Now, you will notice that a number of flagellar proteins only have homologs in the type III secretion system. However, the type III secretion system (TTSS) is not a pre-cursor system to the bacterial flagellum. It probably evolved directly from the flagellar export system (do note that Gophna et al. 2003 are a dissenting view, but in my humble opinion, the evidence is certainly in favor of the hypothesis that the type III secretion system evolved from flagella). So we can ask the question: what percent of the flagellum lacks homologs or only has homologs in the TTSS, which is not a pre-cursor system to the flagellum? A total of 2,804 amino acid residues only share sequence homology with TTSS components. This is added to 3,195, to get 5,999. Thus, approximately 48.7% of the Salmonella flagellum has no known homologs in systems that would pre-date the flagellum.  Finally, we ask the question: what percent of the flagellum have no known homologs in non-flagellar systems? Note that a number of flagellar proteins only share homology with other flagellar proteins and TTSS components. For example, FliM is homologous to FliN and YscQ. FliN is only homologous to FliM and YscQ. Since YscQ could not be a pre-cursor protein, one of these proteins do not share homology with a pre-cursor protein. If FliM is supposed to be a pre-cursor to FliN, then the homology FliN shares with FliM cannot be evidence that FliM descended through non-teleological evolution.  To arrive at a percent of the flagellum that has no homologs that provide evidence of a non-telic origin of the flagellum, in cases like FliM/FliN we will use the shorter protein. This will allow us to be as fair as possible to the non-telic position. We arrive at a total of 471 amino acid residues. Add this to 5,999 and about 52.5% of the Salmonella flagellum has no homologs that provide evidence of a non-teleological origin.


Several flagellar proteins only share structural similarity with other proteins. However, structural similarity can often be the result of convergent evolution – there are only a few thousand different protein folds, contrasted with trillions of different possible amino acid sequences.  Further, in some instances, sequence similarity can also be the result of convergent evolution.

From this brief analysis in this article, I found that more than half of the Salmonella flagellum, in terms of amino acid residues, lack any homologs that provide evidence that it evolved through non-teleological mechanisms.  Some of the remaining homologs can hardly be called significant. The flagellar protein, FliG, shares only about 20% sequence similarity with its only homolog, MgtE.  Also, from the angle of intelligent intervention, where the flagellum was designed at the dawn of life, the remaining proteins it does share fairly significant sequence similarity with could possibly be explained by convergent evolution. I suggest that convergent evolution at the molecular level may be more pervasive than many think.

Is Intelligent Design Dead?

December 5, 2011

Is Intelligent Design Dead?


Recently, a number of critics of intelligent design have said that the intelligent design movement is, well, dead. It all started with Jason Rosenhouse’s blog post “Twenty Years After Darwin on Trial, ID is Dead.” Jerry Coyne followed up on his blog, Why Evolution Is True, agreeing with Rosenhouse’s assesment that the intelligent design movement is effectively dead. So, what’s my opinion on this?


First of all, I’d like to point out that the concept of teleology in biology isn’t dead. It’s been around for a very long time, and that concept isn’t exactly the same thing as the “Intelligent Design Movement.”

That said, back in the days when ID first came out (in the 1990s – I wasn’t an advocate of intelligent design at the time, so I’m talking from the stand point of looking back at the history of the intelligent design movement, not my own personal experience), it seemed like there were a lot of creative, original, inspired ideas going around from the ID side. “We were great,” one could say. We challenged the scientific consensus and proposed research ideas, interesting hypotheses, and explored the various ways that ID could be used to further the advance of the biological sciences. Now, however – and any unbiased observer could see this – many ID proponents are spending their time attacking Darwinian theory, instead of spending their time developing a rigorous intelligent design hypothesis that could truly make robust predictions about the living world. When I look at the posts over at UncommonDescent, it is obvious to me that a change needs to occur within the mainstream ID team. At least 50% of the posts at UncommonDescent, aren’t even remotely relevant to ID and biological origins (well, I suppose by some stretch of the imagination they could be just a tiny, tiny bit relevant). Consider the title of one of the posts at UncommonDescent: “Survey results: Only 5.3% of general philosophers of science accept or lean towards theism.” Now what on earth does theism have to do with biological intelligent design? I really don’t know. Does theism have anything to do with the theory of gravity? Not really, and if the mainstream proponents of ID are genuinely interested in developing a rigorous hypothesis of biological origins, then the theistic language will have to be dropped (or at least minimized). I mean, c’mon, UncommonDescent spends a whole bunch of time devoted to attacking atheism, promoting theism, etc. But what does this have to do with the origin of the bacterial flagellum, for example? If you’re truly interested in biological origins, then we don’t need to be sidetracked by the theism/atheism debate, which is a whole other topic.


There is, of course, the other side of the coin. Papers friendly to ID have been published by academic journals, and researchers like Doug Axe and Ann Gauger are doing some pretty cool stuff in the lab. Much of this research is devoted to discovering the limits to random mutation and natural selection, and without a rigorous intelligent design hypothesis this is the most we can expect at this point. Then there are the folks over at Telic Thoughts, which don’t get as sidetracked as UncommonDescent. The folks over there seem to be genuinely interested in biological origins, and I am glad of their often thought-provoking musings over biological origins. So, too, we have Mike Gene and his blog The Design Matrix, and here again is an example of someone sincerely interested in biological origins. Both at Telic Thoughts and The Design Matrix, we don’t get bogged down with the theism/atheism debate, or with “Neuroscientists study how mindfulness meditation helps people overcome temptation to smoke.” I am thankful for the efforts of the folks at Telic Thoughts and for Mike Gene’s The Design Matrix. These blogs represent what ID as a whole could be if the bulk of its proponents had the interest in developing ID as a rigorous biological hypothesis, instead of talking how the fossil record disproves Darwinian evolution.


In conclusion, ID is not dead, but a number of aspects of ID seem to be in decay these days. The days of the enthusiastic ID proponents thinking about research ideas seem to be waning, thanks to the efforts of UncommonDescent and the like (okay, I know I’ve been picking on you UD guys a lot). The mainstream ID community seems to be content with merely poking holes at Darwinian evolution, which is not good at all. We need to develop a rigorous biological design hypothesis that makes real, robust predictions about the living world. And for this I thank Mike Gene and the folks at Telic Thoughts for pondering over the front-loading hypothesis – a teleological hypothesis that makes real predictions. You guys still retain that creativity and sincerity and that feeling of how ID should be. And I strongly encourage those researchers like Doug Axe and Ann Gauger et al. to continue their lab work – it’s certainly needed these days. I for one, am quite interested in pursuing ID, developing it as a rigorous hypothesis, and researching the predictions made by telic hypotheses like front-loading.


No, ID isn’t dead. But it’s a bit hard to tell these days if it’s the calm before the storm or not. We need more Mike Genes, more “telic thoughts” (is that a pun or not?) and more ID researchers determined to build ID as a rigorous biotic hypothesis.

A Front-loading Prediction

November 1, 2011

If intelligent design is to be accepted by the scientific community than the proponents of the intelligent design hypothesis must do more than merely attacking flaws in non-teleological evolution. Intelligent design proponents must go beyond this and develop a thorough scientific framework from which robust predictions can be generated.

And so I think it’s time for intelligent design proponents to begin focusing on the mechanisms by which the intelligent design of life forms may have been accomplished. The front-loading hypothesis is one such proposed mechanism, and we can begin to draw general predictions from the front-loading hypothesis.


So, what is the front-loading hypothesis? On page 147 of The Design Matrix, Mike Gene puts it this way:

“Front-loading is the investment of a significant amount of information at the initial stage of evolution (the first life forms) whereby this information shapes and constrains subsequent evolution through its dissipation. This is not to say that every aspect of evolution is pre-programmed and determined. It merely means that life was built to evolve with tendencies as a consequence of carefully chosen initial states in combination with the way evolution works.”


By the way, by the phrase “significant amount of information” is not meant a large genome. What is meant is a genome(s) that has been carefully crafted to shape the future of evolution.


Further, as Mike Gene pointed out, front-loading does not mean that all aspects of life were front-loaded. Perhaps only the origin of multicellular life was front-loaded, for example. Or perhaps all the phyla were front-loaded. So how does front-loading work? Well, there are several ways, but one of the ways is this: suppose the first cells contained genes necessary for multicellular existence but genes that were not necessary for unicellular existence. In this way, genes that would be needed in the future would be placed in the first organisms. To ensure that these genes do not decay over time, they can, firstly, be given an beneficial (but not necessary to the unicellular organisms) function, such that decay of these genes in the unicellular organisms would mean a loss of fitness; secondly, these genes could be part of an IC machine that is beneficial to the unicellular organisms. If these genes were part of an IC machine, then decay of these genes would mean decay of the IC machine and thus, again, loss of fitness would result.

Figure. A diagram illustrating how a gene that is not necessary for the existence of the first life forms but is necessary for future multicellular life is placed in the first life so that it will be present when multicellular life evolves. 


When we consider the above points, it is obvious that one general front-loading prediction is that genes necessary for the existence of major life forms (e.g., metazoan life forms; vertebrates; plants; animals; etc.) will be found in ancestral organisms – even though these genes would not be strictly necessary for the existence of the ancestral organisms.


Consider that fish, reptiles, birds, and mammals require the globin proteins to deliver oxygen to their tissues. In short, vertebrates seem to need globins. However, non-vertebrate groups don’t need the function carried out by globins. Nevertheless, consistent with the front-loading prediction, globin does occur in non-vertebrate groups like bacteria.


Thus, we can formulate the following prediction from the front-loading hypothesis:

Genes necessary for the existence of major life forms will always  have deep homology with or will always be found in simpler life forms that do not require those genes for survival; on the other hand, genes that are not necessary for the survival of major life forms will not always be found in ancestral life forms.


Note that absence of significant sequence similarity between a necessary gene in a major life form and genes in other life forms does not invalidate that front-loading prediction, since sequence similarity isn’t the only way we can find those pre-cursor genes. We can also use structural homology, looking at the 3D shape of a protein and comparing that shape with the shapes of other proteins across the web of life. Furthermore, and importantly, if cytosine deamination was utilized by the intelligent designer(s) such that the path of evolution would be channeled in a particular direction, we would have to take this into account when hunting for precursors of genes necessary for the existence of major life forms. How would this work? I’ll describe that in another article (yea, I say that a lot). Suffice it to say that if the above prediction of the front-loading hypothesis is confirmed with more and more research, then the front-loading hypothesis will be considerably strengthened. On the other hand, if that prediction is not confirmed by new research, then my confidence in the validity of the front-loading hypothesis will have to drop.

Your Weekly Dose of Proteins, Week 2

October 9, 2011

Your Weekly Dose of Proteins, Week 2


Today we will talk about a protein known as TolB. TolB is part of a larger multi-protein complex known as Tol-Pal. If I recall correctly, the Tol-Pal system is composed of about five different protein components. See the image below for a space-fill model of TolB and its association with Pal.

TolB and its association with Pal. The green guy is TolB, while the purple guy is Pal.

The neat thing about the Tol-Pal system is that its function isn’t quite known. This is neat because it means that there’s room for research here to uncover its exact function.


Nevertheless, there are several proposed functions of Tol-Pal:

  • The Tol-Pal system may be involved in the integrity of the outer membrane of the bacterial cell.
  • It might anchor down the outer membrane to the peptidoglycan layer.



Incidentally, parts of the Tol-Pal system share structural (and weak sequence) similarity with MotA and MotB, the motor components of the bacterial flagellum. Again, this is a topic to be discussed in a later article. In the meantime, don’t forget to take your weekly dose of proteins!

How to Detect Design

October 3, 2011

How to Detect Design


Perhaps the most common argument advanced against the intelligent design hypothesis is that the conclusion that certain parts of life were designed is an “argument from ignorance” or a “god of the gaps” argument. I must disagree with this claim, since several branches of science (particularly SETI) make design inferences, yet those inferences are not labeled “argument from ignorance” or “god of the gaps.”

What if we detected a triangle-shaped object floating in space? It would be reasonable to conclude that that object was intelligently designed. In fact, this conclusion is supported by the peer-reviewed literature:

“The forthcoming space missions, able to detect Earth-like planets by the transit method, will a fortiori also be able to detect the transits of artificial planet-sized objects. Multiple artificial objects would produce light curves easily distinguishable from natural transits. If only one artificial object transits, detecting its artificial nature becomes more difficult. We discuss the case of three different objects (triangle, two-screen, and louver-like six-screen) and show that they have transit light curves distinguishable from the transits of natural planets, either spherical or oblate, although an ambiguity with the transit of a ringed planet exists in some cases.” (Arnold, L. Transit Light-Curve Signatures Of Artificial Objects. The Astrophysical Journal, 627:534–539 (2005)).

The author goes on to note that:

“Transits of artificial objects also could be a means for interstellar communication from Earth in the future. We therefore suggest to future human generations to have in mind, at the proper time, the potential of multiple Earth-sized artificial structures in orbit around our star to produce distinguishable and intelligent transits.” (emphasis not added)

In short, detecting a triangle-shaped object in space would suggest that that object was intelligently designed – and this conclusion is supported by the peer-reviewed literature (The Astrophysical Journal has a fairly high impact factor, too).

So, would the conclusion that that object was probably intelligently designed be an argument from ignorance, or an “intelligence of the gaps” argument? If that conclusion is not an argument from ignorance, then the conclusion made by the hypothesis of biological intelligence is not an argument from ignorance (or “intelligence of the gaps” argument) either.

Why, then, would a triangle-shaped object in space be indicative of intelligence? The reason is because the shape of that object would be discontinuous from the shapes of objects known to be generated by non-teleological astronomical processes. Thus, discontinuity is one of the ways to strengthen a suspicion of intelligent design. Yet this is not the only way: in his The Design Matrix, Mike Gene proposes four criteria to help gauge our suspicion of intelligent design. These four criteria are, namely, Analogy, Discontinuity, Rationality, and Foresight.

Analogy, Discontinuity, Rationality, and Foresight

Imagine you are an astronaut of the future. You are walking on the surface of Mars, examining the features of this planet closely. You spy a suspicious-looking object a few feet in front of you, and when you bend down to examine it, you are shocked to find that the object is eerily similar to a common mousetrap.

The platform is made out of wood, it has a spring and a hammer, and all the essential components of a mousetrap. Of course, one would conclude that that object was the result of intelligent design. But why?


Firstly, the hypothetical Martian mousetrap would be strongly analogous to human-made mousetraps. The Martian mousetrap would be made out of the same materials terrestrial mousetraps are typically made of, and the Martian mousetrap would have all the components that terrestrial mousetraps have. This extremely strong analogy would very decidedly point in the direction of intelligent design. On the other hand, suppose that the ‘mousetrap’ was made out of clumsy clay parts? While we would almost certainly still conclude intelligent design, that conclusion wouldn’t be quite so strong. Why? Because the level of analogy between something known to be designed by intelligence (in this case, the terrestrial mousetrap) and something we suspect to be designed (the hypothetical Martian mousetrap) wouldn’t be as strong as in the first example. What if the hypothetical “mousetrap” was simply a hole in the ground with some sticky substance like oil inside the hole? This “device” can catch mice: if a mouse happened to walk into the hole, it would get stuck. Yet this “device” is not at all analogous to our terrestrial mousetraps. The level of analogy drops enormously, severely weakening our suspicion of intelligent design. In fact, the analogy is so weak that one might not even conclude design at all – and for a good reason, too. Thus we see that the stronger the analogy between an object suspected to be designed and an object known to be designed, the more reasonable our conclusion of intelligent design is. This would not be an argument from ignorance: it would constitute a positive case for teleology. Arguments from analogy are often used in scientific research, where if X is strongly analogous to Y, then Z is quite probably true for both X and Y.

For example, in a paper called “Comparative analyses of foregut and hindgut bacterial communities in hoatzins and cows,” researchers note:

“Foregut fermentation occurs in mammalian ruminants and in one bird, the South American folivorous hoatzin. This bird has an enlarged crop with a function analogous to the rumen, where foregut microbes degrade the otherwise indigestible plant matter, providing energy to the host from foregut fermentation, in addition to the fermentation that occurs in their hindguts (cecum/colon). As foregut fermentation represents an evolutionary convergence between hoatzins and ruminants, our aim was to compare the community structure of foregut and hindgut bacterial communities in the cow and hoatzin to evaluate the influences of host phylogeny and organ function in shaping the gut microbiome.”

Given that the South American hoatzin (a bird) has an organ with a function analogous to the mammalian rumen, one might predict that the microbiome of both these organs would be also analogous. This is indeed the case, as the abstract of the above paper notes:

“Regardless of the independent origin of foregut fermentation in birds and mammals, organ function has led to convergence of the microbial community structure in phylogenetically distant hosts.”

In this particular case, X and Y are analogous to each other, and so we expect Z (the structure of the microbial community) to be similar. Thus, since X and Y are analogous, then Z is quite probably true for both of them. We can see, then, that reasoning by analogy is not at all uncommon to scientific research, and reasoning by analogy is not necessarily a fallacy.

The nice thing about analogy is that it can actually help us make predictions about the living world. For example, if “at first glance” biological feature X is strongly analogous to feature Y, something known to be designed, then we could predict that the finer details of biological feature X are also analogous to Y. We can ask what Y predicts about X. Furthermore, if the telic predictions are confirmed it would strengthen the case for intelligent design, and it would also provide evidence that the analogy under discussion is an actual analogy, and not just a metaphorical analogy.


We have seen that analogy is one way we can gauge our suspicion that a given feature was intelligently designed: the more analogous that feature X is to something known to be designed, the more confident we can be that feature X itself is the product of teleological mechanisms. Now we come to discontinuity. By discontinuity, I simply mean that there are limits to what non-teleological mechanisms can accomplish. For example, a mousetrap is discontinuous from things that can be generated by non-teleological processes, such as canyons. A triangle-shaped object floating in space is discontinuous from objects that can plausibly be generated by non-teleological processes. This is a very important criterion, and the more discontinuous an object is from things known to be produced by non-teleological mechanisms, the more suspicious we become that that object was intelligently designed.

How can we detect discontinuity? Well, we can do this by seeing how far apart feature X is from things that are produced by non-teleological processes. For example, if cosmological non-teleological processes were known to be capable of generating objects shaped like almost perfect squares, then an object in the shape of a triangle wouldn’t be all that indicative of intelligence. Similarly, if mindless processes were able to generate things strikingly close in similarity to Mount Rushmore, the suspicion that Mount Rushmore was intelligently designed would be weakened.

In biology, we can detect discontinuity by firstly, determining if a system is irreducibly complex (IC), and secondly, scanning the known biological universe to how many precursor systems (if any) pre-date that IC system. The fewer the number of precursor systems that pre-date the IC system, the more discontinuous the IC system is from the rest of the biological universe. Furthermore, if the Darwinian pathways proposed to explain the origin of that IC system are extremely implausible, the more discontinuous that IC system is from the parts of life that non-teleological processes can account for.

Discontinuity is often used by scientists to detect design. I have mentioned the example of SETI science, and this example should be sufficient to dispel any notions that intelligent design is an argument from ignorance, or a “god-of-the-gaps” argument.



One hallmark of teleology is rationality. Several attributes of rationality may be noted here:

  • Specificity
  • Efficiency
  • Flexibility

A rationally designed system will generally exhibit all of the above. Naturally, “bad design” is usually not a hallmark of teleology. However, many instances of “bad design” really are not bad design. For example, the existence of viruses might be considered “bad design.” However, this is taking a human-centric approach. The virus is actually a very cleverly crafted system, well suited for its purpose. In other words, for the virus, its design is rational.

That said, any true instances of irrational design in a system must be considered evidence against the view that that system was the product of teleology. Before we can make this conclusion, though, we must keep in mind that a system might degenerate through non-teleological processes, resulting in an irrational design.

If we do find a system that performs its function in a rational way, then we must consider that teleology might have been involved in the origin of that system. The more rationally designed the system appears to be, the more confident we can be that the system was the product of teleology. Also note that the criterion of rationality can be used to generate telic predictions. For example, if at first glance, a molecular system seems to be rationally designed, then we would predict that further investigation would reveal that it is rationally designed. Consider the bacterial flagellum. If the arrangement and structure of the core flagellar system seems to be rational, then we would predict that further investigation at the molecular level would strengthen the case for the rational design of the bacterial flagellum.


Our final criterion is foresight. This criterion is a bit vague. A system that demonstrates foresight essentially means that the intelligent designer(s) designed that system right from the start. For example, the same DNA molecule is used throughout all of life, meaning that the designer(s) of the DNA molecular and genetic code got the design right the first time. Obviously, it is difficult to determine if a system displays foresight.


Here I have argued that the intelligent design conclusion is not an argument from ignorance or a “god of the gaps” argument. Its methodology of detecting design is as valid as the methodology used by SETI, for example. The various criterion used to deepen our suspicion of teleology constitute positive evidence for teleology.

The main points to take home are as follows:

  • The intelligent design conclusion is not an argument from ignorance or a “god of the gaps” argument as is often assumed by critics of intelligent design.
  • The various criterion used to deepen our suspicion of teleology constitute positive evidence for teleology.
  • These criterion are useful in guiding research and in formulating predictions under the intelligent design hypothesis.