t f p g+ YouTube icon

Behe, Lenski and the “Edge” of Evolution, Part 5: Mixing and Matching

Bookmark and Share

November 29, 2012 Tags: Genetics
Behe, Lenski and the “Edge” of Evolution, Part 5: Mixing and Matching

Today's entry was written by Dennis Venema. You can read more about what we believe here.

Note: In this series, we reexamine the claim made by Intelligent Design proponent Michael Behe to have found a limit to “Darwinian” evolution in light of recent results from the laboratory of Richard Lenski.

Nothing new under the sun

As we noted in the last post, Behe has replied to my arguments to claim that “no new functional elements” arose during the actualization step that produced the first Cit+ bacteria in Lenski’s experiment. Rather, he claims that previously existing Functional Coded elemenTs (FCTs) were merely duplicated:

The gene duplication which brought an oxygen-tolerant promoter near to the citT gene did not make any new functional element. Rather, it simply duplicated existing features. The two FCTs comprising the oxygen tolerant citrate transporter locus -- the promoter and the gene -- were functional before the duplication and functional after. I had written in my review that one type of mutation that could be categorized as a gain-of-FCT was gene duplication with subsequent sequence modification, to allow the gene to specialize in some task. Venema thinks the mutation observed by Lenski is such an event. He has overlooked the fact that there was no subsequent sequence modification; a segment of DNA simply tandemly duplicated, bringing together two pre-existing FCTs.

I have already discussed how this seems to seriously strain the definition of “new.” Whatever one chooses to call such an event, there is an emergent function present that did not exist before (in this case, the production of a citrate transporter when oxygen is present). My point here is not to revisit that discussion, but to extend it and consider its implications for Behe’s overall case for irreducible complexity (IC) in light of what we know about protein structure and function. Since Behe accepts that an emergent function can arise through an exaptation event that cobbles FCTs from different genes together, then there is a large body of evidence about protein structure that Behe needs to address. To understand the importance of this evidence, however, we’ll need to take a brief excursion into some details of protein structure and function.

“Domain architecture” of proteins

As the molecular biology revolution picked up steam in the 1980s and 1990s, researchers began to notice that proteins that were otherwise quite different could have short stretches that were highly similar to each other. As more and more proteins were sequenced, these small “motifs” or “domains” became easier to recognize. At the beginning, not much was known about the function of these types of domains, but the fact that they were conserved between different proteins strongly suggested that they had to be functional. Eventually, the functions of many of these domains were identified. Often, they serve as specific docking sites to allow other proteins to bind and perform a function.

One of the classic examples of this sort of thing is what came to be known as an “SH2” domain. It was first identified in a protein called “Src” and “SH2” stands for “Src Homology 2.” (No, we biologists are not very creative with names at times.) SH2 domains are made up of about 100 amino acids that fold up into a defined shape – a shape that recognizes and binds on to another specific shape on other proteins. Individual SH2 domains can vary a bit, of course, so they don’t all bind to exactly the same partners.

Because the SH2 domain has a specific function (binding to a specific protein) that can be separated from other functions, this qualifies as what Behe would call a FCT, as we have discussed previously. What we see then, when we look at proteins, is that many of them are combinations of several domains (FCTs), each with a distinct function. The overall function of the protein, then, is determined by the combination of domains (FCTs) that it has: some FCTs have enzymatic functions, others direct specific protein-protein binding events, and so on.

Implications for Behe

As we noted before, Behe takes a dim view of the notion that parts for one complex system can be exapted for use in another system:

In Chapter 2 I noted that one couldn’t take specialized parts of other complex systems (such as the spring from a grandfather clock) and use them directly as specialized parts of a second irreducible system (like a mousetrap) unless the parts were first extensively modified. Analogous parts playing roles in other systems cannot relieve the irreducible complexity of a new system; the focus simply shifts from “making” the components to “modifying” them. In either case, there is no new function unless an intelligent agent guides the setup.

In other words, Behe paints a picture of molecular machines with highly specialized parts that cannot be used in other systems without “extensive” modification – and claims that without a designer, no new functions are possible (for either “making” or “modifying” the parts). Yet what we see in nature looks rather different. Yes, the parts are specialized when examined at the level of entire proteins – but a closer look reveals that these specialized proteins are in fact made up of different combinations of many smaller protein domains with known functions– what Behe would call FCTs. Sequence evidence supports the hypothesis that these FCTs are derived from a common ancestral sequence, and that they have been duplicated, rearranged and exapted into many different proteins. As we have seen, many of these FCTs are modular domains that allow for protein-protein interaction – exactly the sort of effect needed to add new components to molecular systems over time.

Since these domains are found in functional proteins, selection acts to maintain their function. This keeps them around and “available” for duplications and rearrangements that produce new genes with new functions - just as we observed previously for the citrate transporter coding sequence and the promoter from a gene expressed in conditions in which oxygen is present. As such, these domains / FCTs are sort of a “spare parts drawer” in the genome that shuffle every so often – a screw here, a spring there – and contrary to Behe’s assertion, the evidence suggests that they can indeed be exapted for new roles and functions. SH2 domains, for example, are very widespread – in humans there are over 100 genes with SH2 domains, and no two of them are exactly alike. Would it be fair to say that each of these genes have the same function? Of course not, unless one was to claim that new combinations of functions (FCTs) were somehow “not new.” Furthermore, given that Behe already is on record for accepting the mechanism in view (duplication and rearrangement of previously existing FCTs into new combinations with emergent properties) it would seem strange to point to combinations of such proteins as an insurmountable problem for evolution to produce over time.

Implications for Axe

While we have not focused on the work of Douglas Axe (a structural biologist and Intelligent Design proponent) in this series, the observation that proteins are made up of smaller domains that can be swapped between different proteins as self-contained FCTs has implications for his lines of argument as well. As we have mentioned briefly in a previous series, Axe is interested in the origins of stable protein structures (protein folds), and claims that new genes and/or protein folds are inaccessible to evolution:

Basically every gene, every new protein fold… there is nothing of significance that we can show [that] can be had in that gradualistic way. It’s all a mirage. None of it happens that way.

The evidence from Lenski’s ongoing experiment demonstrates that new genes can indeed arise as FCTs recombine, and the genomics evidence that suggests that this mechanism is widespread. If indeed new genes can be produced by recombining FCTs to create new proteins with new properties, it now falls to Axe to explain why this is not a threat to his claim that new genes / protein folds cannot be produced through evolution. Lenski’s work is not just a problem for Behe, but for Axe as well.

Summing up

Lenski’s Long Term Evolution Experiment (LTEE) continues to provide an interesting glimpse into the inner workings of evolution – and the more we learn through it, the more the theoretical underpinnings of the ID movement are eroded. As the experiment continues, I expect it to continue this trend – and I will be watching it carefully to see if it does. I suspect that those in the ID movement will do the same.

For further reading:

Basu, M.K., Poliakov, E., and Rogozin, I.B. (2008). Domain mobility in proteins: functional and evolutionary implications. Briefings in Bioinformatics (3); 205-216.
Blount, Z.D., Barrick, J.E., Davidson, C.J. and Lenski, R.E. (2012). Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489; 513- 518.
Jing, J and Pawson, T (2012). Modular evolution of phosphorylation-based signalling systems. Phil. Trans. R. Soc. B 367; 2540–2555.
Michael J. Behe, Darwin’s Black Box: The Search for the Limits of Darwinism (New York: Free Press, 2007).
Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York: Free Press, 2007).
Michael J. Behe (2010). Experimental evolution, loss-of-function mutations, and “The first rule of adaptive evolution”. The Quarterly Review of Biology 85(4); 419-445.

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

< Previous post in series

View the archived discussion of this post

This article is now closed for new comments. The archived comments are shown below.

Page 1 of 1   1
Ashe - #74873

November 30th 2012

SH2 domains seem to be generally useful for transducing signals. This gives us a tentative but intriguing handle on what might be a core signaling parts-list.

Tim - #74898

December 1st 2012


How widespread are these domains in proteins?  Is “domain architecture” an accepted paradigm in the area of genetics / molecular biology currently?  Is the support broad, or limited to just a few recent examples, with presumably more to follow as research progresses?

Dennis Venema - #74922

December 2nd 2012

Hi Tim,

Protein domains are well accepted and known to be widespread. For example, over 700 proteins in the human (and other vertebrate) genomes have what is known as an immunoglobulin (Ig) domain; SH2 and SH3 domains are also widespread (in the hundreds of proteins in humans), as are many, many more. They are all over the place. 

Tim - #74927

December 2nd 2012

Thanks Dennis!

I looked for this on publically available sources on the web, but couldn’t find anything.

Do we know what percentage of proteins contain one or more domains?  And does this increase with the size of the proteins?  For very long/complex proteins, would it perhaps even be the exception rather than the rule that they would be lacking at least one (or more) domains?

I can’t find good numbers on this.  One of the ways I’d like to see this go is if it can address the evolution of proteins comprising ID icons of “irreducible complexity” such as the bacterial flagellum.  Do you have any solid data on this?


HornSpiel - #74951

December 3rd 2012

These domains / FCTs are sort of a “spare parts drawer” in the genome that shuffle every so often – a screw here, a spring there – and contrary to Behe’s assertion, the evidence suggests that they can indeed be exapted for new roles and functions.

Sounds like Venema is describing a hierarchy of functional elements.  It appears the parts are rearrangeable on many different levels. The possibilities are endless once the evolutionary system is in place. He has shown in this article that Behe and Axe’s critiques fall flat because they fail to recognize an intermediate level of structure in proteins.

I want to point out that none of this would be possible without extreme regularity and substitutability in the basic building blocks of chemistry, atoms. In any chemical system one atom can be substituted for any another of the same element. This is, of course, the result of the regularity of the basic laws of physics across time and space—a regularity that begs a “natural” explanation.

This precision of similarity allows self-organizing systems such as crystals or even snowflakes to occur “naturally.”  I am no chemist but I know if an atom of a different type fills a slot, in say a crystal, a related but potentially significant structure/function is realized—such as in a semiconductor.

As we move up the hierarchy to molecules, we see any instance of an amino acid  in a DNA strand can be substituted for another, either of the same or a different type. If of a different type, a slightly different protein will be built. But not only can a single amino acid swap for another, but a whole sequence, a functional element from a higher domain can be substituted or inserted in an amino acid slot.

This pattern repeats on a multiplicity of levels—piggy-backing on Bill Manz’s comment about fractals.

In language the same thing occurs. One word can be substituted for another to give a different but functional sentence, but one can also substitute across hierarchies:  a word for a sentence “Yes!” a phrase for a word “piggy-backing”, or even a sentence for a word in one of those you-really-need-to-have-this-edited sentences like this one. In linguistics we can call this a skewing of grammatical levels.

So there is a regularity in the way complex systems are created and modified, from molecules to language. Larger functional units are created from smaller ones, which are creatively combined. Sometimes hierarchies are even skewed. The only rule is that the result is “functional” in some sense.

Such levels of function are therefore necessarily common in biological systems. Moreover, it is likely that there are levels of structure and a novelty-of-combinations-of-elements in biological systems we have not yet recognized. Therefore any evolution-could-not-have-produced-it declaration is, it seems to me, quite premature.

Ashe - #74957

December 4th 2012

Different binding sites could target different sets of residues/atoms at the same
interface to perform the recognition. Binding sites that are very different in nature can
recognize the same partner.

lancelot10 - #75391

December 18th 2012

The fact that proteins genes etc can be used for other purposes by God’s design does not help the hypothesis of evolution at all . It just shows us that living matter is even more complex than we can imagine.

All the biological systems prove design - eg we can make a water pump out of a car engine but only by ID and manufacture - not by mixing the car parts in a giant bowl.

What evolutionists have yet to explain is a mechanism in operation now and in the past that can change the DNA of one creature into the DNA of another creature and be purely random in nature.

Since the DNA is tightly coiled into a tiny ball in the sperm or egg there is no way that random cosmic rays could blast the DNA of a deer into the DNA of an ocean going whale.  

Why dont evolutionists not go back to basics to come up with even the mechanism of evolution before getting all excited about so called ‘junk’ dna.

Note that both male and female deers would have to have the same mutations for the move towards their journey into the ocean -  what an absurdity of logic to regret for all eternity.


David Buchanan - #75724

December 28th 2012


“change the DNA of one creature into the DNA of another creature and be purely random in nature” ????

Why do evolutionists have to explain this?

lancelot10 - #77459

March 14th 2013

David - evolutionists are required to explain their theory - how it works - the evidence that the mechanism worked in the past and also in the present .  

Evolution states that the DNA of one kind of creature can change into the DNA of another creature such as from fish to mammal or vice versa by purely random mechanisms such as bombardment of sperm or egg cells by cosmic rays.  

Even if this fairy story happened between say two fish awaiting lungs - it would have to continue in a mammalalian direction until everything  in the fishes descendents was good enough for the final fish/ mammal  to sliver onto the land.  

The mathematical probability of this happening is so fantastical that anyone believing must have more blind faith than a YEC ever needs.

Darwin confused breeding with evolution since he did not know about DNA  so he has more excuse than present day evolutionists.   DNA can lose information and it can be damaged but this does not produce a new species - in fact DNA can correct itself - keeping the species survival intact.



Evolutionists talk as if the theory has a mechanism - which it claerly does not.

lancelot10 - #75472

December 19th 2012

“Assuming the existence of all the necessary components - a huge assumption - Dr J. Coppedge statistical probability expert has calculated that the likliehood of a single protein molecule being arranged by chance is 1 in 10 ^161  - since there are around10^80 atoms in the universe one would need 10^81 universes for this one protein to come together” 

Also the protein would have no life since this has to come from God.


Page 1 of 1   1