The Evolutionary Origins of Irreducible Complexity, Part 2

| By on Letters to the Duchess

One of the challenges of discussing evolution within evangelical Christian circles is that there is widespread confusion about how evolution actually works. In this (intermittent) series, I discuss aspects of evolution that are commonly misunderstood in the Christian community. In this post, we continue to examine the evidence that new genes can become part of “irreducibly complex” structures through gradual mechanisms.

Something old and something new; something borrowed and spliced into

In the last post in this series, we introduced a paper by Chen and colleagues that sought to identify new genes in various Drosophila (fruit fly) species. The youngest (i.e. the most recently evolved) gene they found is one specific to Drosophila melanogaster, the species of fruit fly beloved by geneticists as a model organism. The gene is named “p24-2” (not the most imaginative name, but it serves its purpose) and the gene it is duplicated from is called “Éclair”. The Éclair gene is found in a number of Drosophila species. A simplified “family tree” of three Drosophila species (D. melanogaster, D. simulans and D. erecta) is shown below. The duplication event that generated the p24-2 gene happened within the lineage leading to D. melanogaster, but after D. melanogaster and D. simulans separated as distinct species:

Since the entire genomes of these species are now sequenced and available online, it is possible to look at the chromosome region where the Éclair gene is found in all three. By looking at this region in D. melanogaster, we see that the brand-new p24-2 gene is almost right next door to its “parent” gene, Éclair. Below is a screen shot taken when looking at this region using a Drosophila “genome browser” that is freely available online. The red arrow indicates the Éclair gene, and we can see p24-2 is just one gene over, and seems to be nested within another gene called “Unc-115b”. The green arrows are pointing to two different “versions” of how p24-2 is made into an mRNA working copy. The Unc-115b gene (blue arrow) has five different mRNA versions. (One of the p24-2 mRNA versions has a lot of Unc-115b sequence that is not used when the p24-2 protein is made).

(Click Image to Enlarge)

Finding a duplicated gene next door to the sequence it is copied from is pretty common in genomes – when chromosomes are copied or recombined during cell division, side-by-side copies of parts of chromosomes show up every now and then. It’s also not surprising to see a new gene cobbled together with another gene. In this case, Unc-115b and p24-2 are overlapping but separate functional entities: they each have their own protein sequences, but each includes the code of the other as a sequence that does not actually translate into protein. The details of how this “cobbling” happens aren’t important for this discussion, other than to note that the mechanisms are known and not rare. In the chart above, then, the orange sections indicate the active parts of the transcribed sequence, while the gray are sections that are included in the RNA molecule, but do not get used directly to code for the new protein.

When we look at this same chromosome region in D. simulans and D. erecta, however, p24-2 is missing. Éclair and Unc-115b are there, but p24-2 is not, since it arose after D. melanogaster separated from its common ancestors with the other species. (Note: this entire region is a mirror image in D. simulans and D. erecta when compared to D. melanogaster due to a large scale chromosome inversion that covers this whole area. So, while it looks “backwards” compared to the image above, that is not surprising, it’s expected):

(Click Image to Enlarge)

So, with the p24-2 gene in D. melanogaster, we have a bona-fide, recent gene duplication event. This gene is brand new, evolutionarily speaking (less than 3 million years old, given the calculated speciation times of D. melanogasterand D. simulans). Not only is it brand new, it is also essential for survival in D. melanogaster: if you remove it, the fly dies. Obviously, since every other Drosophila species lacks p24-2, this gene is not essential for survival for any other species. It’s new, and now it’s necessary.

Do new, essential genes refute the Intelligent Design (ID) argument from Irreducible Complexity (IC)?

So far, nothing we have discussed explicitly threatens the ID argument from IC, though it does threaten the ID argument that new information cannot arise through evolution, a topic we have discussed in detail before. Michael Behe, the main ID proponent of the argument from IC, has commented on this research by Chen and colleagues (thanks to commenter “Bilbo” for pointing this out). Behe’s rejoinder was to a blog post by biologist and atheist blogger Jerry Coyne, who used the paper by Chen and colleagues to attack Behe’s ideas. Since Behe’s reply deals with his understanding of how gene duplication relates to his argument from IC, I will quote it here at length:

I have never stated, nor do I think, that gene duplication and diversification cannot happen by Darwinian mechanisms, or that “they play almost no role at all” in the unfolding of life. (As a matter of fact, I discussed several examples of that in my 2007 book The Edge of Evolution. That would be silly — why would anyone with knowledge of basic biochemical mechanisms deny that, say, the two gamma-globin coding regions on human chromosome 11 resulted from the duplication of a single gamma-globin gene and then the alteration of a single codon? What I don’t think can happen is that duplication/ divergence by Darwinian mechanisms can build new, complex interactive molecular machines or pathways. Assuming (since he is in fact critiquing them) Professor Coyne has been attentive to my arguments, one background assumption that he may have left unexpressed is that he thinks the newer duplicated genes discovered by Professor Long’s excellent work represent such complex entities, or parts of them.

There is no reason to think so. A gene can duplicate and diversify without building a new machine or network, or even changing function much. The above example of the two gamma-globin genes shows that duplication does not necessarily result in change in function. The examples of delta- and epsilon-globin, which, like gamma-globin, presumably also resulted from the duplication of an ancestral beta-like globin gene, show that sequence can diversify further, but function remain very similar. Even myoglobin, which shares rather little sequence homology with the other globins, has not diverged much in biochemical function.

In his recent work Professor Long discovered that many of the new genes were essential for the viability of the organism — without the gene product, the fruitflies would die before maturity. Perhaps Professor Coyne thinks that that means the genes necessarily are parts of complex systems, or at least do something fundamentally new. Again, however, there is no reason to think so. The notion of “essential” genes is at best ambiguous. We know of examples of proteins that surely appear necessary, but whose genes are dispensable. The classic example is myoglobin. It is also easy to conceive of a simple route to an “essential” duplicate gene that does little new. Suppose, for example, that some gene was duplicated. Although the duplication caused the organism to express more of the protein than was optimum, subsequent mutations in the promoter or protein sequence of one or both of the copies decreased the total activity of the protein to pre-duplication levels. Now, however, if one of the copies is deleted, there is not enough residual protein activity for the organism to survive. The new copy is now “essential”, although it does nothing that the original did not do.

The main points of Behe’s reply can be summarized as follows:

  1. Gene duplications and subsequent changes to the copies (diversification) can and do happen, but the results are nothing really “new”— no new molecular machines or pathways (nor parts of such pathways), nor much in the way of new functions.
  2. Duplicated genes can become essential simply by “sharing” the original function, and then reducing their share to a minimum, perhaps through the amount of protein that each copy makes. Again, this is not anything really new, since the copy doesn’t do anything that the original didn’t do already. So, the finding that some gene copies are essential genes is not a threat to the IC argument.

Note that Behe’s reply makes predictions that can be tested with further research. These predictions might be summarized in this way:

  1. If IC is correct, duplicated genes will not be part of new, complex molecular pathways or machines.
  2. If IC is correct, duplicated genes that are both essential should “share” the original function.

Testing IC with new research

Behe’s reply to the Chen paper is of course hypothetical and speculative – as demonstrated by his own comment that “there is no reason to think” that the duplicated genes are components of new complex pathways or systems. Accordingly, the validity of Behe’s reply depends on its ability to hold up over time as more work is done. Of note, the functions of p24-2 and its parent gene Éclair have been studied intensively since 2010. These studies, as we shall see in the next post in this series, shed quite a bit of light on these questions.




Venema, Dennis. "The Evolutionary Origins of Irreducible Complexity, Part 2" N.p., 11 May. 2012. Web. 18 January 2019.


Venema, D. (2012, May 11). The Evolutionary Origins of Irreducible Complexity, Part 2
Retrieved January 18, 2019, from /blogs/dennis-venema-letters-to-the-duchess/the-evolutionary-origins-of-irreducible-complexity-part-2

References & Credits

Further reading:

Behe, M.J. Darwin’s Black Box: the Biochemical Challenge to Evolution. Free Press, New York, 1996.

Behe, M.J. The Edge of Evolution: the Search for the Limits of Darwinism. Free Press, New York, 2007.

Chen, S., Zhang, Y, and Long, M (2010). New genes in Drosophila quickly become essential. Science 330; 1682-1685.

About the Author

Dennis Venema

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. 

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