The Evolutionary Origins of Irreducible Complexity, Part 3

| By on Letters to the Duchess

One of the challenges for 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.

In the previous post in this series we introduced the p24-2 gene, a brand-new gene identified in a large survey that compared several fruit fly (Drosophila) genomes to each other. The p24-2 gene stuck out like a sore thumb in this survey because it is present in only one fly species (Drosophila melanogaster). This gene arose from a duplication of a nearby gene (the Éclair gene) after D. melanogaster parted ways with other fly species within the last 3 million years. Pairs of recently duplicated genes and their “parent” genes are interesting to biologists studying how new gene functions arise—as well as an excellent opportunity to test the Intelligent Design (ID) argument from Irreducible Complexity (IC), as we discussed in the last post.

Éclair and p24-2 have distinct essential functions

The Éclair and p24-2 genes are part of a larger gene family in flies called p24 proteins. There are nine p24 protein genes in most Drosophila species, but the recent addition of p24-2 in D. melanogaster brings the total for this species to ten. The p24 protein family is a group of proteins that is widespread among diverse forms of life, such as plants, animals, and fungi. The various p24 proteins act as carriers for other proteins as they shuttle them from where they are made in the cell (the endoplasmic reticulum, or ER) to the Golgi apparatus(another location in the cell where proteins are modified and sorted). The p24 proteins do their jobs by binding their “cargo” proteins and loading them into small membrane spheres called vesicles that do the physical shuttling back and forth to different compartments within the cell.

Since p24-2 is a recent duplication of Éclair, the two genes are very similar at the structural level. Indeed, their amino acid sequences are nearly identical, as you might expect:

Of the 206 amino acids in each protein, only five differ between the two genes. (The figure above shows the amino acids for both genes using a single-letter code, and the differences are highlighted). Though these sequences are highly similar, already we see hints that the two genes are not equivalents. In fact, the difference between these two genes is already a little greater than the average difference we see between human and chimpanzee genes, and the separation of these two genes occurred much more recently than the human-chimpanzee split. Also, most of the differences are clustered at the one end of the protein, suggesting that a protein-protein binding domain has been altered. (See here for a description of binding regions that similarly latch onto sections of DNA)

Further work has confirmed the hypothesis that p24-2 and Éclair are not functionally equivalent genes. Several lines of evidence support this conclusion:

  1. Different defects are seen when the two genes are removed. While removing either gene usually results in the death of the fly, some rare flies do survive to adulthood. The survivors, however, have different defects: the loss of the Éclair gene results in female flies that cannot lay eggs, but loss of the p24-2 gene has no effect on egg laying at all.
  2. Éclair and p24-2 are not always found in the same cell types during development. For example, p24-2 protein is not found in the ovaries of adult females, whereas Éclair protein is very abundant in this tissue. This difference likely explains why removing Éclair is so detrimental to laying eggs, but removing p24-2 is of no consequence at all for egg laying.
  3. Éclair seems to share some functions with other p24 proteins that are less closely related to it than p24-2 is. For example, the “Basier” gene is found in all the same tissues in which Éclair is found. If a fly lacks Éclair, then it must have Basier (the flies all die if Basier is also removed). Similarly, when a fly lacks Basier, no loss of Éclair can be tolerated. These two genes work together and share their essential functions.
  4. One target “cargo” of Éclair has been identified - an important signaling protein called Wingless. The Wingless protein needs to be exported out of the cell in order to do its job, and without functional Éclair present, Wingless cannot make it from the ER to the Golgi, which it needs to do in order to be exported. The p24-2 protein, however, is completely dispensable for exporting Wingless. Thus p24-2 and Éclair are involved in transporting different cargo proteins. Éclair shares the function of exporting Wingless with another p24 family member (called Emp24), but notwith its closer relative, p24-2.

In summary, while p24-2 and Éclair are both essential genes, they are involved with different essential functions. They transport different cargo proteins (in some cases in different tissues), and they show different defects when they are removed. While there is some sharing of function among p24 family members, Éclair shares with proteinsother than p24-2.

Implications for the ID argument from IC

In our previous post we discussed ID proponent Michael Behe’s response to the 2010 paper that identified the new genes in Drosophila. In his response, Behe explained why he felt that paper was not a threat to the ID argument from IC:

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… What I don’t think can happen is that duplication/ divergence by Darwinian mechanisms can build new, complex interactive molecular machines or pathways…

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.

We also discussed how Behe’s thoughts could be expressed as testable hypotheses:

If IC is correct, duplicated genes will not be part of new, complex molecular pathways or machines.

If IC is correct, duplicated genes that are both essential should “share” the original function.

As we can now see, these hypotheses have not been supported through additional work on Éclair and p24-2. We now do have good reason to think that p24-2 is involved in its own complex molecular pathway, and that it is not merely sharing an essential function with its parent gene Éclair. While we do not yet have all the details of how p24-2 and Éclair work, we already know that p24-2 performs its essential role without merely propping up the function of its parent gene. We also know that it carries a different cargo that Éclair is carries. It appears to have developed a new protein-protein interaction that allows it to carry something else. This role could not have been essential when it first arose, but it is essential now.

In summary, the evidence strongly suggests that the essential function of the p24-2 gene qualifies as IC in the ID sense, and that this IC function arose through an evolutionary process. Even if ID supporters quibble over the precise details of the Éclair/p24-2 story, the more important issue is one that is hopefully now abundantly clear: evolutionary processes can add new components to already complex molecular systems; such additions cannot be essential when they are added; and additions can later become essential as the system comes to depend on them as other changes accumulate. Given this, the ID argument from IC is susceptible to false positives: IC systems are not reliable indicators of “design” in the ID sense, since evolutionary mechanisms can produce them. In the next post in this series, we will examine other examples of IC systems and the evidence for their evolutionary origins.


Notes

Citations

MLA

Venema, Dennis. "The Evolutionary Origins of Irreducible Complexity, Part 3"
https://biologos.org/. N.p., 17 May. 2012. Web. 16 October 2018.

APA

Venema, D. (2012, May 17). The Evolutionary Origins of Irreducible Complexity, Part 3
Retrieved October 16, 2018, from /blogs/dennis-venema-letters-to-the-duchess/the-evolutionary-origins-of-irreducible-complexity-part-3

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.
  • Boltz, K, Ellis, L, and Carney, G (2007). Drosophila melanogaster p24 genes have developmental, tissue-specific, and sex-specific expression patterns and functions. Developmental Dynamics 236; 544-555.
  • Port, F, Hausmann, G, and Basler, K (2011). A genome-wide RNA interference screen uncovers two p24 proteins as regulators of Wingless secretion. EMBO reports 12; 1144 – 1152.
  • Beuchling, T, Chaudhary, V, Spirohn, K, Weiss, M, and Boutros, M (2011). p24 proteins are required for secretion of Wnt ligands. EMBO reports 12; 1265 – 1272.
  • Saleem, S, Schwedes, C, Ellis, L, Grady, S, Adams, R, Johnson, N, Whittington, J, and Carney, G (2012).Drosophila melanogaster p24 proteins have vital roles in development and reproduction. Mechanisms of Development (in press).

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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