I just came across an article in the journal Science called “Irremediable Complexity?” 1 In the article, the authors describe an evolutionary idea called “constructive neutral evolution,” which was first proposed in 1993. The paper starts out stating something that is quite obvious:
Many of the cell’s macromolecular machines appear gratuitously complex, comprising more components than their basic functions seem to demand.
Of course the cell seems “gratuitously complex” to an evolutionist, since an evolutionist is forced to believe that everything found in cells (as well as the cells themselves) developed as a result of random processes acted on by natural selection. You would not expect amazingly complex things to be produced that way. Nevertheless, when you look at cells, you see all sorts of amazing complexity. Of course, those of us who understand science know that the cell’s machinery is not gratuitously complex. It is simply very well designed by a Designer who built a lot of adaptability and diversity into His creation.
The paper goes on to ask how we can understand such “gratuitous complexity” in light of evolution. The real answer is that you cannot. However, that’s not the answer an evolutionist likes, so the authors have to come up with something else. They quickly reject the widely-held adaptationist belief that the complexity is just the result of natural selection preserving any random changes that improve basic function. While they admit that this view can explain some of the simpler aspects of the cell, it clearly fails when discussing some of the really complex parts of the cell.
Their reasoning is quite valid, but their proposed solution takes even more faith to believe than the adaptationist view!
The authors use the specific case of a eukaryotic cell’s highly-complex method of dealing with introns as an obvious example of why the adaptationist view doesn’t work for the really complex things found in cells. Remember that in eukaryotic cells (the kind of cells that make up plants, fungi, and animals), many genes are interrupted by introns. These introns are stretches of DNA whose information must be removed before the gene’s information can be used by the cell to make a protein.
Since introns contain information that is removed before the gene is actually used by the cell, it was first thought that the introns were “junk DNA.” After all, why would those sequences of DNA be there if their information is just thrown away before the gene is actually used? However, further investigation showed that the introns allow one gene to make several different proteins, because they allow the gene’s information to be spliced together in different ways. Thus, far from being junk, they allow DNA to store information much more efficiently than it would without them. In addition, they may play other vital roles, such as the encoding of small nucleolar RNAs (snoRNAs), which have several important functions in a cell.2
The authors consider the specific case of the mitochondria in the cells of a fungus from genus Neurospora. Mitochondria are responsible for producing most of the energy that a cell uses. They have their own DNA, which is called mitochondrial DNA. In the fungus mentioned above, many of the mitochondrial genes have introns. Most can self-splice, which means they don’t need any extra proteins to remove their information before the gene’s information is used. However, some require an additional protein (TyrRS) to bind to them in order for the gene’s information to be spliced properly. The protein seems perfectly designed to bind to the intron so as to make the gene splicing occur.
Now the adaptationist would say that the introns were initially all self-splicing, but then mutations occurred to make some introns unable to self-splice. Eventually, other mutations somewhere else in the DNA produced TyrRS, which was able to bind to the mutated introns to allow the gene once again to be spliced. However, the authors of this paper make the obvious point that this couldn’t possibly be the way things happened.
After all, a mutated intron that made it impossible to splice a gene would make the cell less likely to survive. Thus, the mutated intron would never get fixed in the population. Natural selection would (probably quite quickly) remove the mutated intron from the organism’s gene pool. Thus, the mutated intron would not be around for the many generations it would take for the TyrRS to evolve.
So what’s the authors’ solution? They say that the TyrRS was already being produced by the fungus’s cells. That way, when the introns mutated so as to be no longer self-splicing, the TyrRS was right there to bind to the introns. Over time, mutations in both the introns and the gene that produced TyrRS made the interaction between the two more efficient, so that when we look at it today, it appears that the TyrRS was designed perfectly for the introns.
Why was the TyrRS already in the cell? Well, the authors have an answer for that:
Specifically, if the binding interaction arose first—fortuitously or for some reason unrelated to splicing—its existence could allow the accumulation of mutations in the intron that would have inactivated splicing, were the protein not bound.
So the fungus just luckily had the TyrRS floating around in its cells. Perhaps it served some other unknown function. When the introns mutated, however, the TyrRS immediately started binding to the introns, and whatever other mystical function it once served was, over time, no longer needed.
In order to overcome the obvious problems inherent in the adaptationist view, then, we have to believe not only in lucky mutations that increase the information in a given genome, but also that for many of the very complex systems in the cell, lots of the machinery needed to deal with those mutations just happened to already be in the cell, perhaps serving some other function that is now completely unknown to us. When the lucky mutations occurred, those unrelated parts started working together, and eventually, the complex machinery we see today was perfected.
Boy, I am glad I am not an evolutionist. I just don’t have that kind of faith!
1. 1. Michael W. Gray, et al., “Irremediable Complexity?,” Science 330:920-921, 2010.
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2. 2. R Nowak, “Mining treasures from ‘junk DNA’,” Science 263:608-610, 1994.
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