Is There an Edge to Evolution? Part 5: It’s All About Numbers

Today's entry was written by David Ussery. Please note the views expressed here are those of the author, not necessarily of The BioLogos Foundation. You can read more about what BioLogos believes here.

Dr. Ussery continues his chapter-by-chapter analysis by focusing on Chapter 8. This time he finds some significant problems with Behe’s extrapolations. Darrel Falk and Dave Ussery have worked closely on this; however, the primary author is Dr. Ussery.

Chapter 8 - Objections to the Edge

I agree with Behe when he says “Time is actually not the chief factor in evolution - population numbers are.” (page 153). Perhaps an analogy can help explain this. In my line of work, we rely heavily on computers. For example, I want to do a comparison of a thousand bacterial genome sequences – if it takes a few days to do a calculation on one genome, then it would take literally YEARS to do the calculations for a thousand genomes. How do we get around this? By using lots of processors in parallel. If we have 1000 CPUs, then in principle, assuming the computers are free and all goes well, we can do the calculation in a few days. Thus, by using parallel processing, one can speed things up tremendously. The argument goes for evolution as well. Although the mutational frequency might be small, if you have enough genomes, the chances of getting the ‘right combination’ is much greater, especially if it happens in parallel along with the occasional recombination of genomes.

Behe’s argument in this chapter is essentially that even with more than several hundred million years of evolution, this is simply not enough time for the ‘right mutations’ to occur in order for the complexity we see around us, in terms of plants and animals, to have evolved via ‘random processes’. On page 163, Behe poses the question: "Yet if it can do so little, why is random mutation/natural selection so highly regarded by biologists?" He then goes on to compare the idea of random mutations with that of "ether", that mysterious substance hypothesized to exist more than a hundred years ago, but thoroughly discredited by Einstein. It is quite clear from this comparison that Behe thinks “random mutation” is a myth believed by most biologists on faith, with little evidence to back it up.

I disagree. I do believe that life’s history is infused with purpose and that this process is God’s process. The question here, from my perspective, is not whether there is purpose or not, but whether the scientific arguments presented in Behe's book make sense and are valid, based on what is currently known in biochemistry and molecular biology. It is those arguments that I address here. To really understand the potential of mutations to build new protein interactions you need to see a much bigger picture than Behe paints. Bacteria have been around since the first ecosystems, more than 4 billion years ago, and are still the most predominant life form on the planet today. I have a table I love to show my students when I'm teaching. It comes from a review article published about a year ago. There are 10³¹ bacteriophages (viruses that attack bacteria) on the earth, and if one were to stretch out their genomes, end-to-end, they would be about a thousand times the length of the Milky Way galaxy! If one were to stretch out all of the bacterial DNA from the planet, it would be close to a MILLION times the length of the Milky Way! So this is an enormous amount of DNA. Since bacteria have very short lifetimes (less than a day) that means that more than that amount of DNA is being replicated every day. With each replication there is an opportunity for genetic change in parallel lines which have the opportunity to mix and match every so often in the history of life. In examining a tiny, tiny fraction of that, a 'mere' thousand bacterial genomes, I am absolutely astounded at the amazing diversity. As I've said before, not a single protein is conserved amongst just this tiny sampling of bacteria we've looked at so far, and many bacterial 'species' have less than half the proteins of one genome found in another genome - of the same species! To what extent does Behe appreciate this vast opportunity to build new combinations of proteins?

Behe makes an astonishing conclusion. He states “the formation of even one helpful intracellular protein-protein binding site may be unattainable by random mutation.” (page 157). Let’s start off by examining what has been published. Go to PubMed, search their more the 20,000,000 articles online. If you type in “evolution, protein binding sites” you will see the article, “Structural features and evolution of protein-protein interactions” along with 5400 other articles on the topic. The abstract for this article includes the sentence:

Here, the interfaces of 750 transient protein-protein interactions as well as 2,000 interactions between domains of the same protein chain (obligate interactions) were analyzed to obtain a better understanding of molecular recognition and to identify features applicable for protein binding site prediction.

This is just one article. Would you agree that perhaps Behe’s statement “the formation of even one helpful intracellular protein-protein binding site may be unattainable by random mutation” is likely not to be too meaningful? It seems that it might be a little premature to bring his summary of the state of biological research to a public audience as he did in this book. There is no question that Behe’s story is very incomplete. You are especially urged to read Kelsey Luoma’s excellent article on this. She is an undergraduate student who did what all good science students do--she went back to check the literature. The literature clearly demonstrates the evolution of new protein interactions.

So Behe is clearly wrong when, on page 154, he says that since “we see no new protein-protein interactions developing in 10²⁰ cells, we can be reasonably confident that, at least, no new cellular systems needing two new protein-protein interactions would develop in 10⁴⁰ cells - in the entire history of life…" Depending upon your math background you might be tempted to think that the difference between 10²⁰ and 10⁴⁰ is not that great. Just in case that is the case, let’s examine how different those numbers are with a little illustration. The DNA from 10²⁰ cells of bacteria would be about 18 light years long – that’s a lot of DNA! However, the length of the DNA from all bacteria, on the face of the planet, living right now (roughly 10³¹ cells), is about 100,000,000,000 LIGHT YEARS long. However, that is just is just the amount of bacterial DNA present right now. Bacteria duplicate as often as once every five minutes. So compared to the DNA in 10²⁰ cells (18 light years) the amount of DNA in 10⁴⁰ cells is 1,800,000,000,000,000,000,000 light years. That’s a lot of DNA. (Remember there are 180,000 miles in one second of a light year. That’s a lot of DNA.) Let’s be careful about telling the public “we can be reasonably confident that, at least, no new cellular systems needing two new protein-protein interactions would develop in 10⁴⁰ cells - in the entire history of life…” The generation of this amount of DNA provides for a lot of opportunity for mutations that would generate new protein interactions.

Let’s look further at what really was done in the experiment with 10²⁰ cells he discusses in the quote from page 154 where he clearly states that no new protein-protein interactions were seen. The fact is that in this experiment they didn’t search the proteome for new protein-protein interactions - they were only looking for one particular type of mutation. So not only did Behe’s extrapolate from a “pin-prick” sample size (10²⁰ cells) to a larger than universe-sized sample size (by comparison), the authors of this study didn’t even begin exhaustively comb the “pin-prick” sample for new protein-protein interactions. It is dangerous to extrapolate over “zillions” of orders of magnitude (from 10²⁰ to 10⁴⁰) even at the best of times. However, Dr. Behe did it for a parameter that had not even been carefully searched to begin with. The investigators did not design the experiment to search for any new protein-protein interactions in the entire protein repertoire of cells- they were just probing for one particular phenotype. Behe is correct that they didn’t see them, but to conclude that they didn’t find ANY new protein-protein interactions is a bit far-fetched, since they weren't looking for them. They were only looking for a small number of highly specific changes, not the proteome as a whole. True, no one reported finding beneficial mutations in the samples studied, for this particular case, but to conclude that they can in general never or only rarely happen is just a hopeful extrapolation.

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