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

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November 19, 2010 Tags: Design

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 we believe here.

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

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.


David Ussery is an associate professor of comparative microbial genomics at the Center for Biological Sequence Analysis at the Technical University of Denmark and on the faculty at the University in Oslo, Norway. Ussery is the co-author of Computing for Comparative Microbial Genomics and has authored or co-authored 130 articles for science and professional journals. He is also a frequent public speaker on the topic of bacterial genomics.

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Alan Fox - #42410

December 3rd 2010

Had a look atAxe’s latest paper  and he still seems to be making the same argument of “1 in a gadzillion” without establishing that there are not in fact many more than one in a gadzillion.


Alan Fox - #42411

December 3rd 2010

Here for the Szostak paper.


Dave Ussery - #42412

December 3rd 2010

I’m curious what people think about this bacteria that seems to not require arsenic.  Here’s a quote from an article about it in the newspaper:

‘This story is not about Mono Lake or arsenic, she said, but about “cracking open the door and finding that what we think are fixed constants of life are not.”’

So perhaps the fundamental constants of life are not as ‘finely tuned’ as previously thought?  We don’t need 6 elements, but only 5, for life to exist???


John - #42414

December 3rd 2010

johan wrote:
“a) Evolution is as politically correct in academia today as you can get, meaning, just mention the word “evolution” and your paper is likely to pass peer review as the editors are as convinced of evolution as you are and you received grants to do evolutionary research.”

This is absurd. Peer review is primarily about the DATA in a paper. Are the data new, do they advance the field?

And there is very little money devoted to evolutionary research. There is far more money devoted to biomedical research, which still tells us a lot about evolution.

“b) ID proponents do get their papers published in secular journals, this is the equivalent of you getting your pro-evolution papers published in creationist journals, so they at least deserve credit for that.”

No paper with an empirical test of an ID hypothesis has ever been published. ID proponents lack the faith to do any such test.

“Doug Axe did a much more careful study, asking for real enzymatic function, not just binding. He also looked at a medium-sized protein domain, about 150 amino acids in length.”

Why did Axe only look at a single protein, johan? How can anyone honestly derive a global conclusion from a single case?


johan - #42415

December 3rd 2010

//So perhaps the fundamental constants of life are not as ‘finely tuned’ as previously thought?//

a) life is based on semantic information, not on the physicality of it’s elements.

b) the “chemical uniformity of life” was hailed to be powerful evidence for evolution, as Niles Eldredge put it:

“The basic notion that life has evolved passes its severest test with flying colors: the underlying chemical uniformity of life, and the myriad patterns of special similarities shared by smaller groups of more closely related organisms, all point to a grand pattern of descent with modification.”

What happens to evolution if we find out that the chemical uniformity is not so uniform? Nothing, because as Dave puts it, “it shows that life is not finely tuned”. Heads evolution wins, tails evolution wins.


johan - #42416

December 3rd 2010

//This is absurd. Peer review is primarily about the DATA in a paper. Are the data new, do they advance the field?//

It’s about the data? Of course, scientists are people in white lab coats who give us only objective answers, we live in such a wonderful world.

Please, pray tell, how can a paper with such a title appear in a biology journal?

Barbara Forrest, “The Religious Essence of Intelligent Design,” Cold Spring Harbor Symposia on Quantitative Biology 74 (2009) 455-462.

Bash ID and your paper is likely to pass peer review no questions asked, only ID theorists could have motives.


John - #42426

December 3rd 2010

I wrote:
“Peer review is primarily about the DATA in a paper. Are the data new, do they advance the field?”

johan replied, strategically omitting my qualification:
“It’s about the data?”

Primarily, yes.

“Of course, scientists are people in white lab coats who give us only objective answers, we live in such a wonderful world.”

Scientists give us new data. The ID movement gives us rhetoric.

“Please, pray tell, how can a paper with such a title appear in a biology journal?”

Is is a biology journal or a symposium volume, johan?

“Bash ID and your paper is likely to pass peer review no questions asked, only ID theorists could have motives.”

Are symposium volumes in general (and this one in particular) peer reviewed, johan?


chunkdz - #42433

December 3rd 2010

Alan Fox: I responded to the first part of your question: Just curious - is this a prediction that flows from Modern Evolutionary Theory… which is a basic enough question and does not need any particular expert to answer it, though Dr. Ussery is free to make a comment, as anyone is here.

Hard to call something a basic question if it hasn’t been answered.  But thanks for the permission to speak!

I linked to the Jack Szostack lab because of their work showing that functionality is widespread in random protein sequences which tends to refute Axe’s “needle-in-a-haystack” argument.

Actually you linked to the Szostak paper as putative evidence that novel proteins evolve from extant proteins. Unfortunately, that Szostak paper says nothing of the sort. And anyway, the fact that novel proteins evolve from extant proteins is orthogonal to my original question.

I suspect that you don’t fully comprehend the question so let’s just wait for Dr. Ussery to weigh in, shall we?


John - #42436

December 3rd 2010

chunkdz wrote:
“Actually you linked to the Szostak paper as putative evidence that novel proteins evolve from extant proteins.”

Which it is.

“Unfortunately, that Szostak paper says nothing of the sort.”

You exalt rhetoric and you ignore evidence. The evidence in my own papers test Axe’s hypothesis more rigorously than Axe has tested it, but the words in my own papers don’t mention Axe’s hypothesis.

Would that make the evidence presented in the figures and tables irrelevant?

“And anyway, the fact that novel proteins evolve from extant proteins is orthogonal to my original question.”

No, it is integral to replying to your question. You’re just unwilling to examine evidence for yourself.


Ashe - #42437

December 3rd 2010

In general Axe’s paper (and many before his) show that it’s very rare to get back functional proteins when large numbers of residues in a protein fold are randomized. In general, Evolutionary theory doesn’t necessarily predict that you get new functions from extant proteins, because they also expect that functional proteins didn’t originally evolve from randomization of large reading frames, but from smaller fragments.

People have obtained folded, functional proteins from random libraries with complexities of 1e13 or so.


Ashe - #42438

December 3rd 2010

Dave:

I’m curious what people think about this bacteria that seems to not require arsenic.  Here’s a quote from an article about it in the newspaper:

I think they replaced phosphorus with arsenic. I think it says a lot about the power of bacteria to adapt to their environment. I like what Joyce said “It’s a really nice story about adaptability of our life form”.


chunkdz - #42444

December 3rd 2010

John:

You exalt rhetoric and you ignore evidence. The evidence in my own papers test Axe’s hypothesis more rigorously than Axe has tested it, but the words in my own papers don’t mention Axe’s hypothesis.

I’m sure your scientific papers are very fascinating.

But as my question was not about Doug Axe or his hypothesis, I’d prefer to wait and let Dr. Ussery answer my question. I hope you understand.


Bilbo - #42447

December 3rd 2010

Apparently Behe has just published another peer-reviewed paper:


http://www.journals.uchicago.edu/page/qrb/papers.html


Alan Fox - #42460

December 3rd 2010

Hard to call something a basic question if it hasn’t been answered.

Would you have preferred a different answer to your question?

Just curious - is this a prediction that flows from Modern Evolutionary Theory…

Have you read ‘The Design Matrix’? See pages 150-152. It would seem the answer is still yes.


chunkdz - #42465

December 3rd 2010

Alan:

Would you have preferred a different answer to your question?

I don’t think you are qualified to say whether the prediction comes from Dr. Ussery’s research unless you’ve followed his research very closely.

Have you read ‘The Design Matrix’? See pages 150-152. It would seem the answer is still yes.

So we’re back to the Szostak study? Tell me, Alan, based upon the Szostak study what percentage of eukaryotic proteins would Modern Evolutionary Theory predict to find homologs for in prokaryotes? 10%? 50%? 90%? Please be specific so that we may falsify your hypothesis experimentally.


Ashe - #42466

December 3rd 2010

Those pages contain a great discussion of some of the discoveries of deep homology, nothing at all though about how this is a prediction that flows from Modern Evolutionary theory.


Alan Fox - #42503

December 4th 2010

I don’t think you are qualified to say whether the prediction comes from Dr. Ussery’s research unless you’ve followed his research very closely.

As I said before, I responded to the first part of your question.

Just curious - is this a prediction that flows from Modern Evolutionary Theory…

(“of course”, clarified as “‘yes” was my answer.”)

Dr. Ussery can speak for himself but his comment above:

I wouldn’t be surprised if many (most?) of the eukaryotic proteins have homologs in bacteria - this just makes sense, given that prokaryotes have been around for the first 90% of life’s history, before animals / plants came along, much more recently.

seems clear enough.

Now, intriguingly, you ask a potentially much more interesting question:

...based upon the Szostak study what percentage of eukaryotic proteins would Modern Evolutionary Theory predict to find homologs for in prokaryotes? 10%? 50%? 90%? Please be specific so that we may falsify your hypothesis experimentally.

Keefe and Szostak conclude (contd next comment)


Alan Fox - #42505

December 4th 2010

(contd from #42503)

We therefore estimate that roughly 1 in 10 [raised to power] 11 of all random-sequence proteins have ATP-binding activity comparable to the proteins isolated in this study.

And they were only examining one potential function - ATP binding. It may be that most sequences may have some potential biological activity. You ask about homologues. Keefe and Szostak were not addressing the issue of homologues in the experiments described in this paper though there is extensive research, for example Hanks and Hunter, 1995 showing how nested hierarchies can be derived from sequences.

So if biological activity is common in random sequences, life in its known diversity may have only exploited a small fraction of available working proteins due to the limitation imposed by evolutionary pathways needing to move through an unbroken chain of viable sequences (if evolution is true).


Alan Fox - #42507

December 4th 2010

Those pages contain a great discussion of some of the discoveries of deep homology, nothing at all though about how this is a prediction that flows from Modern Evolutionary theory.

There are several quotes (staring page149, sorry) that illustrate it is a given among mainstream biologists. Find a black swan.


chunkdz - #42510

December 4th 2010

Alan, a simple “I have no idea” would have sufficed.

But if you ever come up with an answer to this “basic” question let me know. 


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