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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Ashe - #43063

December 8th 2010

259


John - #43064

December 8th 2010

Ashe,

“Anticipated”? Really?

Please present empirical evidence of this anticipation before 1997.


Ashe - #43067

December 8th 2010

John , there could be examples pre-1997 from Mike Gene, I remember him talking about it as far back as 2000, but thats irrelevant, I wasn’t saying that he predicted it pre-1997, I’m talking about the logic of his idea anticipates it. Predictions aren’t necessarily temporal, the best ones are, though. Specific, and anticipatory.


John - #43076

December 8th 2010

Ashe:
“thats irrelevant, I wasn’t saying that he predicted it pre-1997,”

I didn’t say you said that. I asked for empirical evidence of this anticipation.

“I’m talking about the logic of his idea anticipates it.”

Sorry, Ashe, that just doesn’t wash. The idea is consistent with it, maybe, but pretending that there was any anticipation when you have no evidence for it seems deceptive.

“Predictions aren’t necessarily temporal, the best ones are, though. Specific, and anticipatory.”

I’m sorry, but you’re making no sense. In science, predictions are empirical. Got any?


Ashe - #43078

December 9th 2010

The idea is not just consistent with it, it’s anticipatory, with the idea in hand, you expect to find important stuff are really ancient. On the other hand, MS is consistent with the idea, but it did not expect it .  I have given you already an example of an empirical prediction with regard to Bcl-2.


chunkdz - #43083

December 9th 2010

Alan:

So you agree with “homolog sequences can diverge “beyond recognition,””? You understand that if two living species diverged from a common ancestor 3 billion years ago,

And yet Dr. Ussery predicts that we will find them.

“In fact, to be honest, I would be surprised to find very many proteins at all which are present in eukaryotes, and completely missing in single-celled organisms.” - Dave Ussery


chunkdz - #43085

December 9th 2010

John:

“Around 50%, of course.”

I wonder why Dr. Ussery disagrees with you.

“In fact, to be honest, I would be surprised to find very many proteins at all which are present in eukaryotes, and completely missing in single-celled organisms.” - Dave Ussery

John:

“Absolutely not.”

I wonder why Dr. Ussery disagrees with you.

“Just in terms of the vast vast amount of different sequences / structures found in the tiny amount of genomes we’ve sequenced so far.” - Dave Ussery

If two esteemed biologists cannot agree on such a “basic” prediction, then perhaps it’s not such a “basic” prediction after all?


John - #43111

December 9th 2010

Ashe wrote:
“The idea is not just consistent with it, it’s anticipatory, with the idea in hand, you expect to find important stuff are really ancient.”

Sorry, “important stuff” isn’t remotely specific enough. Aren’t ribosomal proteins important and really ancient? It seems that you are moving the goalposts.

“On the other hand, MS is consistent with the idea, but it did not expect it .”

People expect things. Ideas don’t.

“I have given you already an example of an empirical prediction with regard to Bcl-2.”

It was as fuzzy as a palm reading. I asked:
“...but you’re still not there yet, as you haven’t defined finding a gene in empirical terms. What percent identity? Similarity? Or would finding something that has one structural motif or protein fold in common with Bcl-2 be enough for you to claim that the unicellular organism has a member of the family?”

Then, I asked if you had done a BLAST, to which you replied that you weren’t writing a paper, which was a truly bizarre evasion.

Why aren’t you eager to test an empirical prediction?


John - #43114

December 9th 2010

John:
“Around 50%, of course.”

chunkdz: “I wonder why Dr. Ussery disagrees with you.”

“In fact, to be honest, I would be surprised to find very many proteins at all which are present in eukaryotes, and completely missing in single-celled organisms.” - Dave Ussery

Do you not understand the meaning of the word “completely” in this context? It’s what Alan has been patiently explaining to you.


John - #43115

December 9th 2010

chunkdz: “Is it simply the vast variety of bacterial genomes and therefore a game of sheer numbers?”

John: “Absolutely not. Perhaps you should read up on BLAST and do a few runs, but not in the shallow way that “Mike” did. It’s a statistical analysis.”

chunkdz: “I wonder why Dr. Ussery disagrees with you.”

He doesn’t.

“Just in terms of the vast vast amount of different sequences / structures found in the tiny amount of genomes we’ve sequenced so far.” - Dave Ussery

What’s your point? Other than displaying an inability to grasp basic concepts or something much more insidious? Where did he say it was “simply” that?

“If two esteemed biologists cannot agree on such a “basic” prediction, then perhaps it’s not such a “basic” prediction after all?”

If you can’t understand the context of a discussion on a subject you blog about, then perhaps you should examine the evidence for yourself? You don’t do textual analysis very well.


Alan Fox - #43118

December 9th 2010

Deep homology is in fact anticipated by Mike Gene’s idea of front-loaded evolution.

Did Mike’s anticipation pre-date the confirmation of deep homology? This would indeed be impressive. Perhaps you can indicate where Mike first makes this prediction.

I am thinking about predictions about non-coding (“junk”) DNA that arose from people the ID movement post facto.


Alan Fox - #43119

December 9th 2010

Dr Ussery asked way up thread:

I’m curious what people think about this bacteria that seems to not require arsenic.

I don’t know if you saw this post? The general consensus from scientists who have commented in the blogosphere seems to be “underwhelmed”!


Ashe - #43162

December 9th 2010

John:

Sorry, “important stuff” isn’t remotely specific enough. Aren’t ribosomal proteins important and really ancient? It seems that you are moving the goalposts.

Not moving the goalposts at all. Yes ribosomal proteins are extremely important and really ancient. For eukaryotes, also the cadherins, phosphotyrosine based signaling, the MAP kinase, the splicing machinery , integrin signaling. All very ancient processes. I am not surprised at all that these go way way back. Whereas many evolutionary biologists were surprised.

You must have forgotten that I gave a very specific answer to your question with regard to bcl-2, to which you responded that I was now being too “stringint”. That is what is truly bizarre.


Ashe - #43164

December 9th 2010

*stringent


chunkdz - #43167

December 9th 2010

John:

“Where did he say it was “simply” that?”

I said “simply”.

Ussery said “Just”.

 

If you can’t understand the context of a discussion…

Sorry but you can’t blame me for the fact that you and Dr. Ussery have very different predictions for very different reasons.

Perhaps if you waited for clarification from Dr. Ussery it might help.


John - #43193

December 9th 2010

Alan:
“I am thinking about predictions about non-coding (“junk”) DNA that arose from people the ID movement post facto.”

Yes, especially that they can’t even get them right post facto! The funniest ones are those that claim that because some biologists found a function for 1 kb of DNA provisionally categorized as junk, that somehow means that a million-fold more has magically been recategorized too.

Ashe:
“Not moving the goalposts at all. Yes ribosomal proteins are extremely important and really ancient. For eukaryotes, also the cadherins…”

The cadherins? Are you referring to “Mike’s” discovery? What happens when you BLAST the human database with the hypothetical Volvox protein? Does beta-cadherin head the list?

“…phosphotyrosine based signaling, the MAP kinase,...All very ancient processes.”

And why would an intelligent designer have so many receptors feed into so few second-messenger pathways?


John - #43195

December 9th 2010

Ashe:
” ...am not surprised at all that these go way way back. Whereas many evolutionary biologists were surprised.”

Here’s what would surprise me: if an ID proponent would actually propose a feasible followup experiment, including predicted empirical results, when they claim that a new paper (usually cited via press release) supports the notion of ID post facto.

I won’t hold my breath.

“You must have forgotten that I gave a very specific answer to your question with regard to bcl-2, to which you responded that I was now being too “stringint”. That is what is truly bizarre.”

Why? You don’t understand that the binding sites would coevolve?

So what’s your excuse for posting comment after comment instead of spending a much shorter time doing a BLAST? Are you afraid to test your hypothesis?


Ashe - #43214

December 10th 2010

What are you referring to when you say “post facto”? Homologs of Bcl-2 have not yet been demonstrated in unicellular lineages.  Even if I could not find anything with blast, that would not demonstrate that bcl-2 would not be found in unicellular lineages.  Blast just shows the right direction to pursue.

I did not post “comment after comment” talking about this, you asked me about a possible example of an empirical prediction, twice no less, and I have simply given you one (i’ve talked about two in fact). Like I said, I’m not writing a paper here, I’m simply discussing and answering your questions.

And no I’m not just talking about the cadherins that Mike is pursuing although that is certainly relevant. However, I will look into your questions.


chunkdz - #43280

December 10th 2010

John:

“Do you not understand the meaning of the word “completely” in this context? It’s what Alan has been patiently explaining to you.”

Is the beta catenin gene “completely” missing in archaea and bacteria?


John - #43325

December 11th 2010

“Is the beta catenin gene “completely” missing in archaea and bacteria?”

The gene itself, as in an ortholog? Yes. The building blocks, as in Armadillo repeats, no.

Biology is complicated, chunkdz, but not in any way that suggests an intelligent designer. Perhaps you should study it for yourself instead of regurgitating hearsay that appears to support what you wish to be true.

And you would be wise to keep in mind that metaphors and similes are explanatory devices that inevitably break down as one goes deeper into biology.


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