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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John - #43327

December 10th 2010

Ashe:
“What are you referring to when you say “post facto”?”

You offered a perfect example of the genre: “Deep homology is in fact anticipated by Mike Gene’s idea of front-loaded evolution.”

“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.”

What criteria would you propose, then?

“Blast just shows the right direction to pursue.”

I think that you don’t know what you are talking about here.

“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.”

Again, “I’m not writing a paper here” is a non sequitur. You clearly are afraid to examine the evidence for yourself.

“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.”

I doubt it. But being a scientist, I’m willing to admit when I am wrong.


chunkdz - #43339

December 11th 2010

John:

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

Dr. Ussery’s prediction is that we will find homologs for “many (most)” eukaryotic proteins. Not “buiding blocks”.

“Biology is complicated, chunkdz, but not in any way that suggests an intelligent designer.”

Actually, it’s not the complexity of biology that suggests design to me. I see the hallmarks of design in the rational simplicity of biology. Take for instance your example of the Armadillo repeat. If a designer wanted to ensure the evolution of complex multicellular life, tandem repeats would seem to be an absolutely essential design feature for front-loading modularity and future functionality.

Rationality. Foresight.

“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.”

I agree. The deeper we go into biology the more it appears that life are highly advanced nanotechnology.


Rich - #43364

December 11th 2010

John wrote:

“I doubt it. But being a scientist, I’m willing to admit when I am wrong.”

Fact check:

John was proven to be completely wrong (by citations of numerous journal articles) in a claim he made about chimpanzee/human genome comparisons, and not only would not admit it, but would not even reply to the comment.

Recently John claimed *without qualification* that “random mutation” was “a creationist term.”  A humiliating number of references proved him wrong; he then claimed that he really meant something other than what he said, and therefore was not wrong.

John does not admit errors.  And he isn’t the only Darwinist here like that.  Another one refused to admit that he had blatantly misinterpreted an extremely clear passage by Lynn Margulis (someone who has contributed more to evolutionary theory than all the biologist-commenters here put together, and presumably therefore knows what she is talking about when it come to defining neo-Darwinism).

I see no virtue in a terroritorial, professional pride which cannot bring itself to say “I stand corrected.”  I’ve never seen such pride in physicists or chemists.  Biologist-commenters here seem to have a gigantic chip on their shoulder.  I wonder why.


John - #43923

December 16th 2010

Rich:
“John was proven to be completely wrong (by citations of numerous journal articles) in a claim he made about chimpanzee/human genome comparisons, and not only would not admit it, but would not even reply to the comment.”

Where was this? And what’s the evidence that I would not admit it?

“Recently John claimed *without qualification* that “random mutation” was “a creationist term.”

I should have qualified it to reflect the data from PubMed:
mutation: 573873 citations
random mutation: 168 citations

Pretty clear to me.

“John does not admit errors. “

Yet I just did. When will you support or retract your claim about deleting bacterial flagellar components, Rich?

“I see no virtue in a terroritorial, professional pride which cannot bring itself to say “I stand corrected.””

So how many papers from the primary literature did you consult before making a global claim about flagellar components? I’m guessing zero, because your claim is utterly, objectively false.


John - #43924

December 16th 2010

chunkdz:
” If a designer wanted to ensure the evolution of complex multicellular life, tandem repeats would seem to be an absolutely essential design feature for front-loading modularity and future functionality. Rationality. Foresight.”

I’m sure that’s what every son and daughter watching a parent die of Huntington disease thinks. After all, it’s caused by expansion of tandem CAG repeats.

Or color blindness, caused by recombination between what once was a tandem repeat, deleting one of the repeats.

Brilliant design feature!


Rich - #43935

December 16th 2010

Re 43923:

Rich:  “Recently John claimed *without qualification* that “random mutation” was “a creationist term.”

John:  “I should have qualified it to reflect the data from PubMed:
mutation: 573873 citations
random mutation: 168 citations”

Rich:  “John does not admit errors. “

John:  “Yet I just did.”

No, John did not.  He did not retract the error that “random mutation” was a “creationist term.”  He continues to conceal the fact that it’s a term which comes from the founders of the Modern Synthesis, and was central to it, and to ignore the quotations I gave from leading evolutionary biologists.

The honest and accurate admission of error would be:  “I was wrong to say that ‘random mutation’ is a creationist term.  It’s a classic neo-Darwinian term.  I therefore withdraw the cheap shot I took at Behe in connection with this error of mine.”

Note: searching on “random mutation” is inadequate, since the words “random” and “mutation” might well be separated by one or more words.  The idea can be present without the exact phrase.  It would be better to search on “random”.  In any case, the phrase is not a creationist term, so the error remains no matter what the PubMed numbers.


Rich - #43944

December 16th 2010

Re: 43923:

See Would You Like Fries with that Theory, Part 3

Rich: (paraphrase)  Geneticists have sometimes given the figure of roughly 2% difference between the chimpanzee and human genome.

“John”:  “I’m a geneticist, and chimps and humans are far more than 2% different genomically. Where do you get these silly fabrications, Rich?”

Rich:  “Some methods bring the number down below 2%; …”

John:  “None that consider the GENOME do.”

Note the absolute, unqualified nature of these statements. 

Now, note the reply of Rich 23231 below on the same thread, containing many references to a roughly 2% figure for the difference in the genome.

John never replied, nor has he replied when this has been brought up on other threads.
John was in error and would not admit it.

Note that Rich explicitly said that he was not defending or arguing for that figure.  It was immaterial to the original point he was making.  It was John that made an issue of 2%.  Rich did not ask John to agree with the figure.  He asked John to agree that some geneticists gave it.  And John wouldn’t agree.  The literature shows that John was wrong.  And John wouldn’t retract.  He did not admit error.


Rich - #43947

December 16th 2010

Re: 43923

While we are on the subject of that previous thread, there was another error there which John would not admit to.  Consider this exchange (23223):

Rich: “I have no religious commitment to ID,…”
John:  “Rich, I’ve seen your web site.”

and this comment (23188):

John:  “The same factoid is on your web site”

Elsewhere in the same area, John said, “You work in a lab” (23030).

Rich does not work in a lab.  Rich has no web site, and never did.  Rich told John that he had no web site, and that John had clearly been confusing him with someone else, and had been venting anger upon Rich that should have directed at the someone else who worked in the lab and had a web site.  John would not retract.  He would not say:  “I’m sorry for raging at you in comment after comment, when I have clearly mixed you up with someone else.”  This error was brought up on other threads as well, giving John ample chances to retract.  John did not retract.

This is a third example demonstrating that John does not make a rule of admitting errors.


chunkdz - #44022

December 16th 2010

John:

I’m sure that’s what every son and daughter watching a parent die of Huntington disease thinks. After all, it’s caused by expansion of tandem CAG repeats.

Or color blindness, caused by recombination between what once was a tandem repeat, deleting one of the repeats.

Brilliant design feature!


Given that without tandem repeats humans don’t even appear, and your hypothetical family never gets to experience a single moment of love and joy together- emphatically YES! BRILLIANT!

The benefits astronomically outweigh the potential flaws. Brilliant design is always a tradeoff between various constraints. 

Protein based machines are exceedingly brilliant. Well beyond anything humans are currently capable of to be sure.


John - #44499

December 20th 2010

Chunkdz rationalized:
“Given that without tandem repeats humans don’t even appear,…”

How do you know this?

“... and your hypothetical family never gets to experience a single moment of love and joy together- emphatically YES! BRILLIANT! The benefits astronomically outweigh the potential flaws.”

That’s interesting, particularly since I can intelligently design an identical amino-acid sequence that is only 70% identical, suppressing homologous recombination between tandem repeats. Is your designer less intelligent than I am?

“Brilliant design is always a tradeoff between various constraints.”

This tradeoff doesn’t have to happen. I could interrupt tandem repeats with introns in different places, too, but we don’t see that. We see boys dying young from Duchenne muscular dystrophy, much of which is caused by homologous recombination.

“Protein based machines are exceedingly brilliant.”

We weren’t talking about the machines, we were talking about the death and suffering caused by tandem repeats within them. I can see why you’d want to run away from that, though!


John - #44500

December 20th 2010

Rich:
“Note: searching on “random mutation” is inadequate, since the words “random” and “mutation” might well be separated by one or more words.”

Then we agree that Behe’s search was inadequate when he testified:


John - #44501

December 20th 2010

Q. Now, you on Monday showed the court, or maybe it was Tuesday you showed the court that you had done a literature search of articles on the immune system looking for the words “random mutation,” correct?
A. Yes.
Q. But you didn’t search for transpositions, is that correct?
A. That’s correct.
Q. And that word appears in a number of the titles here?
A. It does, but the critical difference is the word random. There’s lots of mutations, and it’s entirely possible that intelligent design or some process of the development of life can occur by changes in DNA, but the critical factor is are such changes random, are they not random, so just there are also many occurrences of the word mutation, but it was not just mutation that is the critical element of Darwinian theory. It is random mutation.
Q. But in modern Darwinian theory transposition is one of the kind of mutations that natural selection acts upon, correct?
A. It is a mutation, and natural selection can act upon it.
Q. So the word mutation didn’t show up, or random mutation, but a form of mutation that natural selection can act upon appears throughout these articles, correct?
A. Yes, that is right.


John - #44509

December 20th 2010

I wrote:
“...I can intelligently design an identical amino-acid sequence that is only 70% identical, suppressing homologous recombination between tandem repeats.”

To clarify, I can design identical amino acid sequences that are only 70% identical at the nucleotide level.


Rich - #44586

December 21st 2010

John wrote (43327):

“I doubt it. But being a scientist, I’m willing to admit when I am wrong.”

In a series of comments above (43364, 43935, 43944, 43947), it was shown that John has several times been wrong and, when confronted with his errors, will not admit them.  That was several days ago. 

John has since posted 4 more comments, none of which responds to the demonstrations of error, even though he specifically asked for proof of one of the errors (43923).

This is not surprising.  He did not respond to some of these demonstrations of error months ago, when they were pointed out to him; so why should he now?

Nor do I expect that John will respond to the revelation in the comments, on Part VI of this topic, that he has not been consistent in his self-representation regarding his employment as a scientist. 

Nor do I expect that John will ever reveal his identity and say directly *to* Michael Behe the things he has said, under the cover of anonymity, *about* Michael Behe.  I wish that he would, because it would be a pleasure to view a scientist and gentleman like MIchael Behe politely dismantle John’s abrasively offered criticisms and leave them lying in pieces all over the floor.


chunkdz - #44597

December 21st 2010

John:

How do you know this?

I read books.

“It seems probable that just as tandem repeats are affected by deletions and expansions in some well-known human diseases, so too are they implicated in the formation of evolutionary breakpoints” - Pantarotti, P., Evolutionary Biology (2010), p148


Tandem repeats are also thought to be responsible for a lot of mammalian evolutionary plasticity. Their modular design allows for great flexibility.

I can intelligently design an identical amino-acid sequence that is only 70% identical, suppressing homologous recombination between tandem repeats. Is your designer less intelligent than I am?

Great. But you would sacrifice flexibility and adaptability.

This tradeoff doesn’t have to happen. I could interrupt tandem repeats with introns in different places, too, but we don’t see that.

I’m not sure how tandem repeats could assist in evolutionary breakpoints if you were constantly thwarting their efficacy.


chunkdz - #44598

December 21st 2010

...we were talking about the death and suffering caused by tandem repeats within them. I can see why you’d want to run away from that, though!

Not running away, John. Here’s two points for you to chew on.

Tandem repeats are concentrated at human chromosomal breakpoint regions. This implies that they are crucial facilitators of human evolution. They confer great flexibility and plasticity, but this comes at the cost of possible disease. A design tradeoff.

I guess one could design a rigid, static genome that plays it safe by severely limiting flexibility and exploration of evolutionary search space. No one will ever die of Duchenne muscular dystrophy because no human will evolve.


Second point: If you are saying that death and suffering are design flaws, then you’ll have to explain why. One could certainly make the argument that the Space Shuttle is a poor design because it’s heat shield fails sometimes. But I don’t see any astronauts backing out of missions. In fact, they seem to be clamoring for a chance to test the design tradeoffs.

That’s because a chance to visit the stars is worth the risk of dying. And a chance to live as a human is worth the risk of an early death.

Brilliant.


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