Is There an Edge to Evolution? Part 2

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October 18, 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 2

An Analysis of Michael Behe’s book, The Edge of Evolution

In his previous post, Ussery discussed his personal reasons for being interested in “The Edge of Evolution.” He went on to discuss two aspects of the book he appreciates, and he showed that he and Behe are in agreement that all living organisms have arisen through common descent from a single ancestral species.

In this post, however, Ussery says that Behe has presented a vastly over-simplified view of what scientists know about the origin of genetic diversity in the history of life. Here is his analysis based on Chapters Two and Three.

The accompanying figure illustrates the amount of genetic diversity in the bacterial world and beyond. It shows that even a single species of bacteria (E. coli) contains a vast reservoir of different genes. The term “orthologous” refers to genes in different species that clearly resemble one another and are thereby believed to have a common ancestry. Genes which are not orthologous are found in the species on the right side but not on the comparator species on the left.

Chapter 2 - Arms Race or Trench Warfare?

This chapter is about one of the classic examples of evolution: malaria and sickle cell anemia in humans. Behe observes (correctly, in my opinion) that the mutations that are responsible for helping some humans fight malaria are bad mutations. 'The first point is that the two examples he cites, sickle and Hemoglobin C (HbC), (two mutations that help the body resist malaria), are quintessentially hurtful mutations because they diminish the functioning of the human body. A second point is that “the mutations are not in the process of joining to build a more complex, interactive biochemical system.” (page 34).

Fair enough—and it is well known that harmful mutations, in the sense of wrecking something or making a pathway not work, occur much more frequently than beneficial mutations. However, Behe goes on to claim that there are “absolutely no studies' to document a molecular basis for the “coherent development of a single trait in a Darwinian arms race.” But this is highly erroneous . True, the example he gives us is not a “good mutation” - but to just blatantly claim that nothing has been done is showing his ignorance of the literature.

For example, consider this from the abstract of a recent review article, with the title “Origins, evolution, and phenotypic impact of new genes,” published in Genome Research. “The array of mechanisms underlying the origin of new genes is compelling, extending way beyond the traditionally well-studied source of gene duplication. Thus, it was shown that novel genes also regularly arose from messenger RNAs of ancestral genes, protein-coding genes metamorphosed into new RNA genes, genomic parasites were co-opted as new genes, and that both protein and RNA genes were composed from scratch (i.e., from previously non- functional sequences).” This is a new article, but many of the references in this article date to long before The Edge of Evolution was written, and some even date to before Darwin's Black Box was published, more than a decade ago.

Then there's another article about recent evolution of beneficial mutations in humans. There are many, many articles published on this sort of idea, and to claim that not a single study has been done is essentially a play on the ignorance of the readers! It is as if the hope is that the readers are ignorant of the scientific literature, and either too lazy or not competent to have a look through PubMed and see what is really out there.

Chapter 3 - The Mathematical Limits of Darwinism

One of my Ph.D. students was a mathematician, and I can still remember trying to read through his paper—lots of formulas—and sometimes they were difficult for me to understand. I have since learned that many people in math departments have a strong disliking for statisticians - I used to naively think that the two are the same. In this chapter, it looks as though Behe has confused mathematics (in the title) with statistics (what is actually discussed in the chapter). What's worse, the numbers he uses are based on bad assumptions, and are way off from what is known in the field by experimentalists doing current research in this area. Thus, unfortunately, his conclusions are not as strong as they might seem at first glance.

First, in calculating the odds of a single mutation in a protein, one has to take into account the chances of a mutation in the DNA sequence, because this is where mutations happen in biology - this is part of the 'central dogma' of molecular biology - that the information flows from DNA to RNA to protein, but not from proteins back to DNA. Thus, if a protein has a particular amino acid changed, this can be traced back to a change in the DNA sequence. Behe says ”resistance to chloroquine has appeared fewer than ten times in the whole world in the past century” - but what is meant by this shorthand is that we have documented evidence of this happening only a few times - that's not the same as knowing definitively that this HAS happened only those few times. Lots of things [like mutations leading to drug resistance] happen all the time that don't get seen and documented.

Then, based on this vastly over-simplified estimate, he suggests that the odds of a parasite developing resistance to chloroquine is one in 1020, whilst the odds of developing resistance to another drug (atovaquone) is one in 1012. Since the former, he says, involves two amino acid changes, while the latter involves on one, from these two numbers, it is concluded that the chance of having mutations which change two amino acids in a protein is a hundred million times lower (10-20 vs 10-12) than that for just getting one.

But this just simply does not make sense. Even within E. coli, the well known work-horse of molecular biology, take the order of amino acids in any one of its 5000 or so proteins, and compare that arrangement to that in other E. coli strains and you will find LOTS of differences. For many proteins in E. coli, the level of identity between strains is around 80% - that is, about twenty out of every hundred amino acids are different - so to say that the odds for a double mutation (2 amino acid changes out of 100), is essentially impossible, when we observe 10 times that amount of diversity (20 differences for every 100 amino acids) in natural populations is speaking from ignorance. We see ten times the number of changes which Behe says is almost impossible all around us within a single species without even the need to generate new mutations.

I’ll discuss the vast differences found with various sequenced E. coli genomes later, but getting back to this chapter and the mutations in the two different spots within a single gene, Behe concludes:

On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since this is many times the age of the universe, it's reasonable to conclude the following: No mutation that is the same complexity of chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years. (page 61, emphasis in the original).

But again, if one takes a deep breath, and looks at what is known, the mutational frequency that we can actually measure in humans is many times greater than that upon which Behe's assumptions are based. His argument is that the chances of getting useful mutations at two sites in the same gene are highly unlikely. But can we assess how likely mutations, which are likely to change the function of a gene, occur? One of the underlying assumptions of molecular biology is that sequence determines structure, and that this structure determines function. Hence, a major structural change is likely to have a different function. So how common are mutations that result in structural changes in proteins?

Surprisingly Common! One out of every 21 births in humans have some sort of STRUCTURAL change (and hence likely a functional change) in a protein, just from insertions from a single transposable element (alu), common in humans. It is already evident that Behe has a real problem with “random” mutations – but I think perhaps he is confusing ‘randomness’ with ‘purposelessness’.1 More about that in my next post.

Notes

1. I think many people don’t really understand randomness - for more on this see David Bartholomew’s excellent book “God, Chance and Purpose - Can God Have it Both Ways?” (Cambridge University Press, 2008), and also my “Purpose-Drive iPod” essay (Christian Century, 23 September, 2008, pages 11-12).


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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Rich - #36912

October 27th 2010

Arthur:

Thank you for your polite and clear answer to my questions.  However, I must say that it’s not convincing.

I never questioned that you can get zillions of mutations in 9 million years.  And I’ll generously leave aside the fact that most mutations are deleterious or useless, which brings your numbers down by several orders of magnitude. 

But zillions of mutations alone is not a model of an evolutionary pathway.  The order of occurrence is crucial, in many cases, if certain structures are to be built.

If I had a random word generator, that spit out 100,000 random words per year, I am sure that after nine million years I would have enough words to write *War and Peace* many times over.  But it is very unlikely that *War and Peace* would be produced even once during that time.  The order of the words is essential. 

Similarly, in evolution, if you don’t get the mutations in a beneficial order, you aren’t going to get an eye or sonar or anything else useful.  You have to somehow preserve small components of these features originally used for something else.  So you need to suggest a series of *n* intermediate structures—where *n* may be quite large—each conferring selective advantage.


Alan Fox - #36936

October 27th 2010

“mutations for thin bones and limbs”—and what genes have to be mutated for that?

I don’t know the answer to that but a single mutation (a G to A point mutation at nucleotide 1138 of the FGFR3 gene causes a glycine to arginine substitution (Bellus et al. 1995, Shiang et al. 1994, Rousseau et al. 1996*) results in dramatic changes to how the bone structure develops in humans. There is no blueprint or diagram stored in the genome; it is control of growth and differentiation of cells that produces the phenotype.

*Link


Bilbo - #36988

October 27th 2010

John:  “Behe equated resistance with mutations on p. 59. Did you read the book?

No, he didn’t.  Yes I did.

Is Behe’s representation of what Nicholas White wrote accurate, Bilbo, or are you not very concerned about Behe’s representations?

If you think Behe misrepresented White, go ahead and make your argument.  The fact that Ussery hasn’t made it should be pretty good evidence that Behe got it right.

Why would Behe cite a review instead of the primary literature, do you think?

So he could avoid the exact same criticism that Ussery leveled against him: 

Then, based on this vastly over-simplified estimate, he suggests that the odds of a parasite developing resistance to chloroquine is one in 1020….

You or Ussery must either show that Behe misinterpreted White, or attack White himself, not Behe.


R Hampton - #37001

October 27th 2010

You should have recognized that the “task” I was speaking of is the task of *explanation* that the Darwinians have before them in order to account for bats.

The task, as you described many times, is to provide a hypothetical route for evolution. In light of this, comments like inference, not data and speculation are meaningless. In addition, inference - which you seem dismissive of - is the foundation of ID: evidence of a designer is not necessary when it/he/she/they can be inferred from the detection of design.

“mutations for thin bones and limbs”—and what genes have to be mutated for that?

Molecular Determinants of Bat Wing Development
Cells Tissues Organs 2008;187:6-12 (DOI: 10.1159/000109959)
http://content.karger.com/ProdukteDB/produkte.asp?doi=10.1159/000109959


R Hampton - #37002

October 27th 2010

Small changes, big results: evolution of morphological discontinuity in
mammals
Journal of Biology 2008, 7:9 (doi:10.1186/jbiol71)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2323037/

...By comparative studies with non-flying mammals, it is now clear that small changes in the spatiotemporal pattern of gene expression during development account for the dramatic changes represented by the chiropteran forelimb, and the genes responsible are beginning to be identified. The continued elongation of digits in bat embryos compared with mouse embryos seems to be associated with the regulation of cartilage growth. One candidate gene involved in this morphological change is Bmp2 (bone morphogenic protein 2), which encodes a secreted signaling protein associated with the regulation of chondrogenesis. Expression of this gene is upregulated in bat development compared with that of the mouse. Another candidate gene is Prx1 (paired-box), which encodes a transcription factor associated with growth of limb bones. A transgenic mouse with a bat Prx1 enhancer showed an increase in limb length apparently resulting from the upregulation of the endogenous mouse Prx1 gene in cartilage.
continued…


R Hampton - #37003

October 27th 2010

(cont.)
...Separation of the digits in vertebrates involves programmed cell death of the interdigital mesenchyme. While this occurs in the bat hindlimb, it is inhibited in the forelimb, resulting in the development of the patagium. This inhibition is due to differential inhibition of the Bmp signaling pathway in the embryonic forelimb, which is also characterized by high levels of expression of the signaling protein fibroblast growth factor 8. Although the processes responsible for the evolution of powered flight in mammals are not yet known in detail, these comparative studies indicate that small changes in the timing and extent of expression in key genes can have large developmental effects.


John - #37035

October 27th 2010

John:  “Behe equated resistance with mutations on p. 59. Did you read the book?”

Bilbo: No, he didn’t.  Yes I did.

Yes, he did precisely that in the first paragraph.

John: ”Is Behe’s representation of what Nicholas White wrote accurate, Bilbo, or are you not very concerned about Behe’s representations?”

Bilbo: “If you think Behe misrepresented White, go ahead and make your argument.  The fact that Ussery hasn’t made it should be pretty good evidence that Behe got it right.”

The fact that you haven’t read the White review or the relevant primary literature is pretty good evidence that you don’t care about the evidence.

John: ”Why would Behe cite a review instead of the primary literature, do you think?”

Bilbo: “So he could avoid the exact same criticism that Ussery leveled against him: “

I don’t understand your claim here.

Bilbo: “You or Ussery must either show that Behe misinterpreted White, or attack White himself, not Behe.”

Why must we show anything of the sort? I’m content with showing that neither Behe nor you care about the actual evidence. Your game is all hearsay.

Why do you think that almost all hearsay is prohibited in legal proceedings, Bilbo?


Rich - #37099

October 28th 2010

R Hampton:

So what’s your point with all these articles?  (Which I suspect you just looked up now, after getting my question, which means that you were merely mining the literature for support for a belief you already held in the absence of the evidence for it.)

If your point is that the evolutionary change from one mammal into another is possible, I grant it.  But if the mutations are *random* (as neo-Darwinism specifies) then you cannot avoid a calculation.  The question on the table is whether random mutations are sufficient to construct a drastically new animal in a particular length of time.  You cannot answer that question without numbers.  And neo-Darwinists won’t provide numbers.  How many morphological changes would be necessary?  They won’t say.  How many mutations, and which mutations, would be required for each morphological change?  Normally they won’t say; at best they give very partial answers, like the ones in your articles.  In other words, the theory can’t provide the numbers necessary to test it for causal adequacy.  Yet you believe it anyway.  Why?  Would you believe in the theories of chemistry and physics if they could not provide quantitative confirmation?  I wouldn’t.


John - #37156

October 28th 2010

Rich wrote:
“So what’s your point with all these articles?”

Refuting your assumption, falsely presented as fact, that “Now, to get from an artiodactyl to a whale, you’ve got to have many CCCs.”

“... which means that you were merely mining the literature for support for a belief you already held in the absence of the evidence for it.)”

Now that is truly twisted. Rich thinks that “mining the literature” for actual data is a bad thing! Better to pretend that science is about arguing about hearsay, I guess.

“If your point is that the evolutionary change from one mammal into another is possible, I grant it. “

Evolutionary change never involves “change from one mammal into another,” Rich. That’s a common creationist canard designed to distract from the fact that evolution happens to populations, not individuals.

“But if the mutations are *random* (as neo-Darwinism specifies)…”

And another creationist canard! News flash, Rich: mutations are not random wrt location, direction, and multiple other parameters. Only wrt fitness. And of course, this isn’t “specified,” it’s empirical, but since you have no data, you have to misrepresent the real science you are attacking.


John - #37157

October 28th 2010

Rich:
“...The question on the table is whether random mutations are sufficient to construct a drastically new animal in a particular length of time.”

What you don’t understand is that mammalian development is not construction.

You’ve inadvertently provided a testable hypothesis and its empirical predictions.

You hypothesize that mammalian bodies and their “construction” were intelligently designed, and your hypothesis about how they were designed predicts “...to get from an artiodactyl to a whale, you’ve got to have many CCCs.”

“You cannot answer that question without numbers.”

Indeed. So gather your courage (if you have any) and look at the cold, hard data. Can you find a SINGLE CCC that differs between artiodactyls and whales? Now, today? My hypothesis predicts that you are afraid to look.

“And neo-Darwinists won’t provide numbers.”

Pure projection.

“How many morphological changes would be necessary?  They won’t say.”

They study the changes and you don’t.

“How many mutations, and which mutations, would be required for each morphological change?  Normally they won’t say; at best they give very partial answers, like the ones in your articles.”

See the following comment.


John - #37158

October 28th 2010

Proc Natl Acad Sci U S A. 2006 May 30;103(22):8414-8
Developmental basis for hind-limb loss in dolphins and origin of the cetacean bodyplan.
Thewissen JG, Cohn MJ, Stevens LS, Bajpai S, Heyning J, Horton WE Jr.

(free full text at pnas.org)

According to Rich, this paper shouldn’t even exist!

How many CCCs were found, Rich? You’ll have to look at the data, not the text, to find out.


Bilbo - #37201

October 28th 2010

John:  “Yes, he did precisely that in the first paragraph.

No, he didn’t.

The fact that you haven’t read the White review or the relevant primary literature is pretty good evidence that you don’t care about the evidence.

Are you saying Behe got it wrong?

Bilbo: “So he could avoid the exact same criticism that Ussery leveled against him: “

John:  “I don’t understand your claim here.

By Behe referring to White, he makes it impossible for people like Ussery to correctly accuse him of making an estimate on oversimplified data.  Ussery made the accusation anyway, but it was a false accusation.

cont.


Bilbo - #37203

October 28th 2010

Bilbo: “You or Ussery must either show that Behe misinterpreted White, or attack White himself, not Behe.”

John:  “Why must we show anything of the sort? I’m content with showing that neither Behe nor you care about the actual evidence. Your game is all hearsay.

If Behe misrepresented White, all of his critics would be out for blood, and we would know about it.  Behe knows this and therefore would be careful about getting it right. The fact that Ussery lied is a pretty good sign that Behe got it right.  It is reasonable to believe Behe, at this point.  If you don’t, go head and look at the primary literature yourself.  Or don’t you care about the actual evidence?  Just playing your own little game?


John - #37230

October 28th 2010

John:  “Behe equated resistance with mutations on p. 59. Did you read the book?”

Bilbo: “No, he didn’t.  Yes I did.”

Behe,p.59:
“Let’s compare the two numbers for the odds of acheiving resistance to atovaquone, where just one mutation is needed, versus chloroquine, where (presumably—since if a single mutation could help, chloroquine resistance would originate much more frequently) two are needed….

Let’s focus on the parenthetical bit, shall we?

What’s the basis for Behe’s presumption? What is the relative fitness of each of the mutants and the double mutant in EACH of the phases of the life cycle in which chloroquine is absent, Bilbo?

Next, note that Behe uses the term “originate” when the data don’t tell us anything about origination. They tell us about fixation in a population.

“By Behe referring to White, he makes it impossible for people like Ussery to correctly accuse him of making an estimate on oversimplified data.”

That’s just insane. Assuming that Behe is correct, a competent, ethical academic would cite all of the relevant primary literature and point out that White came to a similar conclusion. Behe simply quote-mines a review article.


John - #37232

October 28th 2010

Bilbo:
“Ussery made the accusation anyway, but it was a false accusation.”

Then answer the following questions:

What is the relative fitness of each of the mutants and the double mutant in EACH of the phases of the life cycle in which chloroquine is absent?

How many times does cell division occur during the life cycle?

“If Behe misrepresented White, all of his critics would be out for blood, and we would know about it.”

Are you kidding, Bilbo? Do you really think that Behe is that important?

“Behe knows this and therefore would be careful about getting it right.”

Just like the care he took in asserting that HIV hasn’t evolved any new protein-protein binding sites, when Vpu has evolved a function as a pentameric viroporin?

“The fact that Ussery lied is a pretty good sign that Behe got it right.”

You haven’t shown that Ussery lied.

“It is reasonable to believe Behe, at this point.”

No, you desperately want to believe him, but you have no faith.

“If you don’t, go head and look at the primary literature yourself.”

I have, as well as the secondary literature. You won’t, and that says it all.


Bilbo - #37240

October 28th 2010

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC385418/

“Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 1020 parasite multiplications.”


Bilbo - #37246

October 28th 2010

John:  “You haven’t shown that Ussery lied.

True.  It could be that he’s just delusional.  Or that he had someone else right the review and then signed his name to it.  I could see him giving the job to some grad student, who had a much lower standard of ethics and did the lying.  In fact, from the challenge that Ussery first issued to me, I tend to think that this third option might be the case.  It could be that Ussery didn’t know that his student lied his head off.  John, you aren’t one of Ussery’s students, are you?


John - #37247

October 28th 2010

Bilbo,

You’re not reading what you’re cutting and pasting. Try to sincerely answer the questions:

What is the relative fitness of each of the mutants and the double mutant in EACH of the phases of the life cycle in which chloroquine is absent?

How many times does cell division occur during the life cycle?

And a third: where does White equivocate between resistance arising (i.e., a mutation becoming fixed in a population) and the mutations themselves occurring?


R Hampton - #37400

October 29th 2010

The question on the table is whether random mutations are sufficient to construct a drastically new animal in a particular length of time.  You cannot answer that question without numbers.  And neo-Darwinists won’t provide numbers.  How many morphological changes would be necessary?  They won’t say.  How many mutations, and which mutations, would be required for each morphological change?

Your question is like asking, how many steps does it take to walk from the Lincoln Memorial to the U.S. Capitol. The actual answer depends on the path taken, if you meander then you will take more steps. Now if the U.S. Capitol was never your intended destination because you had none, then calculating the steps would be impossible since there are an infinite number of paths that can intersect with that locale. You could only reasonably calculate the shortest number of steps, and the average number of steps taken (if you detailed histories of people making the trek).

In this analogy, ID theorists have (incorrectly) determined the average number of steps taken per unit of time and claimed that such a meandering walk - while not impossible - can not be done in less than a day…
continued


R Hampton - #37402

October 29th 2010

Of course, ID’s claim is only as good as its assumption on a single step takes X amount of time. What Science has done with IDs claim is to show that it is terrible flawed due to a misuse of Information theory. Because the an actual time between individual steps occur more quickly, the meandering walk is definitely possible. And once we have established the possibility, the actual path - while important to know - is not necessary to conclude that such a walk occurred.

ID’s only other recourse, then, is to say the walk was actually assisted with a ride on a bus, cab, etc. and/or that a tour guide led the walk, step-by-step. But without any evidence of a tour guide or a bus ticket or cab fare, their supposition is just that. It fails as a scientific theory.

Now Rich demands that an evolutionary path can not be accepted unless it can be a specific, though hypothetical, step-by-step meandering route is presented. While this might comfort Rich, Science is more concerned with trying to understand the actual meandering path based on the evidence of the stops made along the way. Yet even this Rich rejects the findings because best they give very partial answers.

What else can Science do but ignore people like Rich?


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