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 - #37410

October 29th 2010

R Hampton:

Your analogy is fundamentally flawed, in that it presumes from the outset precisely what is to be proved, namely, that the walk in question in possible in a certain fixed amount of time.  You’re cherry-picking by choosing a walk that can be done in a brief time even by many very inefficient routes.  But if one had to walk from Earth to Pluto or to the Andromeda Galaxy, would 9 million years of non-stop walking be enough?  One can’t determine that without calculation—what’s the longest human stride, how many strides per hour can be taken, etc.  Similarly, to be sure about whale evolution one needs to know the smallest possible number of mutations needed, the most optimistic order of mutations, the most optimistic number of offspring per generation, etc. in order to calculate whether even the shortest evolutionary route is feasible within 9 million years.  But you, like so many others here, accept on sheer faith that there must be a feasible route.  You don’t even have the minimal amount of healthy skepticism—necessary for all good science—to ask the biologists if they have any such numbers.  You just defer to their authority.  Passive, uncritical, deferential—you’re the NCSE’s dream public.


Bilbo - #37415

October 29th 2010

John,  I don’t see the relevance of your questions to anything I’ve said, nor to your claim that Behe equates mutations with resistance.


Bilbo - #37416

October 29th 2010

And I’m still a little bit curious, John.  Are you one of Ussery’s students?


R Hampton - #37419

October 29th 2010

You’re cherry-picking by choosing a walk that can be done in a brief time even by many very inefficient routes.

Not true. As I previously (and many times before, such as with this links to the papers of Dr. Sean D.  Devine) Science has demonstrated that the walk is possible. For example:
- Information Theory, Evolution, and The Origin of Life, Hubert P. Yockey, Cambridge University Press, 2005
- Evolution of biological complexity, PNAS April 25, 2000 vol. 97 no. 9 4463-4468
- The Origins of Order: Self-Organization and Selection in Evolution, Stuart A. Kauffman, Oxford University Press, 1993
- Selforganization of matter and the evolution of biological macromolecules, Naturwissenschaften. 1971 Oct;58(10):465-523.


John - #37423

October 29th 2010

Bilbo wrote:
“John,  I don’t see the relevance of your questions to anything I’ve said,…”

Then you should be eager to answer them! But you aren’t.

“... nor to your claim that Behe equates mutations with resistance.”

Doesn’t Behe claim that the probability 10^-20 has something to do with mutations?

Does White? What are the other factors that are important to fix a resistance allele in a population? Does Behe consider any of those?

Did you bother reading what White wrote in the rest of the review?

“And I’m still a little bit curious, John.  Are you one of Ussery’s students?”

No. So since I’ve answered your question, why don’t you make a good-faith effort to answer my questions?


Colin - #37441

October 29th 2010

Behe’s estimation for the probability of chloroquine resistance developing is based on observations of its occurrence and numbers of infected hosts. The two key point mutations are discussed to further the readers understanding and provide some explanation as to why it took longer to develop resistance, but were not related explicitly to the probability. He labels that probability, ‘Chloroquine Complexity Cluster’ or CCC. A CCC does not specify two point mutations.

Based on the sheer numbers of malarial parasites, It can be reasonably assumed that if malaria reproduced at the rate of mice, chloroquine resistance would be safely out of reach.


John - #37448

October 29th 2010

Rich wrote:
“Similarly, to be sure about whale evolution one needs to know the smallest possible number of mutations needed…”

Why? We already know the percent identity between a representative sample of orthologous genes, and isn’t that perfectly compatible with measured mutation rates?

“... the most optimistic order of mutations,”

Why? What genetic difference is dependent on another one preceding it?

“... the most optimistic number of offspring per generation,…”

Why?

“... etc.”

Since you offered no reason for the ones preceding the “etc.” I’m skeptical that there are any more.

“... in order to calculate whether even the shortest evolutionary route is feasible within 9 million years.”

So please point us to an artiodactyl/cetacean pair of orthologs that you think differs by more than 9 million years, Rich.


John - #37469

October 30th 2010

Colin:
“Based on the sheer numbers of malarial parasites, It can be reasonably assumed that if malaria reproduced at the rate of mice, chloroquine resistance would be safely out of reach.”

Sorry, Colin, but that makes no sense at all.

To give you an idea as to why it is completely unreasonable, consider the following statement:

“I would also want to see relevant information such as what is the population size of the organism in which these mutations are occurring, what is the selective value for the mutation, are there any detrimental effects of the mutation, and many other such questions.”

If you agree, where does Behe address the relevant parameters of selective value for the mutation and detrimental effects of the mutation? Remember, there are multiple phases to the P. falciparum life cycle, and chloroquine is absent in some of them; therefore, the fitness will vary wildly.

If you disagree, why?


Arthur Hunt - #37471

October 30th 2010

Here is the paragraph from which Behe got the 10^-20 value for a CCC (which, remember, is the estimated frequency of occurrence of a double mutation in PfCRT):

“Chloroquine resistance in P. falciparum may be multigenic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear (13). At least one other as-yet unidentified gene is thought to be involved. 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 10^20 parasite multiplications. “

Behe pretty plainly is misrepresenting White in using this paragraph as he does.


Rich - #37508

October 30th 2010

R Hampton:

You wrote (37419):

“Science has demonstrated that the walk is possible.”

For someone who quotes Aquinas so often, you are strangely uninformed about the meaning of the word “demonstrate.”  The sort of hand-waving arguments in your sources (not one of which provides a complete hypothetical evolutionary pathway for even one major organ, system, or body plan) are not “demonstrations” in Aquinas’s sense.  But of course, you haven’t read any of them, have you?  You’ve just pulled the titles up off the internet, as you always do.  You would be more convincing if you demonstrated personal knowledge of the subject-matter.

All statements of the form “science has demonstrated” are illegitimate.  “Science” is an abstraction.  “Science” doesn’t demonstrate anything.  Individual scientists make arguments By reifying “science,” you are trying to make the arguments of specific individuals seem more impressive than they are.  “Science has spoken” functions for you and others here as the equivalent of “God has spoken”—once “science” has spoken, it’s considered blasphemous to disagree.  Save this rhetorical ploy for the yuppies from the Blue States.  They’re the only ones who will be taken in by it.


Colin - #37515

October 30th 2010

John:

It’s reasonable to request that extra information (from your quote), but for the purposes of discussing Behe’s argument it is over complicating the matter, since the probability for a CCC is based on observation of occurrence, not on theory.

Let me ask you, can we agree that the probability of malaria developing a mutation that will give it resistance to chloroquine is incredibly small? If so, why is it so? Is it considered a difficult step by evolutionary standards?


Bilbo - #37553

October 30th 2010

Bilbo wrote:
“John,  I don’t see the relevance of your questions to anything I’ve said,…”

John:  “Then you should be eager to answer them! But you aren’t.

Why should I be eager to answer something that is completely irrelevant to what I’ve been saying?

”... nor to your claim that Behe equates mutations with resistance.”

Doesn’t Behe claim that the probability 10^-20 has something to do with mutations?

Yes.

Does White?

He seems to.

What are the other factors that are important to fix a resistance allele in a population? Does Behe consider any of those?

How is that relevant to the question of whether Behe equates mutations with resistance?

Did you bother reading what White wrote in the rest of the review?

How is it relevant to what I have written?

“And I’m still a little bit curious, John.  Are you one of Ussery’s students?”

No. So since I’ve answered your question, why don’t you make a good-faith effort to answer my questions?

No, you have not made a good faith effort to answer my questions.


John - #37561

October 30th 2010

Colin wrote:
“It’s reasonable to request that extra information (from your quote),…”

It also is reasonable to request that you offer your opinion on the quote I offered, because it is highly relevant, despite Bilbo’s insane claim that selection coefficients are irrelevant to determining the probability that an allele becomes fixed in a population.

“...what is the selective value for the mutation, are there any detrimental effects of the mutation…”

Are these not relevant parameters, and are they not relevant in every phase of the P. falciparum life cycle, particularly those in which it is not exposed to any chloroquine?

“... but for the purposes of discussing Behe’s argument it is over complicating the matter, since the probability for a CCC is based on observation of occurrence, not on theory.”

But then Behe pretends that it’s just about mutation.


John - #37563

October 30th 2010

Colin:
“Let me ask you, can we agree that the probability of malaria developing a mutation that will give it resistance to chloroquine is incredibly small?”

Not at all. Your phrasing shows a complete lack of understanding.

1) Malaria is a disease. Diseases cannot “develop a mutation.”
2) P. falciparum cannot “develop a mutation” either. Mutations simply happen.

“If so, why is it so? Is it considered a difficult step by evolutionary standards?”

Because there are certainly resistant alleles present at different frequencies in different subpopulations population. The probability that White was addressing was the probability that a resistant allele becomes FIXED in one of those subpopulations. That depends on its relative fitness in EACH of the phases of the life cycle, including phases in which chloroquine is absent.

Sorry, Colin, but if you can’t comprehend the differences between a resistance mutation occurring, a resistant allele being present in a population at low frequency, and the fixation of that allele at a high frequency by selection, you’re hopeless.


John - #37564

October 30th 2010

Bilbo:
“Why should I be eager to answer something that is completely irrelevant to what I’ve been saying?”

Interesting. Before you said that you didn’t see the relevance. So are you now saying that the person who said the following is wrong?
“I would also want to see relevant information such as what is the population size of the organism in which these mutations are occurring, what is the selective value for the mutation, are there any detrimental effects of the mutation, and many other such questions.”

Me: ”Does White [claim that the probability 10^-20 has something to do with mutations]?”

“He seems to.”

Seems to? Where? White clearly understands that selection is highly relevant and extremely complex. You are now claiming that selection is irrelevant!

“How is that relevant to the question of whether Behe equates mutations with resistance?”

Because they are relevant to fixation of the resistant allele.

“No, you have not made a good faith effort to answer my questions.”

Which ones?


Bilbo - #37577

October 30th 2010

Ussery’s latest thread (http://biologos.org/blog/the-edge-of-evolution-a-note-from-dr-ussery/) ignores all the evidence I have presented here that he is either delusional or a liar.  My comments to this effect at that thread continue to be deleted.  Perhaps they won’t be deleted here as well.


Bilbo - #37580

October 30th 2010

John:  “Interesting. Before you said that you didn’t see the relevance. So are you now saying that the person who said the following is wrong?

No.  Just irrelevant to what I have been saying.

Me: ”Does White [claim that the probability 10^-20 has something to do with mutations]?”

“He seems to.”

Seems to? Where? White clearly understands that selection is highly relevant and extremely complex. You are now claiming that selection is irrelevant!

Where did I claim that?

Bilbo:  “How is that relevant to the question of whether Behe equates mutations with resistance?”

John:  “Because they are relevant to fixation of the resistant allele.

How does this show that Behe equates mutations with resistance?

Bilbo:  “No, you have not made a good faith effort to answer my questions.”

John:  “Which ones?

The ones where I ask you how all your questions are relevant to what I’ve been saying.  I have presented evidence that Ussery is either delusional or a liar.  You have failed to address any of that evidence.


John - #37589

October 30th 2010

Bilbo, you are denying that Behe attributes the rarity of chloroquine resistance to mutation, are you not?

He clearly does so on p. 59 and his failure to assess the fitness of the resistant alleles throughout the life cycle. If you don’t agree that Behe is attributing the frequency to mutation, please show me where he addresses the fitness throughout the life cycle.

How can the following quote possibly be irrelevant to a discussion of the frequency at which a mutant allele becomes fixed in a population?
“I would also want to see relevant information such as what is the population size of the organism in which these mutations are occurring, what is the selective value for the mutation, are there any detrimental effects of the mutation, and many other such questions.”


John - #37590

October 30th 2010

Rich wrote:
“Individual scientists make arguments”

That’s not what real scientists limit themselves to doing. Real scientists offer empirically testable hypotheses, and the vast majority of scientists test their hypotheses empirically.

No one in the ID movement has sufficient faith to test an ID hypothesis. They run away.

“By reifying “science,” you are trying to make the arguments of specific individuals seem more impressive than they are.”

He’s talking about the data produced by science, not the arguments. You are trying to hide the lack of faith, including your own, that characterizes the ID movement.


Colin - #37640

October 30th 2010

John:

I was aware that I was using “malaria” incorrectly, but probably gravitated towards it because it saves me typing a few extra letters. I was also aware of some of the finer details of how a mutation may or may not become fixed in a population, but thought it was unnecessary to write with such detail in a forum.

Your pedantic and argumentative replies might give you an opportunity to regurgitate some knowledge, but unfortunately prevents any real discussion of Behe’s argument. And one year after reading the book I am yet to find an opponent who has bothered to try to understand his argument.


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