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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Arthur Hunt - #36475

October 26th 2010

Several thousand mutations per individual.  Nolo contendere.  But do all of these bear on the form and function of the adult offspring?  ...

If just 5% of all DNA in a mammalian genome is protein-coding, then 1 in 20 mutations will affect a protein coding gene.  (There’s a reason I opted for the generous estimate of 20.) If a new individual has 20 mutations, it will have a change in one protein-coding gene.  If we are speaking about a stable population of 30,000 individuals, then each new generation will “yield” a new mutation in each protein-coding gene in the population (assuming a gene complement of 30,000 - a fair estimate).  In a hundred generations, we are talking about 100 mutations per protein-coding gene.  If a generation is 50 years (a fair estimate for a slow-growing mammal), then we need 5000 years to produce this sort of diversity within the population.  Etc., etc., etc.

This is if only 20 new mutations occur in a new individual.  If it is 1000 or more (as some studies suggest), then .... well, I think we can all use a calculator.

The bottom line - mutation frequency is not going to be much of a limiting factor for any sort of evolution, even in large, slow-growing mammals.


Arthur Hunt - #36477

October 26th 2010

Suppose we contemplate the transformation of a shrewlike creature into a bat, by means of random mutations.  Can you tell me which nucleotides have to be altered to give the shrewlike animal a bat’s wings?  A bat’s sonar?  We need this information for any calculation of the probability that the transformation could have occurred in X million years.
Where can I find it?

Well, we can easily estimate the upper bound of the number of genes that may be involved in such transformations. (Don’t ask me to state the obvious.) And the previous comment gives us a start to figuring roughly how long it would take to generate a respectable degree of variation within a ca. 30,000-strong population. This is, I would argue, a start towards estimating a limit, imposed by just considerations of mutation frequency, that relates to the improbability of such transitions.


Arthur Hunt - #36481

October 26th 2010

A postscript - I’m deliberately trying to keep things simple, which means ignoring for now the fact that more than x individuals are needed to make sure that x mutations will occur in a population, given an average frequency of 1 mutation per individual.

In other words, spare us the stats pedantry.


Rich - #36482

October 26th 2010

Arthur Hunt:

I’m offering no pedantry.  I’m asking for a pathway.  What genes have to be altered?  How would they have to be altered?  If we knew that (along with other information, such as the size of litters of small mammals of that type, number of generations, etc.)  we could estimate how long the process would take, on the assumption that the mutations are genuinely random.  Then, if the calculation showed that bats would likely need 5 million years, or 50 million years, or 500 million years to evolve, we could measure that against the time allotted by the fossil record, and we would have an empirical/mathematical test of Darwinian theory.  But as far as I know, no Darwinian has attempted to set forth an evolutionary pathway from one creature to another in a way which allows for such hard-nosed mathematical inspection of the theory.


Alan Fox - #36518

October 26th 2010

But as far as I know, no Darwinian has attempted to set forth an evolutionary pathway from one creature to another in a way which allows for such hard-nosed mathematical inspection of the theory.

You’re asking for the impossible, Rich. Current knowledge does not even allow us to understand how the genomic information in the embryo in an organism results in the growth and development of that organism into adulthood. What we can do is compare genomes of many organisms and observe the similarities which fit very nicely with nested hierarchies. All evidence forms a pattern of relatedness. Evolutionary theory is incomplete but progressing. There is no alternative scientific theory. I am surprised that, while demanding the impossible from evolutionary theory, you appear to credit “Intelligent Design” as having more than a catchy title. ID theories (such they can be so described) explain nothing, are useful for nothing.


Rich - #36525

October 26th 2010

Hello, Alan.  Glad to have you back—I think.

“Current knowledge does not even allow us to understand how the genomic information in the embryo in an organism results in the growth and development of that organism into adulthood.”

If that’s the case (as I in fact knew that it was), evolutionary biologists should not speak with the confidence that they do.  They should treat their theories as plausible speculations, not scientific achievements on a par with those of Newton and Pasteur.

“What we can do is compare genomes of many organisms and observe the similarities…”

Right.  That’s what all Darwinians (atheist and TE) do.  Genetic and morphological comparisons bear almost the entire weight of Darwinian speculation.  Virtually every argument made here, whether by columnists or commenters, amounts to:  “Well, these fossils/genomes are a lot alike, so they must be related to each other historically.”  But the conclusion does not follow logically from the data.  It’s a *possible* conclusion from the data, but not a necessary one.  More important, even granting the historical connection (as Behe does) still leaves one in doubt about the adequacy of proposed mechanisms.  I’m asking for proof of adequacy.


gingoro - #36541

October 26th 2010

Rich@36525
“If that’s the case (as I in fact knew that it was), evolutionary biologists should not speak with the confidence that they do.  They should treat their theories as plausible speculations, not scientific achievements on a par with those of Newton and Pasteur.”

Well put Rich well put!  This is exactly the kind of reason that I object to much of what is called “Computer Science”.  In general in CS we have knowledge of a lot of techniques that work most of the time as well as techniques that fail most of the time.  Sure there is some theory, some science in areas like data compression and encryption, information theory and in my own specialty compilers in terms of parsing theory.
Dave W


gingoro - #36543

October 26th 2010

Dave Ussery@36536@36538
I think these are both excellent posts and only wish that more people would take Dave’s attitude. 

This is the kind of reason that while I think Behe’s idea of IC is interesting but that I would like to see a case where it is agreed that some instance of IC is actually un-evolvable.  In spite of what Bilgo has written I would see Dave Ussery as a friendly critic of ID as opposed to someone like Coyne or Miller who simply dismisses it totally. 
Dave W


John - #36628

October 26th 2010

Rich wrote:
“If were familiar with the teachings and practice of Christianity, you would know that “bearing false witness” does not mean “making an error” or “stating something without adequate proof.” “

I don’t claim either of those things, so your attribution of them to me is false.

“It means willfully telling an untruth about another person which could lead to that person’s legal or moral condemnation by the community. “

Yep, exactly what pds did wrt David Ussery when he claimed, “I don’t think the studies you cite support your assertion.” We all know that pds did not look at the studies and has no intention of ever looking at the studies.

“You have accused several people here of doing that.”

Indeed I have. And I stand by that. You’re one of the worst offenders.

“And aside from the fact that “bearing false witness” isn’t about intellectual arguments, but about people, it’s a very serious moral and spiritual charge.”

You are running away from any argument on intellectual grounds, which in science involves evidence. You and pds reject consideration of the evidence, except hypocritically when you see a potential opening to attack.


John - #36637

October 26th 2010

Bilbo wrote:
“Where did Behe write this?  The correct answer is Behe did not write this.  What Behe said was (as I already pointed out at #35266):”

”The ratio of the two numbers shows that the malarial parasite is a hundred million times (108) less likely to develop resistance [not “mutations] ….”

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

============
“What Behe actually wrote (as I already pointed out at #35261):

”...Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year time the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion. [16]  In shorthand scientific notation, that’s one in 1020.” (p.57)”

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

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


John - #36640

October 26th 2010

Rich wrote:
“That’s exactly what “John” does when accuses several ID people here of “bearing false witness” because they disagree with his interpretation of the facts.”

No, Rich, I do no such thing. I accuse people of bearing false witness when they ignore the facts (the actual data) while pretending to be familiar with them. Here’s an example from you and Art:

R:  “Now, to get from an artiodactyl to a whale, you’ve got to have many CCCs.”

A:  “Prove it.  For example, provide some quotes from some accomplished ID-friendly biochemist that shows,...that a “CCC” ...must have been required, to the exclusion of any of the numerous other molecular mechanisms that underly developmental processes, to produce a different between an artiodactyl and a whale.”

A:  “One request, Rich - don’t go moving goalposts.  You raised the issue of CCC’s in the context of artiodactyls -> whales, it’s up to you to support your assertion with facts.”

R:  “And if you want to drop CCCs, that’s fine.”

I second Art’s demand of you, RIch. He clearly doesn’t want you to drop CCCs, so your suggestion that he does is disingenuous.

Show us JUST ONE of the “many.” You won’t.


John - #36645

October 26th 2010

pds wrote:
“I have already responded to your criticisms, and you seem to ignore it.”

Both utterly false. You have claimed,  “I don’t think the studies you [Ussery] cite support your assertion,” without looking at the studies.

You also wrote,  “Instead of your rambling personal attacks, why don’t you just summarize a study that you think contradicts what Behe actually said.  That will show me whether you understand what Behe is saying.  That should be easy for you.”

I cited just such a study:
Sekita Y, et al. 2008. Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta.
Nat Genet 40: 243–248.

How did you determine that the data from this study:
1) are not a specific example, and
2) do not directly contradict Behe’s assertion?

You have not addressed these data.

“You repeatedly misrepresent my comments.”

I have not misrepresented you in any way.

“I find your tone and style unpleasant.”

Obviously, no one enjoys having his bluff called when he is bluffing. You were bearing false witness when you made your claim about the evidence.

“I don’t plan to respond to you further.”

Predictable. You never really responded to begin with.


Rich - #36702

October 26th 2010

Arthur Hunt:

I won’t deal with John because of his manners, but I will say this to you:

My statement about needing CCCs was a surmise.  I did not mean to present it as the settled result of science, or as if I had done some calculation.  It just struck me that they would be necessary.  So I admit I could be wrong. 

The way to show that I am wrong is to provide me with a hypothetical evolutionary pathway that does not require any CCCs.  The moment I see it, I will eat humble pie and retract my statement as a scientific error.

The problem I find with all debates about what Darwinian processes can and cannot do is that no one on either side speaks concretely enough to even visualize the processes being endorsed or rejected, let alone quantify them.  “Drift”, “selection” and “random mutation” are all big generalities.  Turning a shrewlike animal into a bat is a specific task.  With specific tasks, if the model is good, we should be able to assign hypothetical steps, and provide some numeral data for each step.  But as no Darwinian will do this, ID people tend to stay on the same vague level, trying to rebut with purely qualitative arguments.  The debate thus goes nowhere; science requires testable numbers.


John - #36706

October 26th 2010

Rich wrote:
“My statement about needing CCCs was a surmise.”

Yet you presented it as a fact.

“I did not mean to present it as the settled result of science, or as if I had done some calculation.  It just struck me that they would be necessary.  So I admit I could be wrong.”

You are. Why not just admit that you really have no idea?

“The way to show that I am wrong is to provide me with a hypothetical evolutionary pathway that does not require any CCCs.”

The way to show you that you are wrong is to send you to the primary literature to look at what is known about developmental genetics, but you are afraid of the data. If you had the courage to look at the data, you’d see that the known differences don’t involve any new CCCs, but we all know that you won’t.


John - #36709

October 26th 2010

Rich:
“The moment I see it, I will eat humble pie and retract my statement as a scientific error.”

You made a claim of fact. The honorable, Christian thing to do is to support it yourself or retract it. The cowardly thing to do is to put the burden of proof onto others.

“The problem I find with all debates about what Darwinian processes can and cannot do is that no one on either side speaks concretely enough to even visualize the processes being endorsed or rejected, let alone quantify them.”

Your claim of fact doesn’t depend on Darwinian processes, it depends on knowledge of the mountains of evidence we already have from comparative developmental genetics and an understanding of how developmental mechanisms, not evolutionary ones, work. Your false claim was based on YOUR false assumption that is completely at odds with the evidence.

“But as no Darwinian will do this, ID people tend to stay on the same vague level, trying to rebut with purely qualitative arguments.”

We’re specific. You made a claim of “many” when you can’t even name one.

“The debate thus goes nowhere; science requires testable numbers.”

We’re reducing many to just one to ease your burden of proof. Go for it!


Arthur Hunt - #36714

October 26th 2010

Rich: I’m asking for a pathway.  What genes have to be altered?  How would they have to be altered?  If we knew that (along with other information, such as the size of litters of small mammals of that type, number of generations, etc.)  we could estimate how long the process would take, on the assumption that the mutations are genuinely random. 

Alan: You’re asking for the impossible, Rich. Current knowledge does not even allow us to understand how the genomic information in the embryo in an organism results in the growth and development of that organism into adulthood.

At the top of this thread, I said: I think a comprehensive review of the pertinent literature will inevitably lead one to conclude that the best one can do is to arrive at a range of values for relevant parameter

(continued)


Arthur Hunt - #36717

October 26th 2010

Returning to my thought, the mutation numbers I have mentioned recently can easily be thought of as a sort of limit.  Specifically, if one pulls out the trusty HP21, it is easy to calculate that, for my hypothetical population of 30,000 individuals, in 500,000 years (a relative blink in evolutionary time), this population will “generate” between 10,000 and 1 million different mutations (on average) for every protein-coding gene.  That’s about every conceivable sort of mutational change one could hypothesize.  If we grant that an evolutionary transition involves at least some protein-coding genes, then this amount of variation should easily suffice.

Put another way - mutation rates, the generation of new variability, and the like pose absolutely no probabilistic problems for evolutionary change, even in large and slow-growing animals.  If one is fishing for probabilistic problems for evolution, mutation is not the place to look.

Put yet another way - the wildly-unlikely scenario wherein many thousands of different genes are involved in an evolutionary transition, a scenario that represents a sort of most inaccessible limit, is in fact not at all improbable in the long term, when speaking just of variation.


John - #36726

October 26th 2010

Rich, afraid to look through the primary literature for himself, wrote:
“Turning a shrewlike animal into a bat is a specific task.  With specific tasks, if the model is good, we should be able to assign hypothetical steps, and provide some numeral data for each step.  But as no Darwinian will do this,…”

Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):16982-7.
A second wave of Sonic hedgehog expression during the development of the bat limb.
Hockman D, Cretekos CJ, Mason MK, Behringer RR, Jacobs DS, Illing N.

Only in your warped mind are the real scientists afraid or unwilling to test hypotheses.

Do you see any CCCs there?


R Hampton - #36736

October 26th 2010

Turning a shrewlike animal into a bat is a specific task

sigh…another logical fallacy. When animals evolve, the mutations that are selected and preserved are in response to natural selection, sexual selection, et al. There is no specific direction and no specific task other than survival and reproduction.

From fossil evidence, we know that the bat predecessors climbed trees and thus it’s likely they first evolved the ability to glide between trees, like some species of squirrels. For flight to be possible though, we can surmise the climbing/gliding predecessor acquired mutations for thin bones and limbs. Because thin limbs would make the organism less robust and slower, its quite likely that they first found a protective habitat before said mutation occurred.

So here we have a flying-squirrel like creature with in a habitat that offers a fair amount of protection. Some of its offspring develop thin limbs and survive. Those with thinner limbs glide farther and so advantage spreads. In time, their fingers become longer offering a more wing-like shape. in turn their offspring become even better gliders. And so on and so forth…


Rich - #36904

October 27th 2010

R Hampton:

“Logical fallacy” is the wrong phrase for the error you are accusing me of.  What you should have said is that I was misrepresenting Darwinian evolution.  But of course I wasn’t, and you know, from hundreds of my posts, that I know how Darwinian evolution works.  I am of course fully aware that Darwinian evolution is supposed to be undirected; how would I be an ID sympathizer otherwise?  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.

“We know that bat predecessors climbed trees”—inference, not data.

“It’s likely”—speculation.

“We can surmise”—I’ve just been attacked by two people for “surmising” something about CCCs without presenting evidence.  I wonder if they will do the same to you, or whether the usual double standard around here will continue to apply (Darwinists can get away with modes of argument that are not allowed to ID people).

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

Basically, you’ve told yet another purely qualitative narrative, based on imagined transformations of morphology, and *assumed* your pathway exists.


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