26 January 2006

Lonnig's "Dynamic Genomes" paper: A quick critique.

In the comments section of my most recent post on the Discovery Institute's publication track record, Spike made the following suggestion:
Here is the only scientific paper that one can link from the Discovery Institute’s list of “Peer-Reviewed, Peer-Edited, and other Scientific Publications Supporting the Theory of Intelligent Design (Annotated)” http://www.discovery.org/scripts/viewDB/index.ph… . (The rest you have to pay the publishers for, I suppose):


1. Can you, dear reader, understand it?
If so, could you explain it to us lay people?

2. Is it science?

Caveat Poster I have no special allegiance to “Darwinsists” (whatever those are), evolutionists, scientists or the people who feel they represent the Truth of Evolution. So don’t play into OSC’s hand and don’t use logical fallacies.

If you want to dismember this paper, do so on rational, scientific grounds. Por favor.
I started out intending to examine the entire paper, but it's taken me a while to thoroughly respond to (or dismember, if you prefer) just one of the claims. I do have other things to do, so I'm going to restrict my response to addressing his claims about the lack of differences seen between organisms. This doesn't mean I agree with the rest of the paper - it just means that I only have so much time available for this right now.

The bulk of Lonnig's paper, at least as I understand it, seems to center around the question of how, given the large number of different ways that it is possible for a genome to change, is it possible for any of the various features seen in organisms to remain the same. In other words, if mutations are common, then why don't we see more differences between different groups of organisms:
Becoming fully aware of the features specifying dynamic genomes as mentioned above, the overall impression most students of genetics inevitably have gained, could perhaps best be stated by the words assigned to the Greek philosopher Heracleitus of Ephesus (about 544 BC to ca. 475 BC), describing the essence of nature by his famous verdict: panta rhei, ouden menei (“all things flow, nothing abides”). For almost ‘everything’ in the plant and animal genomes seems to be in a permanent process of flux so that in the long run one should hardly expect any constant genomic (and corresponding morphological) characters at all. (p.104)
There is really no way to say this nicely, so I will be blunt. If Lonnig is trying to suggest that we should not see conserved genes-and as far as I can tell that is exactly what he is saying-then he has an abysmally appaling understanding of evolutionary biology.

Stabilizing selection (occasionally known as purifying selection)is a basic part of our modern understanding of evolution. In simple terms, stabilizing selection is nature's way of saying, "if it ain't broke, don't fix it." In slightly more technical terms, stabilizing selection is a type of natural selection that occurs when the version of a trait that is currently present in the population is the one that is associated with the highest fitness. The Wikipedia article linked to at the start of the paragraph cites human birth weight as one example of stabilizing selection.

Stabilizing selection is, at the absolute minimum, something that needs to be considered as a possible explanation for a lack of evolutionary change in a trait. Lonnig devotes something like half of that paper to discussing stasis, and why he thinks stasis is a problem for evolution, but he does not mention the concept of stabilizing selection anywhere in his paper. He is either unaware of the concept, or he deliberately decided to completely ignore the concept. Stabilizing selection is typically discussed in introductory biology classes, so it's difficult to believe that he didn't know about it.

Something else that Lonnig does not seem to mention is that we can actually predict, at least to a certain extent, how variable specific regions of DNA are likely to be within and between species. For example, the regions of DNA that code for proteins that are involved in basic cellular processes tend to be less variable than the regions of DNA that code for proteins involved in the organism's interaction with the environment.

But you really shouldn't take my word for it, especially when it's easy to look at examples. I'm going to try to err on the side of making the explanation too simple, so I apologize if I'm covering things that you already know.

Histones are a type of protein that is involved in packaging DNA. The shape of this protein is extremely critical to its function, and the sequence of amino acids in the protein determines its shape. Packaging DNA is a basic cellular function, and is critical to the function of the cell. This means that mutations that change the protein are likely to disturb the function of the protein. As a result, stabilizing selection will tend to weed out mutations that result in changes to the protein.

I'm going to list part of two DNA sequences. I'm going to give the first 30 letters of the sequences. Sequence 1 comes from a jellyfish (GenBank accession AY428830.1). Sequence 2 comes from a bivalve mollusk (GenBank accession AY654989.1). To make the differences between the sequences easier to spot, I'll use capital letters to mark the differences.
1: aga aaa tcA acC gga ggA aaa gcA cct CgT
2: aga aaa tcT acT gga ggC aaa gcC cca AgA
There are two things that you should notice about these sequences. The first is that there is actually a fair amount of variation between them - 6 of the 30 bases are different. The second is the way I've grouped the letters into sets of three. This is a portion of DNA that gets translated into a protein, and it takes three letters ("bases") to specify one amino acid. Next, I'm going to provide the protein translation for each of those sequences. Lower-case letters will be used to show differences.
As you can see, the DNA sequences are different, but the proteins that result are identical. (In fact, the entire protein sequences for this histone in these two species are identical, not just these ten amino acids.)

To an evolutionary biologist, this type of signal indicates that this particular gene is both very important to the proper function of the cell and very sensitive to change. That is certainly the case with histones.

Next, we'll look at a protein that is involved in interactions with the environment. The fly genus Drosophila has a protein called alcohol dehydrogenase (or "adh"), which it needs to live in areas where there is ethanol production, such as the rotting vegetation where many of these insects live.
The larger of the two flies in the picture is Drosophila differens. This is a species unique to Molokai, and is part of the Hawaiian Drosophila. The smaller fly is Drosophila melanogaster, the famous "fruit fly" used in genetics labs all over the world. I'm not going to go to the lengths that I did above to look at the genes, but a quick comparison of adh from these two species (GenBank accessions M63303.1 and M36580.1) showed that the DNA sequences were 78% similar, and that there were differences in the proteins. These two flies are much more closely related to each other than a jellyfish is to a clam, so it is clear that this gene is much more variable than the histone we looked at before.

When we see a protein that is more variable, it usually indicates that the protein can tolerate more change and still function properly and/or that the protein's primary function in some way involves the animal's environment. If the protein can function in a slightly changed form, then it becomes possible to pass on mutations that slightly change the protein. If the protein is involved in interacting with the environment, then it may need to be different in animals living in different environmental conditions.

Lonnig's list of possible ways for genomes to change is completely irrelevant to understanding why some proteins are evolutionarily conserved. The histone gene shows much less variability than the alcohol dehydrogenase did, but that doesn't mean that mutations occur any less often in the DNA that codes for the histone. It doesn't mean that any of the different ways that the gene could be mutated don't happen with histone genes. It just means that any mutations that do occur in the histone DNA can only get passed on to the next generation if they don't change the protein. Mutations that don't get passed on to the next generation are evolutionarily irrelevant.

Natural selection can be a force for change, but it can also be a stabilizing force. It all depends on the circumstances. In the case of basic cellular functions, it is usually a stabilizing force. We are separated from the first cells by an amount of time that is too vast to comprehend. The basic cellular processes were pretty much optimized a very, very long time ago. It should come as no surprise that selection usually acts to stabilize the genes responsible for basic cellular processes.

Looking up at this post, I see that I've written quite a bit more than I had intended to, and looking at the clock, I see that my "quick" critique has taken three hours, so I'm going to wrap things up. Even though I wasn't able to dismember the entire paper, I hope I've demonstrated two main things:

1. Even in cases where a protein is exactly the same in widely separated species, the DNA that codes for the protein may differ. In other words, the function may be static, but the genetics are not. In this sense, Lonnig's claim is somewhat misleading, if not just plain wrong.

2. A lack of divergence in a gene (or any genetic trait) between two different groups of organisms is not a problem for evolution. In fact, such similarities can (and do) often result from the stabilizing action of natural selection.


Anonymous said...

Thank you for the time and lucidity of your thoughts.

RPM said...

Good primer on molecular evolution. Two comments:

1. I hate the term stabilizing selection. And while it can be forced into a popgen framework, stabilizing and purifying selection are different. You are talking about purifying selecting here. Of course, I prefer to phrase the difference between histones and Adh as differences in selective constraint.

2. You write, "Something else that Lonnig does not seem to mention is that we can actually predict, at least to a certain extent, how variable specific regions of DNA are likely to be within and between species."
I would add that we can even use the divergence between species to predict the variation within species (ie, HKA, McDonald-Kreitman).

Anonymous said...

You dumbed it down just enough so I could understand it. Thank you for the time and effort.

Anonymous said...

Lonnig seems to barely skip over punctuated equilibria in its different versions, reverting to criticism of the strict constant gradualist model that very few biologists now agree with. He also seems not to have heard of the evolutionarily stable strategy.

Anonymous said...

Thank you for your summary.

Is this the same paper that was "published in the peer-reviewed Washington Journal of Biology" (or whatever it is called) by one of the associate editors sneaking it past the others only to have the others revoke it's inclusion later?

The IDers always trumpet this one published, SCIENTIFIC paper being accepted in a real journal, but leave out the "removed later" part.

Anonymous said...

> The IDers always trumpet this one published, SCIENTIFIC paper being accepted in a real journal, but leave out the "removed later" part.

Silly, this is another paper.

Roadtripper said...

Very informative. Simple enough to follow, but detailed enough to learn quite a bit from, actually. Thanks.

Anonymous said...

Thanks for the analysis/rebuttal. I'm sure a lot of us would like to see even more critiques of Lonnig's paper - if, of course, you had the time. This was certainly helpful to me, though.
It actually seems that - and I'm going to severly dumb this down - the "random chance" that IDers are so dismissive of is the primary reason evolution managed to produce who we are today. Genetic mutation is an absolute necessity for species survival in changing environments. Again, I've dumbed it down, so feel free to flame/correct me!

Anonymous said...


Thank you for this quick critique. I agree with the others who've said that you made it easy enough for us non-scientists to understand.

I'll also post to Panda's Thumb.

Thanks again!


Anonymous said...


Here is what the had to say about a paper a DI Fellow got published in their journal:


The paper by Stephen C. Meyer, "The origin of biological information and the higher taxonomic categories," in vol. 117, no. 2, pp. 213-239 of the Proceedings of the Biological Society of Washington, was published at the discretion of the former editor, Richard v. Sternberg. Contrary to typical editorial practices, the paper was published without review by any associate editor; Sternberg handled the entire review process. The Council, which includes officers, elected councilors, and past presidents, and the associate editors would have deemed the paper inappropriate for the pages of the Proceedings because the subject matter represents such a significant departure from the nearly purely systematic content for which this journal has been known throughout its 122-year history. For the same reason, the journal will not publish a rebuttal to the thesis of the paper, the superiority of intelligent design (ID) over evolution as an explanation of the emergence of Cambrian body-plan diversity. The Council endorses a resolution on ID published by the American Association for the Advancement of Science (http://www.aaas.org/news/releases/2002/1106id2.shtml), which observes that there is no credible scientific evidence supporting ID as a testable hypothesis to explain the origin of organic diversity. Accordingly, the Meyer paper does not meet the scientific standards of the Proceedings.

Anonymous said...

thank you for that lucid explanation ...it's also sorta strange to realize that Iders will resort to any kind of underhanded trick to get their junk science published .....im a christian theist and i find that type of dishonesty discredits real christians ...so please continue to expose ID for what it is ...maybe they'll stop this nonsence of equating God with human ignorance

Anonymous said...

As a nonbiologist I can not say much, except for four things:

1. I would be very suspicious about a paper that says this about itself in the abstract: "In agreement with several researchers".

2. I would be very suspicious about a paper when those agreements are mainly books and mainly from the three authors of the proposed model themselves (Loennig, Behe, Dembski).

3. I would be very suspicious about a paper that makes so many citations and points on a sparse argument.

4. I would be very suspicious about a paper that doesn't seem to show anything about that it's supposed to show. At least, I can't find any quantitative argument whatsoever from the proposed mechanism.

JS said...

Apart from joining the general praise, I'd also like to point out that a favorite creationist argument has always been (and still is) that mutation cannot produce real change.

Is is just me, or is this guy saying that mutation produces too much change?

So, mutation can't produce change, but on the other hand mutation produces waay too much change, is that what he's saying?

Anonymous said...

He acknowledges change I believe - he says that 99.99 % of species can be explained by natural selection. (Or maybe by ID preexisting information - I'm not sure that he exactly means with "the points enumerated above" since he enumerated so many...)

But he never uses his theory to explain the two questions he makes:

(a) why are these characters stable at all and (b) how is it possible to derive stable features from any given plant or animal species by mutations in their genomes?

No quantitative explanation, what I can see. None.

Anonymous said...

Maybe I should add what I'm really looking for is a testable explanation. The ability to make a quantitative prediction is showing that a hypothesis has some power. And it can make a good test.

Ginger Yellow said...

I see a lot of arguments like this from IDists. I suspect that a majority of them don't just disbelieve evolution, but believe in some form of vitalism. They keep on trying to deny basic, empirical facts of genetics like mutation rates that would be true and known even if evolutionary theory hadn't been thought up yet.

Anonymous said...

I went to the trouble of reading the Lonnig paper and it was a hoot. TQA exposes the major problem with it (though personally I would not have used the term 'purifying selection' though that does communicate the ideas). There are many problems with this paper. If there is any interest in further critiques I would be willing to throw in a few comments. (They quote a paper that I wrote 20 years ago so I have some idea how far they go to distort scientific discourse to push their nutty ideas).

Mike Syvanen