A Tale of Three Creationists, Part 3

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February 7, 2011 Tags: Genetics

Today's entry was written by Dennis Venema. You can read more about what we believe here.

A Tale of Three Creationists, Part 3

Reasons to Believe, Scurvy, and a (Guinea) Pig in a Poke

After the recent exchanges between Fazale Rana of Reasons to Believe (RTB) and myself, I had intended to move on to other important issues. However, Rana’s final response to my critique is so inaccurate - and so badly misleads his audience - that to not reply would be irresponsible. There is no room for a “pig-in-a-poke” in science or the church.

If you have been following this series, you will know that one of the strongest pieces of evidence in favor of common ancestry between humans and chimpanzees (and other organisms) is a large number of “broken” genes, otherwise known as pseudogenes. When they are damaged in exactly the same way and exactly the same spot in closely related organisms, by far the simplest explanation is that they are copies of a single gene that was damaged in a common ancestor.

One way of illustrating this is to think of a 25 page manuscript: pretend that there is a mistake of one letter out of the 75,000 letters. Let’s say that a “g” had been inadvertently removed from the word “missing”, so that it now reads “missin.” Now let’s say that you collect 10 copies of this manuscript from various people and five of them have exactly the same mistake—the word “missing” on page 22, line 15, word 7, is spelled “missin” instead of missing. Every one of the other 74,999 letters in the 25 pages is perfect. Would you not conclude that the five identically mistaken manuscripts are derived from a single source? Would you not have to strain very hard to come up with an alternative explanation?

Rana is similarly desperate. The RTB model—based as it is on their specific interpretation of scripture— requires that they find an alternative to the common descent model overwhelmingly accepted by biologists. Rana feels a need to respond to pseudogene evidence since it so powerfully supports the creation of humans through an evolutionary process. The fact that different mammalian species, including humans, have many pseudogenes with multiple identical abnormalities (mutations) shared between them is a problem for any sort of non-evolutionary, special independent creation model. The fact that shared mutations are present in patterns that match other independent lines of evidence such as sequence identity (see here and here) and shared synteny (see here) only makes matters worse. The data from these different areas are congruent and I am not aware of any paper in the peer-reviewed scientific literature that attempts to argue for a non-evolutionary interpretation of these data.*

The topic of Rana’s rebuttal is a single portion (termed the tenth exon) of a single pseudogene, the GLO pseudogene, which, when not broken, makes an enzyme required for vitamin C biosynthesis. In “dry-nosed” primates (a group which includes humans,) this gene is “broken.” It is because of this that we get scurvy if we do not ingest enough vitamin C in our diet. Many of the mutations in the GLO pseudogene are shared between humans and other primates, indicating that these mutations have been inherited from a common ancestor. The only other possible explanation is that a large number of identical mutations occurred independently in many species – something so improbable as to be not worth considering. Yet this is exactly the strained interpretation that Rana chooses to argue for:

Comparison of the rat’s exon X (10th exon) DNA sequence with those in humans, chimpanzees, and orangutans reveals a number of the same mutations in the same locations for the primate sequences. Of particular significance is position 97 in which it appears as if a deletion took place in the primate sequences. Evolutionary biologists argue that this deletion and the other shared mutations are clear evidence for common ancestry, with these changes having occurred before apes diverged from Old World monkeys.

The RTB genomics model offers a different explanation for the similarities in the primate DNA sequences. The shared features are interpreted as the outworking of nonrandom, reproducible changes that happened independently in humans, chimpanzees, and orangutans.

Rana then goes on to claim that there is empirical evidence for the RTB view. The GLO gene is also a pseudogene in guinea pigs, but this species lost GLO function independently of the primate common ancestor. Not surprisingly, the mutations in the guinea pig pseudogene are different from those in the primate pseudogene, but Rana claims that there are a few shared mutations between primates and guinea pigs in exon X:

Support for this interpretation comes from comparisons of the primate exon X sequences with the corresponding region of the guinea pig GLO pseudogene. The structure of the guinea pig GLO pseudogene is dramatically different than that of the human pseudogene. Presumably, guinea pigs and primates lost this gene independently. If mutations were random, then few if any of the changes in the primate and guinea pig exon X sequences would be the same. Yet, as biologist Peter Borger points out, fifty percent of the mutations in the primate and guinea pig exon X sequence are identical. In addition, the guinea pig exon X region shows a mutation at position 97, the location in the primate genomes where a deletion took place. These shared features could not have resulted because guinea pigs and primates shared a common ancestor. Instead, they must reflect nonrandom, reproducible changes.

In other words, the RTB genomics model can reasonably account for the shared features of the GLO pseudogene in primates without resorting to common ancestry as the explanation.

There are several problems with this argument, but none would be apparent to a non-specialist. On the face of it, it seems like a strong case. If indeed there are shared mutations in two independent gene-to-pseudogene conversion events, it would lend (some) credence to Rana’s assertion that all shared mutations are the result of non-random events. The GLO pseudogene sequences in question are as follows. At six sites (in yellow) the human and guinea pig sequences match each other but differ from the rat (purple). The anti-evolutionary source Rana cites (PDF) claims that these sites are the result of independent mutation to the same nucleotide. (Position 97, which has a single-nucleotide deletion in humans and other primates, is shown in blue.)

Despite Rana’s insistence that there is only one possible explanation for this pattern, there are two possibilities. The possibility that Rana does not discuss is this: the human and guinea pig sequences match because they are not mutations, but rather the original ancestral sequence of the functional GLO gene that was present in the last human – guinea pig common ancestor. This would make the rat sequence at these six positions the mutations, not the human / guinea pig sequences. There is a simple way to test this hypothesis, of course: examine the GLO sequence of other mammalian species in this region. If many other species match the human and guinea pig sequences, then we know this sequence is the ancestral sequence. If many other species match the rat sequence, the rat sequence is ancestral and the evidence supports multiple independent mutations in the primate and guinea pig lineages. Unfortunately for RTB, even a cursory examination of other species in this region demonstrates that the human / guinea pig sequence is ancestral. At each of the six positions, the consensus sequence matches the human / guinea pig sequence. The so-called “shared mutations” are not mutations at all:

The RTB model thus has no support for the proposal that shared mutations observed between species are the result of non-random, parallel mutation events. As such, Rana’s assertion that the RTB model adequately accounts for shared mutations in pseudogenes is incorrect. Unitary pseudogenes with shared mutations remain an insurmountable problem for RTB.

Beyond the scientific flaws in this argument, what I found troubling about Rana’s response is that this analysis I have presented here is nothing new – it has been known for years (see for example here and here). Rana should have known about this. But even if he didn’t the fact remains that it would have been easy for Rana to test the claims himself. For example, I assembled the alignments in this post using public databases and search tools freely available on the web. (It would have been possible simply to use figures presented elsewhere, but I wanted to (a) confirm the data myself, and (b) ensure that the relevant sequences have not been updated with corrections in the last few years). If I can do this, Rana should be able to do so as well, especially before presenting flawed arguments to non-specialists (such as RTB supporters or public in general) who will take him at his word.

As the young earth creationist, Todd Wood, pointed out in the conclusion to his recent series on RTB, the reasons behind this unfortunate pattern in RTB scholarship are somewhat irrelevant. What matters is that believers know that until RTB makes amends, their model is untrustworthy. Indeed, if RTB had developed a scientifically credible model to explain shared pseudogenes from an anti-common descent perspective, Todd Wood would be very interested (since he, being a young earth creationist, does not believe in common descent). Todd’s view of the RTB model, however, agrees with mine - and he too has called on RTB to correct their errors:

Venema and I have documented a sad but consistent and ongoing pattern of erroneous summaries of published works on the part of RTB (Rana and Ross, but mostly Rana).There's really no way to deny these mistakes have been made or to explain them away, so what are you going to do about them? I recommend apologizing for the mistakes, correcting them if you can, and instituting some kind of serious fact-checking filter on everything you publish…

As far as I'm concerned, RTB's credibility is completely shot. I would recommend that no one accept any of RTB's arguments without fact-checking their claims first. I do not know whether these problems are due to lazy scholarship, ignorance, intentional deception, or ideological blinders. What I do know is that you cannot trust Reasons to Believe.

Hopefully in the coming days RTB will follow Todd’s advice. Please, Dr. Rana, for the sake of RTB’s followers (and the church as a whole), let your audience know that you have made a mistake. Let them know that the RTB model is flawed. Admit that it misrepresents well-established science. Then start the work of making it right. This, after all is how real science works. We admit when old ideas don’t work anymore and we move on.

I would also suggest that you surround yourself with people who have expertise in this area of biology. Please have your ideas thoroughly vetted by those who know the field. As your brother in Christ, I would be happy to work with you in arranging that. While I cannot speak for Todd personally, I have every confidence that he too would be willing to help with an honest overhaul of the RTB model. Without that (significant) overhaul, however, the RTB model is a (guinea) pig in a poke. Caveat emptor.

* - “I previously stated in this post that I was convinced that no geneticist at a secular, research university would see this data differently. I have now received what I consider reliable information that this is not the case, but rather that there are at least a few biologists at secular institutions who privately hold to a young earth creationist view. As such, they do see the data differently, though for religious reasons. I should have been more clear: I am convinced that there is no biologist at a secular institution who objects to a common ancestry interpretation of these data for scientific reasons. Certainly, if there is such an individual, they have not made their case in the scientific literature, the proper place for contesting current scientific consensus.”


Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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Gregory - #50468

February 8th 2011

In the English text by Dutch biologist Jan Lever (1922-2010). “Where Are We Headed? A Christian Perspective on Evolution” (Michigan, 1970) an attempt is made to ‘integrate’ evolutionary biology with Christianity.

Lever writes: “Life has existed on this earth for several billion years…Suffice it to say here that man is much older than was formerly thought. His age may range from one to two million years. Just as we cannot deny that the earth is a sphere, so we cannot deny that the earth and all of its inhabitants are much older than was commonly thought in the past.” (20)

“The relation of Christian faith and natural science…occurs at the point where man, with all his scientific knowledge, in principle has no answers to his questions because they concern most profoundly the ultimate origin of reality, the ground and meaning of existence in general, and thus also of his own existence. / This implies that Christian and non-Christian alike can and indeed must have the same time-contingent picture of reality even though their respective life and world views, and thus their faiths, may vary greatly.” (23)


Gregory - #50470

February 8th 2011

“When we know, for example, that animals have existed for millions of years already, it is simply wrong to ask whether the ‘days’ of Genesis have reference to long periods of time.” (23)

“Does it really make any difference whether we conceive of God as having formed man out of the dust of the earth or whether he made man come forth from the highest living organisms?” (41)

“For those who believe that God is the creator of this entire earthly reality, the process of evolution described by the natural science in the present-day picture of reality becomes a grand manifestation of God’s intentions and activities.” (42, 43)

“Out of this long chain of evolution lasting billions of years there was finally born this amazing creature, one in whom this earthly reality has come to stand openly before God. Evolution thus terminated in this revelatory encounter with God.” (47)

“The modern development of natural science – its methods are increasingly followed in the other sciences – carried the process of evolution to a higher level. That was undeniably a good thing. But we also saw that the greatest problems now confronting us are ethical and ideological in character.” (54)

Thanks for provoking, P. Borger.


Gregory - #50472

February 8th 2011

http://stevebishop.blogspot.com/2011/01/jan-lever-1922-2010.html

Perhaps a story for BioLogos to pick up on, consistent with its mission plus international flavour?


Marshall - #50486

February 8th 2011

Here is Todd Wood’s response to this particular post and the RTB article (and the Borger paper approvingly cited within it).


Argon - #50490

February 8th 2011

Dennis Venema - #50466: Shared mutations come in a pattern - and this pattern was predicted by common ancestry.

I kinda agree. It was certainly extremely supportive of common descent that variation tends to come in discernible patterns and that the patterns generally map with analyses of morphological & biochemical patterns. But to ‘predict’ that shared variations and differences would have displayed a pattern requires that we know something about the nature and rate of mutations. For example, high mutation rates will erase evidence of historical connections over time. Extremely slow rates would make it hard to differentiate between lineages. Problems arise at either extreme. It was fortunate that rates of change have varied such that signals revealing historical relationships persist.

With what we know about mutations rates today and the details of how mutations arise & fix, I think we can indeed predict that patterns supporing common ancestry will be found. Prior to understanding the details (say, 50-60 years ago), it may have been hard to make a claim with nearly that level of certainty.

In any case, the time since likely divergence of lineages remains the best overall predictor of variation.


pluribara - #50573

February 9th 2011

Dear readers of this weblog…

Yesterday I left a few comments (four or five).

I pointed out that de nature of biological systems (hierachical protein networks operating in networks) cannot be explained by the current Darwinian biological pardigm, since natural selection is not acting on individual nodes of those networks. But only on networks as a whole.

I also pointed out that the difference between man and ape is quantitaive an huge (about 15% instead of 2%) and that the difference is qualitative (novel miRNA genes unique to human).

I also pointed out that RNA viruse originate in the genome from junk-DNA (known as ERVs, LINEs and SINEs). I pointed out that this novel view solves the RNA virus paradox.

It took me about 30 minutes to opload all these novel hypotheses.

The funny thing is: the moderator of this blog removed them all.

Why is that?

No other hypotheses allowed but Darwin’s?

You are free to remove this message, again, but if you do, it does not contribute to your credulity.

Have a nice day.

Peter Borger


pluribara - #50577

February 9th 2011

On my weblog, I was misinformed about the removal of my contributions, here. Please consider may e-mail as not submitted.

Have a nice day,

Peter


pluribara - #50578

February 9th 2011

Surely they can. You are looking at super-hotspots that already mutated in the past, you know.

Look at the Kerala studies with mtDNA. Kerala beaches in India have a high background radiation due to thorium-rich beaches. Almost all mutations in the Kerale population of fischermen were located on known hotspots. Read my paper in the JoC for details.

Mutations are non-random w.r.t. the position (an often nucleotide too) where they are introduced in a DNA sequence.

It explains molecular homoplasy.

It is the end as biology as we know it. But now worries, I wrote a book in which I set up an entire set of novel hypotheses how to understand biology in the 21st century.

Cheers,
Peter

~~~~~~~~~~~~~~~~


pluribara - #50579

February 9th 2011

Jan Lever recently wrote another book, that was published just after he died a few month ago. In one of his contemplations he has a rendezvous with Jesus. Jesus sets Himslef next to Jan, but He doesn’t say a word.

That is tale telling, isn’t it? Jesus has nothing to say to Mr Lever. Nothing but silent pity.

Mr Lever has destroyed Christianity in the Netherlands.

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


pluribara - #50580

February 9th 2011

But not all. We can see that from unique genes. Why are patterns that confirm common descent so important, wheras novelties are dismissed?

In my opinion, the hierarchy is easily explained by 1) the optimal genetic code, 2) optimal design, 3) non-random mutations.

Togeterh they create an illusion of common descent, but the details in molecualr phylogeny show that it cannot be universal common descent. There must have been more than one origin. Baranomes with frontloaded evolvability.

~~~~~~~~~~


sy - #50585

February 9th 2011

I must admit that I am confused by some of Peter Borger’s comments. I wonder if you could clarify some points. 1. Why do you mention an “optimal” genetic code. It has been demonstrated that the actual known genetic code is not at all optimal, there are many much more optimal theoretical codes. The actual code is about half way down the list of optimal codes. 2. What do you mean by optimal design? Again it is simple to find basic and sometimes major design flaws in most creatures. (human teeth, or at least mine, being one example). 3. You seem to stress mutational hot spots, which certainly exist, and it is known that sequence environment plays some role in mutation frequency, but these hot spots are not always that hot. How do you distinguish the effects of selection from ...well, whatever else you think might be responsible for hot spots?
I am most interested in your statement that systems biology refutes Darwinism. I dont understand that at all. Are you referring to the target of selection being the whole system? Why would that negate the development of complex networks?

I know you have published this material, but I wonder if you could provide some answers (using technical language and references) here.


Argon - #50613

February 9th 2011

sy - #50585: I am most interested in your statement that systems biology refutes Darwinism. I dont understand that at all.

I’m curious about his claim as well because that revelation no doubt comes as a shock to many ‘systems’ biologists and people working in developmental biology. I approach Dr. Borger’s certainty with a grain of salt given that so many discoveries in biology and genetics have be predicted by Creationists to be the death knell for evolution (Glen Morton’s collection of predicted ‘death of evolution’ claims here: http://home.entouch.net/dmd/moreandmore.htm)

From a Creationist perspective, I would think that the flexibility and redundancy Peter notes as features of many biological networks (although certainly not all) would make it much harder to create a good model of why unrelated ‘Kinds’ exhibit sequence and gene order similarities. Organization and function at the network level needn’t determine the organization and function at the genetic sequence level, and vice versa. And yet generally we do observe correlation.


Maurizio - #50615

February 9th 2011

Fascinating discussion.

Dr. Borger (I assume you have a PhD) - I notice most of the publications you state are found in the Journal of Creation. I’m assuming this is peer reviewed. Have you attempted to get your research published in more mainstream or secular scientific journals?

If the research/data is valid, I can’t see why it wouldn’t be considered for publication.

In Christ,

Maurizio


Dennis Venema - #50625

February 9th 2011

I see that Todd Wood has noticed this discussion, and has a post up that deals with Borger’s papers (including papers not available without a subscription).

The bottom line? Todd’s not impressed. He has the same concerns about Borger’s work that I do. Borger has not provided a remotely plausible objection to common ancestry. Click on over an have a read - it’s worth your time.


Argon - #50630

February 9th 2011

The problem for Dr. Borger, as Dennis notes in reply #50466 and Todd also sees, is how all these proposed mutational biases happen to so frequently converge to generate a largely consistent pattern that looks like a nested hierarchy. Borger claims it’s homoplasy. But why do sequences across groups consistently converge toward a particular direction? This is particularly odd because ‘within species’ variation tends toward divergence from earlier generations.

I’m sorry Peter but I just don’t see how your claims follow from your premises.


Larry - #50637

February 9th 2011

After reading Peter Borger’s first few posts I realised that I didn’t have a clue what he was talking about. After reading the rest of them, and his articles, I realised that neither does he.


Gregory - #50646

February 9th 2011

“Mr Lever has destroyed Christianity in the Netherlands.” - Peter Borger

That is of course totally absurd. The person who said it should get some professional help.

Rest in Peace, Jan Lever.

In The Brothers Karamazov, Dostoevsky’s Grand Inquisitor also meets Jesus, who doesn’t say a word to him. Did Dostoevsky ‘destroy Christianity’ in Russia?


Ken - #50687

February 10th 2011

RTB’s approach to biology is a little bizarre to say the least. Following the links to their website eventually led me to this recently published article. I tracked down the papers referenced there only to find that the original research does not make any of the claims that Rana suggests in his article. What is going on here? Is he simply inventing any argument he can think of and then citing random articles, hoping that anyone reading his articles won’t bother to check his sources?


pluribara - #50694

February 10th 2011

Freeland SJ, Knight RD, Landweber LF, Hurst LD. Early fixation of an optimal
genetic code. Mol Biol Evol 2000; 17: 511-518. Optimal = optimal.

[to be contued]


pluribara - #50695

February 10th 2011

<2. What do you mean by optimal design? Again it is simple to find basic and sometimes major design flaws in most creatures. (human teeth, or at least mine, being one example).>

By optimal design I mean optimal from ontogeny. Of course YOU think you can point out suboptimal designs, but remember that an organisms cells, all organs, stem from one singel cell. That sets some design restrictions some see as “poor design”. For instance, the inverted retina in vertebrates. But did you ever look into the ontogeny of this design? Probably not. It turns out that the “inverted” retina can only be designed in this way, because the parts that could give rise to “your optimal design” are already determined to form other structures.

http://www.pnas.org/content/94/6/2098/F1.large.jpg

[to be continued]


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