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Signature in the Pseudogenes, Part 2

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May 17, 2010 Tags: Genetics

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

Signature in the Pseudogenes, Part 2

As we indicated in Part 1 of this series, pseudogenes are remnants of once-functional genes. Since they are segments of a DNA molecule, they are faithfully copied and passed along generation after generation through the millennia of time. For this reason, they serve as excellent markers. They allow us to trace ancestry.

Consider, for example, the lineage shown in the diagram at right. In this example, Species A and B diverged from a single ancestor (red) fairly recently. Since there has been little time for them to evolve, the species are similar to each other.

Species A, B, C are also derived from a common ancestor (blue). That ancestor lived much longer ago, so the three species have had more time to diverge. Thus they may look quite different from each other. Finally, a very long time ago, there lived an even more ancient ancestor (yellow). This one gave rise to all four of these species. Having had lots of time to evolve, this ancestor’s descendents have become increasingly different from one another.

With regard to pseudogenes, the theory of common descent makes a prediction. Let’s say that in sequencing a genome, one finds a specific pseudogene (we’ll call it ‘y’) in Species A, but it is not found in Species B (see below).

If the theory of common descent is true:

  1. The event which gave rise to pseudogene ‘y’ occurred recently. It could not have been present in the common ancestor highlighted in red in the diagram to the left; otherwise both Species A and B would have had it.
  2. Since the Species A/Species B common ancestor didn’t have the pseudogene, earlier ancestors could not have had it either.
  3. Species C and D, because they are derived from those earlier ancestors, would not have pseudogene ‘y’ either.

With the sequencing of many genomes, it is now a straightforward matter to test this hypothesis. This can be done not by examining one or two genes, but by examining hundreds, even thousands. Do all pseudogenes fit into this sort of pattern? We will examine this question by considering one particular subset.

Our sense of smell is made possible through a set of proteins, the olfactory receptors, found on the surface of cells lining the nasal cavity. Airborne compounds bind to these receptors, thereby sending signals to the brain, which then interprets the pattern of binding as a particular odor.

Recently it has become apparent that many mammals have lost some of their olfactory receptor proteins through mutation of the genes which produce them: the mutated genes have been converted into non-functional pseudogenes. It is possible to compare the distribution of numerous olfactory receptor pseudogenes in several primate species.

Let’s first consider 15 pseudogenes1 present in humans but not in chimpanzees. According to the theory of common descent, these 15 pseudogenes have arisen since humans and chimps last had a common ancestor about six million years ago. If this is so, we would predict that none of the 15 pseudogenes will be present in primates believed to have diverged even earlier. As illustrated at right, this is exactly what we find when examining gorilla and orangutan genomes.

What about other olfactory pseudogenes? Do they follow the same sort of pattern? Are they in the “correct” places? Indeed they are – every one:


Six pseudogenes with identical inactivating mutations are found in all four species. Humans and chimpanzees share twelve identical pseudogenes (6 plus 3 plus 3) in common, but humans and gorillas share only nine (6 plus 3). These nine, as predicted, are a subset of the twelve shared by humans and chimpanzees.

Using pseudogene evidence alone, in the absence of any other line of evidence (gene homology, shared synteny, anatomy, etc), it would assemble these species into the same pattern of relatedness as any of the others. Indeed for the 47 pseudogenes studied, not one is out of place. We can tell when in the ancestry each arose relative to the others, and no cases exist where the same pseudogene appears in a manner inconsistent with the proposed lineage. Also recall that this is only 47 pseudogenes within a single family of genes: many, many more have been analyzed and they give parallel results.

As compelling as this pattern is, pseudogene data can also be extended to much more distantly-related species. All mammals, for instance, are predicted to be the evolutionary descendents of egg-laying ancestors. Indeed, the fossil record contains species classified as “mammal-like reptiles” as well as “reptile-like mammals” that blur the distinction between these groups. The evolutionary prediction that mammals are descended from egg-laying ancestors was tested recently using the hypothesis of shared synteny to look for the inactivated remains of a gene devoted to egg-yolk production in the human genome. This gene, called the vitellogenin gene, is used as a component of egg yolk in a wide array of egg-laying species. This research group wondered if it would be possible to find the remains of the vitellogenin gene in the human genome. To help in their search, they employed the prediction of shared synteny.

You may recall from our previous post on synteny that over time, blocks of genes in diverging species are increasingly “broken up” into smaller and smaller blocks. Very closely linked genes, however, can stay together for a very, very long time. Using this knowledge, the researchers:

  1. Located the (functional) vitellogenin gene in the chicken genome,
  2. Took note of the gene “next door” to the vitellogenin gene in the chicken,
  3. Looked to see if this neighboring gene was present in the human genome (it was – a functional version of this gene is found in humans),
  4. Looked in the same relative spot next door to this gene in the human genome, and
  5. Discovered the mutated remains of the vitellogenin gene in the human genome in precisely this location.

While it might be possible to present a (strained) argument for the presence of olfactory receptor pseudogenes in humans, the mere presence of the mutated remains of a gene required for making egg yolk in the human genome should give even the most ardent anti-evolutionist pause. That this gene was found using the prediction of shared synteny between humans and chicken only adds to the impact.

Common ancestry is an elegant, parsimonious explanation for the pattern of pseudogenes that we observe, yet many Christians reject common ancestry for theological reasons. The challenges for a non-evolutionary explanation of this data, however, are many:

  1. Why do humans (or any species for that matter) have so many inactivated genes?
  2. Why does the distribution of these inactivated genes match precisely the pattern of relatedness (phylogenies) predicted by other, independent criteria? Why are there no “out-of-place” pseudogenes?
  3. Why are pseudogenes found in the precise locations predicted by shared synteny?
  4. Why are some of these inactivated genes dedicated to functions that make no sense for the species that harbors them (e.g. defective genes for egg-yolk production in placental mammals like humans)?

To be blunt, if this pattern is not to be accepted, why did God put it in place for us to discover? And if this pattern is not to be trusted, how can anything in genetics be certain? As a colleague once commented, this pattern “would deceive all honest investigators” if in fact it is not accurate.

Many believers are troubled by the idea of humans sharing ancestry with other forms of life (and its attendant theological issues). Consider the opposite, however: suppose that common ancestry is in fact incorrect. The trouble is this: the data doesn’t go away. In this case, one still has to explain why the data looks the way it does: why did God choose to create independent species with this pattern? Even among anti-evolutionists there is no satisfying answer to this question. Time and again, what we see from Christian anti-evolutionary organizations is not an attempt to wrestle with the data, but rather to obfuscate it.

These lines of evidence are becoming more and more widely known among believers and non-believers. If Christians continue to insist on denying the implications of this (very solid) science, we greatly risk setting a stumbling block before our brothers and sisters in Christ, or bringing the faith into disrepute with those whom we seek to reach with the Good News.

Notes:

1. Of course, there is always a possibility that the same gene may acquire a mutation and become a pseudogene independently in other species. In this case, the inactivating mutations in the two species will be different, and they will be classified as “species-specific” events. It is also possible that species-specific mutations can obscure previously shared mutations (for example, the complete deletion of a previously-mutated pseudogene).

References:

Brawand, D., Wali, W. and Kaessmann H. 2006. Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation. PLoS Biology 6: 0507-0517. Available free here

Gilad, YG., Man, O., Paabo, S., and Lancet, D. 2003. Human specific loss of olfactory receptor genes. Proc. Natl. Acad. Sci. 100: 3324-3327. Available free here

Zhang, ZD, Cayting, P., Weinstock, G. and Gerstein, M. 2008. Analysis of of nuclear receptor pseudogenes in vertebrates: how the silent tell their stories. Mol. Biol. Evol. 25: 131-143. Available free here


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.
Darrel Falk is former president of BioLogos and currently serves as BioLogos' Senior Advisor for Dialog. He is Professor of Biology, Emeritus at Point Loma Nazarene University and serves as Senior Fellow at The Colossian Forum. Falk is the author of Coming to Peace with Science.

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Malcolm - #13908

May 17th 2010

Excellent article. The line “Time and again, what we see from Christian anti-evolutionary organizations is not an attempt to wrestle with the data, but rather to obfuscate it” is one that really struck a chord. Most people could accept others looking at this data and saying something like “you know, it really, really looks like common descent but I just can’t accept it.” Instead we get distortions, misinformation and what is clearly deliberate misrepresentation (lying?) from anti-common descent organisations. Whatever one’s views about evolution and science in general, this behaviour should be unacceptable to Christians everywhere.


Malcolm - #13909

May 17th 2010

Thought I’d also recommend Dr. Venema’s talk on this from the ASA last year.

Human Genomics: Vestiges of Eden or Skeletons in the Closet?


beaglelady - #13915

May 17th 2010

This just illustrates the purposeful arrangement of pseudogenes.  God put the the “mutated remains of the vitellogenin gene” right where he knew you’d be looking for it.  No way this could happen by chance!


Charlie - #13917

May 17th 2010

What came first the chicken or the egg?  Well I guess the gene vitellogenin gives us the answer, the egg.

Beaglelady,

It didn’t happen by chance.  Our “very distant” ancestors, the same ancestors as the egg laying animals alive today, had the functional vitellogenin gene.  When that gene was no longer necessary for our human lineage, we eventually lost it (or parts of it) through “random” mutations” making in non-functional.


Glen Davidson - #13919

May 17th 2010

With regard to pseudogenes, the theory of common descent makes a prediction.

I’d just add that these are statistical predictions.  Events could happen by chance to give the “wrong” outcome, so that, say, the ancestor of five lineages had the pseudogene, yet all but one of the descendant kept it.

I make this caveat because some act as though evolution were dogma which insists on a particular outcome, and if it fails in any instance it is wrong, wrong, wrong.  Science isn’t like that, its predictions involve contingencies in most cases, and is subject to various contingencies.  It’s the overall probabilities that matter, and the probability that all of the signs of relatedness are due to coincidence or whim of some intelligence is extremely low.

Glen Davidson


beaglelady - #13921

May 17th 2010

Charlie,

For Pete’s sake, that was a joke!


Esley Heizer - #13928

May 17th 2010

Great article. I truly wish I could get some Christians I know to visit this website and read it with an open mind. They might come to see evolution as God’s handiwork and not lie perpetrated by scientists bent on the destruction of Christianity.


Headless Unicorn Guy - #13942

May 17th 2010

This just illustrates the purposeful arrangement of pseudogenes.  God put the the “mutated remains of the vitellogenin gene” right where he knew you’d be looking for it.  No way this could happen by chance!—beaglelady

As in “God Created It That Way Ex Nihilo.”  Omphalos by Gosse, taken to the genetic level.

For Pete’s sake, that was a joke!—beaglelady

Unfortunately, BeagleLady, today is an age of extremes.  As far as you go into absurdity as a joke, there is going to be a True Believer out there who’s gone twice as far and is Dead Serious.


Charlie - #13948

May 17th 2010

Beaglelady,

Whoops, sorry. Sarcasm is hard to pick up on written text


unapologetic catholic - #13950

May 17th 2010

Charlie the yolk’s on you

Excellent article.  Well explained and nicely done.


Chris Massey - #13953

May 17th 2010

Dennis and Darrel,

Fantastic article! I really appreciate the clarity with which you present technical matters. Using language like the “gene next door” really helps those of us who don’t stare at fruit flies for a living

I have a question (and maybe this is what Glen Davidson was getting at) but I’m given to understand that we may discover some situations in which a pseudogene in an ancestral population won’t be found in all descendants (and not just because it has been deleted). If the pseudogene has not reached the point of fixation in the common ancestor, is it possible that some branches of descendants will have the pseudogene and others will not, depending on the frequency of the pseudogene in the subpopulation from which they diverged?


Dennis Venema - #13955

May 17th 2010

Hi Chris,

Your question is perceptive, and you are right: if a pseudogene has not gone to fixation in a population prior to divergence then we may see the pseudogene in some descendent species but not others.

Best,

Dennis


beaglelady - #13956

May 17th 2010

As in “God Created It That Way Ex Nihilo.”  Omphalos by Gosse, taken to the genetic level.

Ah yes, Omphalos, the Biblical Belly-Button Book.  Somehow I get the feeling it would be taken quite seriously these days.


Glen Davidson - #13958

May 17th 2010

Ah yes, Omphalos, the Biblical Belly-Button Book.  Somehow I get the feeling it would be taken quite seriously these days.

Isn’t ID basically the same “argument”?  Everything looks like you’d expect from evolution (other than being “irreducibly complex,” etc.), but it took an intelligent designer to make everything look like no foresight was involved.

Sure, it’s not directly the appearance of age, but it is the appearance of evolution over vast periods of time, even though it’s nothing of the sort—not in the designed aspects, anyway.

Glen Davidson


Frank - #13959

May 17th 2010

“Even among anti-evolutionists there is no satisfying answer to this question. Time and again, what we see from Christian anti-evolutionary organizations is not an attempt to wrestle with the data, but rather to obfuscate it.”

Is this true? It would seem not.

http://www.answersingenesis.org/articles/aid/v3/n1/smell-of-change-pseudogenes

http://www.answersingenesis.org/tj/v14/i3/pseudogenes_genomes.asp

http://www.answersingenesis.org/tj/v18/i3/mistakes.asp

http://creation.com/images/pdfs/tj/j21_3/j21_3_118-127.pdf

http://www.answersingenesis.org/articles/arj/v2/n1/exogenization-vs-endogenization


Chris Massey - #13962

May 17th 2010

Frank,

That is an impressive list of articles that do precisely what Darrel and Dennis say anti-evolutionists do. They obfuscate.

The first, for example, identifies an OR pseudogene that retained some limited function. This is the standard creationist ploy. Whether it be “junk DNA”, Alu repeats or pseudogenes, creationists find some functionality amongst the noise and pretend that this undermines the argument.

In reality, it’s utterly beside the point. A gene can be mutated such that it doesn’t perform its original function, but still retains some vestigial or novel function. That doesn’t mean it’s not a pseudogene. And most importantly, it does nothing to explain the pattern of inheritance that so clearly demonstrates common ancestry.


beaglelady - #13984

May 18th 2010

Isn’t ID basically the same “argument”?  Everything looks like you’d expect from evolution (other than being “irreducibly complex,” etc.), but it took an intelligent designer to make everything look like no foresight was involved.

True. And if God is just a capricious magician,  and creation has no rhyme or reason, who are we to question it?


HornSpiel - #13991

May 18th 2010

Franl,

Thanks for interacting with this site. I took a look at one of your references: http://www.answersingenesis.org/tj/v14/i3/pseudogenes_genomes.asp.

The reasoning was IMHO very muddled. It seemed they went out of their way to make things confusing. Take this sentence from the “Summary” (Abstract):

Evidence for pseudogene function continues to accumulate, and is much more significant than the actual number of known functional pseudogenes.

It apparently means that functional pseudogenes are rare, but when they are functional, they are significant. How does that counter the claim that pseudogenes are markers that demonstrate inheritance and lines of descent? Can you explain to me in simple terms what this article is trying to say?

I hope you keep reading and thinking about these matters.


Frank - #13996

May 18th 2010

I have never been here before, but I was directed here via a link from elsewhere - http://www.gty.org/Blog/B100516 . As someone else pointed out there it is inaccurate to say there are no creationist answers to these points and I thought it was a correction that needed to be made.


Alex - #13998

May 18th 2010

I was listening to Greg Koukl over the weekend. He made some very interesting points at the beginning that he had heard at a recent Intelligent Design conference. Stephen Meyer, Paul Nelson, and Doug Axe presented that;

- No naturalistic explanation for the origin of information
- DNA is not destinate, it does not build bodies on the macro scale, only micro scale, and the other sources involved in building bodies are not capable of being influenced by evolutionary mechanisms; they do not mutate
- In order for required produce evolutionary effects to occur mutations must show up in the egg. These types of early changes however turn out to be lethal by the time it gets to an adult, embryonic lethals.


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