Universal common ancestry in the hotseat III

Toward a Consensus: An Open Letter to BioLogos on the Genetic Evidence
Cornelius Hunter

Dennis Venema, professor of biology at Trinity Western University and Fellow at BioLogos, has written a series of articles that have been noted by evolutionists for their clarity and persuasiveness. So as a collector of evidences and reasons why evolution is a fact, I was interested to see Venema's articles. What does the professor have to say to help confirm what Samuel Wilberforce rhetorically called "a somewhat startling conclusion"?


One of Venema's basic points (see  here and here ) is that the genomes of different species are what we would expect if they evolved. Allied species have similar genomes, and genetic features fall into evolution's common descent pattern:If indeed speciation events produced Species A-D from a common ancestral population, we would expect their genomes to exhibit certain features when compared to each other. First and foremost, their overall genome sequence and structure should be highly similar to each other -- they should be versions of the same book, with chapters and paragraphs of shared text in the same order. Secondly, the differences between them would be expected to fall into a pattern.
Does the evidence confirm these evolutionary expectations? Venema answers with an emphatic yes.

Here Venema is appealing to the empirical evidence. He is comparing the evidence to the theory of evolution, and finding that the evidence confirms evolution's predictions. This means the theory can be empirically evaluated. And if evolution can be genuinely evaluated empirically, then it is, at least theoretically, possible for evolution to fail. If the evidence can confirm evolution, then it also can disconfirm evolution.

This is important because focusing the attention on the evidence means the non-scientific arguments go away and science is allowed to speak. What does it say? Here I will take the opposing view, for it seems that what the science shows is that Venema's claim, that the genetic evidence confirms evolutionary predictions, is inaccurate.

This is not to say that evolutionary explanations cannot be offered. As philosophers well understand, another sub-hypothesis is always possible. Such hypotheses raise more profound questions of parsimony, likelihood, and so forth. But it seems that such philosophical questions ought to be addressed after there is a consensus on what the empirical evidence has to say. The goal here is to move toward that consensus. Venema, and evolutionists in general, make a straightforward claim about the evidence. We ought to be able to dispassionately evaluate that claim.

Of course I realize that reaching consensus is not as simple as reading an article. There will be differing interpretations by fair-minded critics. And the topic of origins is certainly not always dispassionate. If you argue against evolution you will be disparaged. My response to such attacks has and always will be to forgive.

One final preliminary is simply to point out that it is a challenge just to do justice to this story. A thorough treatment could easily require an entire volume. But a few, typical, examples will have to suffice. They can provide readers with an approximate understanding how the evidence bears on Venema's claim.

What Does the Evidence Say?

For starters, phylogenetic incongruence is rampant in evolutionary studies. Genetic sequence data do not fall into the expected evolutionary pattern. Conflicts exist at all levels of the evolutionary tree and throughout both morphological and molecular traits. This paper reports on incongruent gene trees in bats. That is one example of many.

MicroRNAs are short RNA molecules that regulate gene expression, for example, by binding to messenger RNA molecules which otherwise would code for a protein at a ribosome. Increasingly MicroRNAs are understood to be lineage-specific, appearing in a few species, or even in just a single species, and are nowhere else to be found. In fact one evolutionist, who has studied thousands of microRNA genes, explained that he has not found "a single example that would support the traditional [evolutionary] tree." It is, another evolutionist admitted, "a very serious incongruence."

Trichodesmium or "sea sawdust," a genus of oceanic bacteria described by Captain Cook in the 18th century and so prolific it can be seen from space, has a unique, lineage-specific genome. Less than two-thirds of the genome of this crucial ammonium-producing bacteria codes for proteins. No other such bacteria has such a low value, and conversely such a large percentage of the genome that is non-coding. This lineage-specific genome, as one report explains, "defies common evolutionary dogma."

It is not unusual for similar species to have significant differences in their genome. These results have surprised evolutionists and there does not seem to be any let up as new genomes are deciphered.

The mouse and rat genomes are far more different than expected. Before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:

Before the launch of the Rat Genome Sequencing Project (RGSP), there was much debate about the overall value of the rat genome sequence and its contribution to the utility of the rat as a model organism. The debate was fuelled by the naive belief that the rat and mouse were so similar morphologically and evolutionarily that the rat sequence would be redundant.
The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

One phylogenetic study attempted to compute the evolutionary tree relating a couple dozen yeast species using 1,070 genes. The tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. It was "a bit shocking" for evolutionists, as one explained: "We are trying to figure out the phylogenetic relationships of 1.8 million species and can't even sort out 20 yeast."

What is interesting is how this false prediction was accommodated. The evolutionists tried to fix the problem with all kinds of strategies. They removed parts of genes from the analysis, they removed a few genes that might have been outliers, they removed a few of the yeast species, they restricted the analysis to certain genes that agreed on parts of the evolutionary tree, they restricted the analysis to only those genes thought to be slowly evolving, and they tried restricting the gene comparisons to only certain parts of the gene.

These various strategies each have their own rationale. That rationale may be dubious, but at least there is some underlying reasoning. Yet none of these strategies worked. In fact they sometimes exacerbated the incongruence problem. What the evolutionists finally had to do, simply put, was to select the subset of the genes that gave the right evolutionary answer. They described those genes as having "strong phylogenetic signal."

And how do we know that these genes have strong phylogenetic signal. Because they gave the right answer. This raises the general problem of prefiltering of data. Prefiltering is often thought of merely as cleaning up the data. But prefiltering is more than that, for built-in to the prefiltering steps is the theory of evolution. Prefiltering massages the data to favor the theory. The data are, as philosophers explain, theory-laden.

But even prefiltering cannot always help the theory. For even cleansed data routinely lead to evolutionary trees that are incongruent (the opposite of consilience). As one study explained, the problem is so confusing that results "can lead to high confidence in incorrect hypotheses." As one paper explained, data are routinely filtered in order to satisfy stringent criteria so as to eliminate the possibility of incongruence. And although evolutionists thought that more data would solve their problems, the opposite has occurred. With the ever increasing volumes of data (particularly molecular data), incongruence between trees "has become pervasive."

What is needed now is less data. Specifically, less contradictory data. As one evolutionist explained, "if you take just the strongly supported genes, then you recover the correct tree." And what are "strongly supported" genes? Those would be genes that cooperate with the theory. So now in addition to prefiltering we have postfiltering.

Another issue are the striking similarities in otherwise distant species. This so-called convergence is rampant in biology and it takes on several forms.

Consider a paper from the Royal Society on "The mystery of extreme non-coding conservation" that has been found across many genomes. As the paper explains, there is currently "no known mechanism or function that would account for this level of conservation at the observed evolutionary distances." Here is how the paper summarizes these findings of extreme sequence conservation:

... despite 10 years of research, there has been virtually no progress towards answering the question of the origin of these patterns of extreme conservation. A number of hypotheses have been proposed, but most rely on modes of DNA : protein interactions that have never been observed and seem dubious at best. As a consequence, not only do we still lack a plausible mechanism for the conservation of CNEs -- we lack even plausible speculations.
And these repeated designs, in otherwise different species, are rampant in biology. It is not merely a rare occurrence that perhaps evolution could explain as an outlier. That the species do not fall into an evolutionary tree pattern is well established by science.

Furthermore, these repeated designs do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. So now the evolutionist must not only believe that there are many of these repeating design events, but that in most cases, they repeat multiple times, in disparate species.

Evolutionists have labeled this evidence as recurrent evolution. As a recent paper  explains:

The recent explosion of genome sequences from all major phylogenetic groups has unveiled an unexpected wealth of cases of recurrent evolution of strikingly similar genomic features in different lineages.
In addition, many instances of a third more puzzling phylogenetic pattern have been observed: traits whose distribution is "scattered" across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.

Of course these puzzling, striking similarities cannot be explained by common evolutionary history. Instead, they are explained by common evolutionary forces:

As ancestrally shared features are the result of a common evolutionary history, shared features evolved by recurrent evolution are often the result of common evolutionary forces acting on different lineages.
If the pattern fits the evolutionary tree, then it is explained as common evolutionary history. If not, then it is explained as common evolutionary forces.

With all of this contradictory evidence, even evolutionists have realized in recent years that the traditional evolutionary tree model is failing. As one evolutionist  explained, "The tree of life is being politely buried."

There are many more fascinating examples of biological patterns that are not consistent with the expected evolutionary pattern. These are not anomalies or rare exceptions. Here we have focused on the genetic level since that was the theme of Venema's article. It seems that the species and their genomes do not fall into a consistent evolutionary pattern as evolutionists such as Venema claim. This does not mean evolutionists cannot explain any of this. They have a wide spectrum of mechanisms to draw upon, of varying levels of speculation and likelihood. These explanatory mechanisms greatly increase the theory's complexity. They raise questions of realism, and whether the theory is following the data, or the data is following the theory.

But such questions are for another day.

The point here is that evolutionist's claims that the genomic data broadly and consistently fall into the evolutionary pattern and expectations do not seem to reflect the empirical data. This is the first step in moving the discourse forward. We need to reach consensus on what the evidence reveals.

In a subsequent post I will continue with an examination of the next evidences Venema presents.

The design debate through the looking glass

Design through the Looking Glass

Evolution News & Views 

You don't have to hold an amino acid up to a mirror to see its mirror image. Amino acids (except for one, glycine) come in pairs, like gloves, on the real-world side of the looking glass. So do the sugars used in DNA and RNA; they are assigned a "handedness" based on conventional rules of describing their orientation in 3-D space. In all other physical respects, chemical and thermodynamic, they are identical in their activity. This makes them difficult to separate.

The phenomenon is known as chirality. The chiral "isoforms" are called enantiomers of each other. Left-handed enantiomers are preceded byL- (from Latin levo) as in L-alanine, while right-handed enantiomers are preceded by D- (fromdextro) as in D-ribose. A mixture of both hands is said to be racemic, or heterochiral. A pure mixture of one hand is called homochiral.

With only rare exceptions, all living things use just one "hand" of these molecular gloves: left-handed amino acids in proteins, and right-handed sugars in nucleic acids. How this came about has long been a mystery, as four Chinese scientists from Tsinghua University in Beijing explain in Nature Chemistry:

Despite biology's seemingly limitless diversity and the vastness of its territories that permeate into virtually every corner of the Earth, at the fundamental level of biochemistry, all known forms of life are narrowly defined by a single version of molecular machinery based on L-amino acids and D-ribose nucleic acids. Although rare examples of the use of D-amino acids, such as D-aspartic acid in animal brains, and L-sugars, such as L-arabinose in plants, do exist, the central dogma and most of the biological macromolecules have followed the homochirality established by life's earliest ancestors. Processes that led biology onto this particular chiral path have remained largely elusive, even though experimental evidence for breaking the mirror symmetry has been reported and many theoretical models have been proposed.[Emphasis added.]

As it stands, no experimental or theoretical model explains the origin of life's homochirality by natural processes. Some experimenters have produced a slight enantiomeric excess of one hand or the other, but usually with non-biological chemicals, and nothing approaching the purity of life's chiral molecules. Proteins and nucleic acids cannot work with mixed handedness. A single wrong-handed building block is enough to destroy DNA, RNA, and proteins. As we saw last year, checkpoints ensure that life's building blocks remain homochiral.

This purity of handedness baffles materialists, because their causal toolkit only includes natural law and chance. The probability of getting a single-handed polymer from racemic ingredients is comparable to getting a string of coin tosses coming up all heads. The longer the sequence, the more improbable it becomes -- quickly swamping the chance hypothesis. Yet as Wang et al. state, our knowledge of natural laws isn't helping solve the problem.

Recently, an in vitro selected catalytic RNA capable of incorporating nucleotides in a cross-chiral fashion without enantiomeric cross-inhibition was reported. The fact that no known laws of physics and chemistry preclude biology's use of either of the two chiral systems, mirror-image twins of one another, has led to an intriguing question as to whether a parallel mirror-image world of biology running on a chirally inverted version of molecular machinery could be found in the universe or be created in the laboratory.

Turning from origins to application, they describe their initial attempts to create mirror-image life:

We reasoned that towards synthesizing a mirror-image biological system, an imperative step would be to reconstitute a chirally inverted version of the central dogma of molecular biology with D-amino acid enzymes and L-ribose nucleic acids--although reconstituting a mirror-image, ribosome-based translation systemthrough the total synthesis of all the ribosomal RNA (rRNA) and protein building blocks is still beyond the current technology, the totalchemical synthesis of (small enough) mirror-image polymerases might be feasible. Here we set out to synthesize such a mirror-image polymerase and to test if two steps in the central dogma, the template-directed polymerization of DNA and the transcription into RNA, can be carried out in a synthetic mirror-image molecular system (Fig. 1a).

(For present purposes, we won't dispute the central dogma, although biologist Jonathan Wells has written extensively on its problems.)

These scientists did, in fact, succeed in getting some template-driven polymerization and transcription of opposite-handed amino acids. It was very slow, but it demonstrates that, in principle, life could exist in a mirror image of itself. Alice through the looking glass would appear identical to her mirror image, but would not be able to eat opposite-handed food!

Commenting on this work for Nature, Mark Peplow explains why synthetic mirror-image biomolecules have desirable properties:

In principle, looking-glass versions of these molecules should work together in the same way as normal ones -- but they might be resistant to attack by conventional viruses or enzymes that have not evolved in a looking-glass world.

That makes mirror-image biochemistry a potentially lucrative business. One company that hopes so is Noxxon Pharma in Berlin. It uses laborious chemical synthesis to make mirror-image forms of short strands of DNA or RNA called aptamers, which bind to therapeutic targets such as proteins in the body to block their activity. The firm has several mirror-aptamer candidates in human trials for diseases including cancer; the idea is that their efficacy might be improved because theyaren't degraded by the body's enzymes. A process to replicate mirror-image DNA could offer a much easier route to making the aptamers, says Sven Klussmann, Noxxon Pharma's chief scientific officer.

Wang et al. took the smallest known polymerase enzyme, just 174 amino acids long, and laboriously constructed a right-handed counterpart. They succeeded in getting it to extend a primer from 12 nucleotides to 18 nucleotides in 4 hours. Getting it to 52 nucleotides took 36 hours -- a "glacial pace," Peplow remarks. Nevertheless, it was an important discovery. Both the normal and mirror-image enzymes worked independently, without interference, when mixed in the same test tube.

The Design Inference

The researchers admit it would be a "daunting task" to build a mirror-image version of a ribosome where translation could take the left-handed RNA and translate it into a right-handed protein. Building a "looking glass cell" is a far-off dream. At this stage, though, we can draw some conclusions about chance and design.

Peplow confirms that homochirality remains a vexing problem. He surely would have said otherwise if a likely non-random cause were known.

In their research paper, the Tsinghua researchers also present their work as an effort to investigate why life's chirality is the way it is. This remains mysterious: it may simply be down to chance, or it could have been triggered by a fundamental asymmetry in nature.

But Steven Benner, at the Foundation for Applied Molecular Evolution in Alachua, Florida, says it's unlikely that creating a mirror form of biochemical life could shed any light on this question. Almost every physical process behaves identically when viewed in a mirror. The only known exceptions -- called 'parity violations' -- lie in the realm ofsubatomic physics. Such tiny differences would never show up in these biochemical experiments, says Benner.

Benner and Peplow just conceded that natural law cannot explain homochirality. To a materialist, that leaves chance. For a short polypeptide of 100 amino acids to have formed by chance would be ½ x ½ x ½ ... 100 times: 1 chance in 2100, which is approximately 1 in 1030. There aren't enough probabilistic resources to make this likely to happen in a primordial soup of racemic amino acids. But then, even if it did, homochiral DNA or RNA would have to form independently out of its own racemic building blocks. There's just no realistic chance of success in a materialistic world. Intelligence, by contrast, can easily select one hand over the other; consider how quickly an eight-year-old could sort a pile of coins into heads and tails.

Another conclusion from this paper is that homochirality as observed in life is contingent: i.e., it could exist in the opposite mirror-image form. There is no chemical or thermodynamic reason why proteins must be left-handed as opposed to right-handed, or why nucleic acids must be right-handed as opposed to left-handed. The experiments show that chemical reactions can proceed just as well in a mirror-image world. When a choice has been made one way to the exclusion of other possibilities, and it is beyond the reach of chance, it gives indication that intelligence has embedded information into the system.

Finally, these researchers demonstrate empirically how intelligence can embed information into a system. They purposefully selected building blocks of one hand to construct their polymerase. They had a goal, and a means of reaching it. If we rightly judge their work as a product of intelligent design -- as glacially slow as it was -- how much more the products of a cell that work rapidly and accurately, using machinery at a level of sophistication beyond our ability to imitate?

It's logical. If a system on the far side of the looking glass is intelligently designed, then the system on the near side is also intelligently designed. Only a fun-house mirror could distort that conclusion.

Universal common ancestry in the hotseat II

The Vitellogenin Pseudogene Story: Unequally Yolked

Ann Gauger

Synteny refers to how well chromosomal sequences from different species align with one another. Genes can be in the same general order and location between species, for example rat and mouse, or chimp and human. If they align well, evolutionists take the alignment as evidence for common ancestry. Sometimes, the gene sequences may be interrupted by deletions or insertions, and stop codons, which prevent the gene from making functional protein.

These "inactivated" genes are calledpseudogenes, and are taken by evolutionists as further evidence for common descent. Their presence is explained as the remnants of once functional genes broken by mutation and no longer needed by the organism.

"Why should a designer litter the genome with so much trash?" the evolutionists say.

One particular story that combines ancient pseudogenes and synteny to argue for common descent is circulating on the web, right now. See here for comments yesterday by Evolution Newson "Functional Pseuodogenes and Common Descent." The story is several years old, but it's popular because it seems to confirm the old evolutionary idea that our long ago ancestors were egg-laying creatures that then evolved to live-bearing placental mammals. And it's being challenged because of new evidence coming from ENCODE and other genome projects.

Egg-bearing animals use proteins called vitellogenins to transport nutrients in their egg yolk. Each vitellogenin is a very long complicated protein composed of many exons (stretches of DNA that must be copied into RNA and then spliced together into one contiguous piece before being translated into vitellogenin). An article by Dennis Venema lays out the supposed story: humans retain the remnants of DNA that used to code for egg yolk proteins called vitellogenins. Since humans don't lay eggs, the argument goes, these "vitellogenin" pseudogenes, now long since mutated into near unrecognizability, must be inherited from common ancestors who did lay eggs. Venema claims that all three human "vitellogenin" pseudogenes, VIT1 through VIT3, show traces of sequence similarity to the functioning vitellogenin genes of the chicken.

All of this argument depends on three ideas: 1) we share common ancestry with egg laying animals, 2) any sequence similarity is due to ancestry not function, and 3) there was just one function for the vitellogenin gene, and that was making vitellogenin. Any function now is due to secondarily evolved function.

This story is based on a 2008 paper by Brawand et al. that discusses yolk proteins in egg-laying animals and mammals. In that paper they identified the region of the chicken genome where vitellogenin genes are located, then found the similar regions in humans, dogs, and various marsupials and platypus, to see if vitellogenin pseudogenes could be found in the right syntenic neighborhoods.

Patches of sequence similarity to the chicken genome that might be interpreted as pseudogenes can be found in syntenic regions of marsupial genomes. Evidence for vitellogenin pseudogenes in human and dog genomes, on the other hand, is very weak. It is practically nonexistent for vitellogenin genes VIT2 and VIT3 (it is not statistically significant compared to the genomic background). The remaining gene, VIT1, has two patches of similarity in its putative former coding sequence, according to a supplemental figure in the paper.

The best of them is a patch 150 bases long (out of 42,637 total bases for the gene!) that has roughly 50 percent identity, by my estimation, and a few deletions to help make things match up. According to the authors, there is a 95 percent chance that the amount of similarity between VIT1 for humans and dogs, and the chicken VIT1, is not due to random chance -- but that's just at the borderline for statistical significance. (They don't specify exactly what sequences they were comparing, so I am guessing it was the one whose sequence they reported in the paper.)

So what if the similarity is statistically significant? What apparent similarity there is could well be due to an overlapping gene with an entirely different function that is present in that stretch of sequence in the chicken, marsupial, dog, and human genomes. (I am guessing it is present in the other genomes -- I know it is present in humans.) Indeed, there is evidence of another gene with other possible functions in that region of the genome. As reported byTomkins:

...the alleged vtg [vitellogenin] fragment in human is not a pseudogene remnant at all, but a functional enhancer element in the fifth intron of a "genomic address messenger" (GAM) gene. This GAM gene produces long noncoding RNAs that have been experimentally shown to selectively inhibit the translation of known target genes, a majority of which are implicated in a variety of human diseases. Messenger RNAs from this gene are also expressed in a variety of human brain tissues. The alleged 150 base vtg sequence contains a variety of highly conserved mammalian transcription factor binding domains, nucleosome depleted open-active chromatin, is hypo-methylated, associates with RNA polymerase 2 in long-range chromatin interactions, and binds the Mafk transcriptional regulator. These combinatorial data clearly show that it is a functional enhancer element in a GAM gene expressed in the human brain -- strongly challenging the idea that this sequence is an egg-laying pseudogene genomic fossil.The long non-coding RNAs mentioned above are widely believed to have many important regulatory functions in the cell. They are implicated in long- and short-range interactions between genes, the way the DNA loops, whether genes are sequestered or not -- all these things and more are affected.

Let's summarize some of the main points we have discussed:

1. A similar arrangement of genes exists among mammalian genomes and the chicken genome in the neighborhood of the chicken vitellogenin genes, with the very important exception that in mammals, the vitellogenin genes are either absent or pseudogenized.
2. This similar order could be due to ancestry or functional reasons.
3. In humans the evidence for a vitellogenin pseudogene fragment is very weak.
4. It is possible that any sequence similarity there might be due to a shared function, because of the regulatory gene that exists in the same region. (This despite Venema's disparaging comments to the contrary. See above.)
5. If the sequence similarity is due to function, then it need not indicate common ancestry, or the former presence of an egg-laying protein in the human genome --
6. That is, if there is sufficient sequence similarity to make the claim in the first place.
7. Claiming exaptation, à la Venema, is a post hoc argument based on the prior assumption of common descent. It goes like this:
1. There is sequence similarity to vitellogenins in the human genome.
2. It must be due to common descent.
3. There is evidence of another possible function for the sequence.
4. It must have evolved as a secondary function, because we know that it was originally vitellogenin.
8. Claiming a functional reason for the similarity is a creationist dodge.
9. Claiming exaptation sounds like a dodge to me.

Universal common ancestry in the hotseat.

Functional Pseuodogenes and Common Descent

Evolution News & Views 

V.J. Torley and our colleague Cornelius Hunter have continued their discussion about common descent, a subject on which, as John West notes, advocates of intelligent design don't all agree. Airing such disagreements, if done in a respectful and substantive manner, is of course a healthy thing. Writing at Uncommon Descent, Dr. Torley raises an interesting point, directed at Dr. Hunter and citing theistic evolutionist Dennis Venema:

In the comments to one of your posts, you thanked a reader for linking to an article stating that the protein vitellogenin confers several beneficial effects upon bees, in addition to being used to make egg yolks. Humans possess a broken copy of the gene which makes this protein; they no longer need it. So my final question is: why do you not consider this gene to be vestigial -- especially when Dr. Jeffrey Tomkins's claim that the remaining gene [vitellogenin] fragments in human beings are functional has been soundly refuted by Dr. Dennis Venema?

Actually, if you read Venema's response to Tomkins, Venema appears to concede Tomkins's central point that the VIT1 gene could be functional. Here's what Venema writes:

He [Tomkins] argues that the 150 base pair fragment of VIT1 is "not a real pseudogene" but rather regulatory DNA for an unrelated gene -- DNA that functions to direct where and when another gene is transcribed. This gene falls into a class of genes known as "long non-coding RNAs" -- genes that are transcribed into RNA but do not code for proteins. These genes are thought to arise quite easily over the course of evolution, and many are thought to have little or no function (for a good but technical review, see here). Specifically, the VIT1 fragment Tomkins acknowledges sits in an intron of this gene (part of the gene that is spliced out of the RNA copy after it is transcribed from DNA). Tomkins summarizes the evidence -- such as it is -- that suggests this sequence might have a regulatory function. If this fragment is a functional part of an unrelated gene, he argues, it makes sense to understand it as the result of special creation, rather than the evolutionary remnant of a once-functional VIT1 gene in the lineage leading to humans.

Tomkins has presented evidence that the VIT1 pseudogene sits in part of an intron that is transcribed and produces long non-coding RNAs of the type we know often have function. What does Venema say next? Does he contest this evidence for functionality? No. According to Venema the "major problem" with Tomkins's argument isn't the evidence for functionality in the VIT1 pseudogene. Rather, he focuses on critiquing a false dichotomy that Tomkins has supposedly advanced:

The major problem with this argument is that it subscribes to a false dichotomy: that this sequence is either a VIT1 pseudogene fragment or a functional part of another gene. From an evolutionary perspective, there is no issue with it being both. Part of evolutionary theory is the expectation that occasionally some sequences, after losing their original function, may come under natural selection to be repurposed to another function. The technical term for this process is exaptation, and many examples of it are known. Certainly a long, non-coding RNA gene could arise at this location in the human genome and this sequence could be exapted as a regulatory sequence -- but there is no hint of admitting this possibility in Tomkins' work. Once again we are reminded that he is not writing for a scientifically informed audience, but rather for a lay audience that will not know about the possibility of exaptation and expect him to provide evidence that it is not a factor in this situation. Rather, it seems enough to Tomkins to suggest that the sequence is functional -- and that this alone will be enough for him to convince his readership that this fragment is "not a real pseudogene."

Of course Venema is correct that finding function for this pseudogene is no refutation of Darwinian evolution. But his focus on this point distracts from the main issue here. And what's that?

The main issue is that evolutionists havecommonly argued that non-functionality in shared pseudogenes is what provides evidence for common ancestry. They argue that God would not put "broken" shared DNA in multiple speciesand thus this must be evidence for common ancestry over intelligent design (or special creation, or whatever). We've seen many theistic and atheistic evolutionists treat pseudogenes in precisely this manner:

• Richard Dawkins writes that "genomes are littered with nonfunctionalpseudogenes, faulty duplicates of functional genes that do nothing." (Richard Dawkins, A Devil's Chaplain: Reflections on Hope, Lies, Science, and Love (New York: Mariner Books, 2004), 99, emphasis added.)
• Kenneth Miller writes that the "human genome is littered with pseudogenes, gene fragments, 'orphaned' genes, 'junk' DNA, and so many repeated copies ofpointless DNA sequences that it cannot be attributed to anything that resembles intelligent design. " (Kenneth Miller, "Life's Grand Design," Technology Review, 97 (February/March, 1994): 24-32, emphasis added.)
• Francis Collins and Karl Giberson write in The Language of Science and Faith that pseudogenes are "broken," and it is "not remotely plausible" that "God inserted a piece of broken DNA into our genomes." In their view, pseudogenes shared across different species establish "conclusively that the data fits a model of evolution from a common ancestor." (Karl Giberson and Francis Collins, The Language of Science and Faith: Straight Answers to Genuine Questions(InterVarsity Press, 2011), 49, emphasis added.)
• Darrel Falk writes that one "might be tempted suggest that the reason why God put a deletion into the ape lineage is because it would make the gene more ideally suited to carrying out its purposes in apes. That might well have been a valid argument if this was afunctioning gene. However, it is not. The gene has no function. " (Darrel Falk,Coming to Peace with Science (IVP Academic, 2004), 188, emphasis added.)
• Denis Alexander writes: "[O]ur own genomes are loaded with 'pseudogenes,' stretches of DNA that are so similar to functional genes that there is no doubt where they came from, yet so full of mutations that they are functionally incapable of making protein, as can be shown experimentally in the laboratory" (Creation or Evolution, p. 112). He goes on to say that "pseudogenes ... have lost their function" (p. 204), calling them " derelict genetic fossils" (p. 205) or a "dysfunctional gene" (p. 206). He even calls them "nonfunctional genes" (p. 119).
• Even Venema makes a big deal about the idea that pseudogenes are non-functional: "Pseudogenes (literally, 'false genes') are gene sequences that have been inactivated by mutation that persist in the genome as nonfunctionalsequences. ... once inactivated, a pseudogene accumulates mutations only slowly because the proofreading mechanisms that govern DNA replication do not distinguish between functional and nonfunctional DNA sequences." (Emphasis added.)

In fact, in that same article, Venema goes on to say this specifically about the vitellogenin pseudogene. Immediately after calling pseudogenes "nonfunctional," he gives the example of the vitellogenin pseudogene:

The human genome thus contains the mutated remains of a gene devoted to egg yolk formation in egg-laying vertebrates at the precise location predicted by shared synteny derived from common ancestry.

So Venema calls pseudogenes "nonfunctional," gives the "vitellogenin pseudogene" as his primary example, and then goes on to use the supposed nonfunctionality of the vitellogenin pseudogene as evidence against intelligent design and for common ancestry.

He says much the same on BioLogos's website where he uses similar language to say that "pseudogenes are remnants of once-functional genes" and repeatedly calls them "non-functional." (See here and here.) And again he uses the vitellogenin pseudogene as an example, citing "the mutated remains of the vitellogenin gene."

Now Venema argues that the vitellogenin "pseudogene" in humans simply lost its original function and is now being used for a different function. Perhaps, he might argue, even if we are using the vitellogenin "pseudogene" for some function, the fact that we aren't using it to make egg yolk shows that we inherited it from a common ancestor we shared with chickens. This too would be a misguided argument.

First, proteins often have multiple domains that allow a protein to interact with different molecules in different contexts within a cell. At best, the human vitellogenin "pseudogene" only represents a small fraction of the chicken version of the gene. One could initially surmise that the fragment (or fragments) of the vitellogenin "pseudogene" that humans have (and use for some function) may not be the part (or parts) crucial only for making egg yolk in chickens. We may be using it for a non-egg-yolk related function that's also found in chickens.

But in this case, according to Tomkins (2015), the human "vitellogenin pseudogene" seems to be producing a long non-coding RNA (lncRNA), not a protein. LncRNAs are known to have all kinds of functional roles in humans, and are especially known to be involved in gene regulation. In this more likely case, perhaps the chicken vitellogenin gene produces not only egg yolk-related proteins, but also RNAs that haveother roles or functional interactions in chickens. We may be using our "vitellogenin pseudogene" for a similar RNA-based function or interaction that chickens do. For example, perhaps in addition to producing a protein, the chicken vitellogenin gene also produces RNAs with some regulatory role, and humans use our version of the "vitellogenin gene" for some similar RNA-based regulatory role. Indeed, Venema's discussion of the human "vitellogenin gene" seems to admit that something like this could be a possibility.

In either case, our "vitellogenin pseudogene" and the chicken version would turn into a mere example of homologous DNA performing a homologous functions -- something we see all the time in biology and which can be explained by common design just as easily as by common descent. It doesn't appear that the specific function of our "vitellogenin gene" has been explored yet, and this would be an interesting question to investigate. The hypotheses offered here could very well turn out to be true.

But doesn't have to be the case, however, to defeat the vitellogenin argument for common ancestry. That's because, as a second point, even if humans are using our "vitellogenin gene" for entirely different purposes than chickens do, this still doesn't provide evidence for common ancestry. Why? Because we often see in technological designs that similar parts can be used for very different purposes. A plastic ring in one design might be used for blowing bubbles, but in another it helps seal the connections between two pipes. Or a plastic container in an outboard boat motor holds fuel, but in another technological design it holds dishwashing liquid. Using similar parts for different purposes is easily accommodated by common design.

Moreover, when we in biology see this sort of phenomenon -- similar parts performing different functions -- it is usually taken as evidence against common ancestry, not for it, as the textbook Explore Evolution notes:

In another surprising twist, biologists have also discovered many cases in which the same genes help to produce different adult structures. Consider, for instance, the eyes of the squid, the fruit fly, and mouse. The fruit fly has a compound eye, with dozens of separate lenses. The squid and mouse both have single-lens camera eyes, but they develop along very different pathways, and are wired differently from each other. Yet, the same gene is involved in the development of all three of these eyes.

According to neo-Darwinian theory, the development of non-homologous structures should be regulated by non-homologous genes. So, many biologists were taken aback to discover that non-homologous eyes (from an insect, a mollusk, and a vertebrate) could be regulated during their development by homologous genes, like Pax-6. Stephen Jay Gould called this discovery, "...unexpected under usual views of evolution...."

To summarize, biologists have made two discoveries that challenge the argument from anatomical homology. The first is that the development of homologous structures can be governed by different genes and can follow different developmental pathways. The second discovery, conversely, is that sometimes the same gene plays a role in producing different adult structures. Both of these discoveries seem to contradict neo-Darwinian expectations.

(Explore Evolution, Second Edition, pp. 44-45)

Thus, examples where homologous genes perform non-homologous functions are said to provide a conundrum for common ancestry; it would be a mistake to cite similar DNA being used for different purposes as evidence forcommon ancestry.

But this speculation about the function of the human "vitegellenin" gene is an aside, because if we look at the arguments that are actually being made and what we already know to be true, the argument from vitegellenin for common ancestry is defeated. Here is what's really going on:

1. Evolutionists have often claimed that DNA elements like the VIT1 pseudogene are "non-functional."
2. Evolutionists claim that these pseudogenes provide special evidence for evolution because God would not create different species with shared non-functional DNA in the same location. Therefore, they argue, pseudogenes must be evidence for shared ancestry.
3. Tomkins presented evidence that the VIT1 "pseudogene" is indeed functional in humans.
4. Evolutionists responded not by disputing Tomkins's evidence for functionality in the human VIT1 "pseudogene." Rather, they shifted the argument, saying in effect, "Well, common ancestry/evolution isn't refuted simply by finding a function or a pseudogene."

One might reply to point (4) as follows: We never said that functional pseudogenes refute evolution. But functional pseudogenes do in fact refute a central part of a major argument that evolutionists have made against ID and forcommon ancestry. Venema does not seem to contest the evidence that Tomkins cites showing that the vitellogenin "pseudogene" is functional. Although Venema does not explicitly concede the point, by its very nature his argument is one that accepts its functionality.

No, the evidence raised by Tomkins suggesting vitellogenin "pseudogene" functionality in humans poses a major problem for those who make the case that the vitellogenin pseudogene provides compelling evidence for common ancestry. Tomkins's argument has hardly been "soundly refuted" by Venema.

File under "well said" XXVI

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