universal common ancestry in the hotseat IV

The Naked Ape: An Open Letter to BioLogos on the Genetic Evidence, Cont.
Cornelius Hunter

In a previous article I reviewed BioLogos Fellow Dennis Venema's articles (here and here) which claimed that the genomes of different species are what we would expect if they evolved. For instance, allied species have similar genomes, and genetic features fall into evolution's common descent pattern. I argued that this claim is inaccurate and that the scientific evidence tells a very different message.
In a later article Venema focused his claim on the specific case of human evolution, and the similarity between the human and chimpanzee genomes. As before, Venema finds this genetic evidence to be a compelling confirmation of evolution:

The first line of evidence in favor of humans sharing ancestry with other forms of life is straightforward -- there are other species that have a genome that is nearly identical to our own -- the genomes found in great apes such as chimpanzees, gorillas and orangutans. Compared to our "book," the "books" of these species match at the chapter and paragraph level -- all three species have DNA sequences that have the same genes in the same basic order as we do. There are subtle differences, of course -- blocks of sequence that have been rearranged through breakage and rejoining of chromosomes, as expected -- but the overall pattern is clear.
...
Taken together, what we observe when comparing the overall structure of the human genome to other primates is that (a) our genomes do indeed have the features one would predict them to have if they are copies of a shared ancestral genome, and (b) the differences we do observe are easily accounted for by well-known mechanisms. These observations strongly support the hypothesis that our species arose through an evolutionary process.

It does not seem that the evidence supports evolutionary theory as Venema concludes. In fact, there appear to be several significant problems with this claim, as I will explain.
First, as we saw in my previous article, the genetic data from the different species do not fall into the expected evolutionary pattern. Here Venema focuses on the high genetic similarity between the primates, claiming it confirms evolution. But if this is what is required to confirm evolutionary relationships, then the substantial genetic differences that are so often found between otherwise similar species must falsify evolutionary relationships in those cases.
But evolutionists have never entertained any such doubts. Those evolutionary relationships are intact, according to evolutionists, and this suggests that the high similarity between the primate genomes never was required for evolutionists to believe they evolved from a common ancestor.
So it appears that Venema's claim, that the high genetic similarity between the primates confirms their evolutionary relationship, is more of an "after the fact" claim rather than a confirmation of a genuine evolutionary prediction. In fact, given the substantial morphological differences between humans and the other primates, evolutionists had indeed expected greater genetic differences:

The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small.

So it does not appear that the high similarity between the chimp and human genomes was predicted by evolution, or is required by evolution. Beyond that, given the high similarity between the chimp and human genomes, there are many inconsistencies with evolution, as we shall see next.
The Gorilla Genome Is Strangely Similar to Both the Chimp and Human Genomes
When the human and chimpanzee genomes were compared a few years ago, the human genes showed some surprising differences in a few places, such as in genes thought to be related to hearing. Evolutionists called it "accelerated" evolution and they said that it was due to the development of human language. However it turns out that the gorilla genome has a similar pattern. And that doesn't make sense since gorillas don't have our advanced verbal skills:

Much of the 15% is in sections of the genome that do not code for proteins. But the researchers also looked at functional gene changes. They found that certain genes -- including some involved in hearing and brain development -- had gone through more rapid changes than expected in both the gorilla and human lineage. Some of these rapid changes are puzzling: the gene LOXHD1 is involved in hearing in humans and was therefore thought to be involved in speech, but the gene shows just as much accelerated evolution in the gorilla. "But we know gorillas don't talk to each other--if they do they're managing to keep it secret," says [lead author] Scally.

So now evolutionists are calling it "parallel accelerated" evolution, because the same accelerated evolution, by random mutation, must have happened independently, in the human and gorilla genomes. But why would the same "accelerated evolution" occur in the gorilla? It wasn't developing human language. Perhaps there is some other reason, but why then wouldn't that "accelerated evolution" occur in the chimpanzee? It doesn't make sense with evolution, for we must say that random mutations just happened to create the same pattern twice.
The gorilla genome also shows similarities to the chimp genome, including duplications that are not present in the other primates. Evolutionists say these various chimp-gorilla similarities were coincidences, occurring repeatedly by chance in the two different species:

We show that both the gorilla and chimpanzee genomes have experienced independent yet convergent patterns of structural mutation that have not occurred in humans, including the formation of subtelomeric heterochromatic caps, the hyperexpansion of segmental duplications, and bursts of retroviral integrations.

These events must have occurred independently and in parallel.
Viruses
Human uniqueness is expansive. Relative brain size, hairless sweaty skin, striding bipedal posture, long-distance running, ability to learn to swim, innate ability to learn languages in childhood, prolonged helplessness of the young, ability to imitate and learn, inter-generational transfer of complex cultures, awareness of self and of the past and future, theory of mind, increased longevity, provisioning by post-menopausal females, difficult childbirth, and cerebral cortical asymmetry are just a few from a long list of features that make humans exceptional.
Another such unique feature is at the genome level: the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolution these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well. Therefore this lack of endemic infectious retroviruses in humans is inconsistent with evolution:

Other than the recent introductions of HIV and human T leukaemia virus (HTLV) into humans from other animals, humans seem to be devoid of species-wide endemic infectious retroviruses. By contrast, like most other mammals studied, other hominids and non-human primates (NHPs) do have such viruses. Indeed, given the remarkable corroboration between the phylogenetic trees of primates and their lineage-specific simian foamy viruses (SFVs) our common ancestors with other hominids almost certainly had SFVs. The same is probably true of the lineage-specific simian infectious retroviruses (SIVs) found in most NHPs. Assuming that the common ancestors of hominids carried multiple endemic infectious retroviruses, how did the human lineage eliminate them? Given that humans remain susceptible to re-infection with both SFVs and SIVs from other hominids, this seems unlikely to be explained solely on the basis of more efficient host restriction systems. Rather, there seems to have been an episode in which the ancestral human lineage was somehow 'purged' of these endemic viruses.

In other words, the endemic infectious retroviruses do not align with the expected evolutionary pattern. The human lineage must, somehow, have been purged of these endemic viruses. Perhaps such a purging occurred, and future research may be able to strengthen that hypothesis. But as it stands, this evidence is not consistent with evolution.
Chimp-Human Genome Beneficial Differences Are Few
As noted above, evolutionists were surprised by the high similarity between the chimp and human genomes. With so few differences, how could evolution construct such tremendous differences? But not only is evolution limited to a relatively few genetic modifications to create the human, but according to evolution the majority of even those modifications would likely have had little or no consequence or even would have been slightly harmful. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles.

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to "neutral and slightly deleterious alleles." So not only are evolution's random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to "neutral and slightly deleterious alleles."
In fact the beneficial mutations in protein-coding genes, which presumably would be important in evolving the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.
Chimp-Human Genome Differences Have Discrepancies
Furthermore, the chimp-human genome differences show some strange patterns, with unexplainable variation towards the ends of most chromosomes, and with the chromosomal banding patterns.
A common response from evolutionists is that these discrepancies are small in magnitude. That is true, they are small in magnitude. But that is not what counts. Molecular spectra that make magnetic resonance imaging (MRI) possible are also small in magnitude. That doesn't mean they don't count. What is important is that the chimp-human genome differences show patterns that evolutionary theory struggles to account for. The evidence is not consistent with the theory, by a wide margin.
The chimp-human genome differences have also been described using sliding 1-Mb windows. Those results also showed nonrandom variations, but later research found that those variations correlate with the observed de novo human mutation rate patterns. The research paper concluded that the variation in chimp-human genome differences "is only partly explained" by the mutation rate patterns. But these results raise the specter that the variations in the chimp-human genome differences seen in 1-Mb windows may be explainable by a known phenomenon.
This suggests the possibility that future research may also explain the variation towards the ends of chromosomes, and with the chromosomal banding patterns. But that was not the claim. Evolutionists such as Venema claim that today's evidences "strongly support the hypothesis that our species arose through an evolutionary process."
Chimp-Human Alternate Splicing Differences
You may have learned in your high school biology class that genes are segments of DNA, but it is a bit more complicated than that. For starters, in the higher species a gene is often not a simple continuous segment of DNA but rather is interrupted several times by intervening segments. So there are the coding segments (called exons for expressed regions) and then there are the intervening segments (called introns for intervening regions).
When a gene is transcribed, the transcript contains both the exons and introns. It is then spliced by a complicated spliceosome machine that removes the introns from the gene copy and glues the exons together.
One of the features of the exon/intron genetic architecture is that it allows for alternative splicing schemes. In fact, incredibly, a given gene can have thousands of different forms depending on how the spliceosome machine edits the gene.
When it was discovered that the human genome contained about twenty five thousand genes it seemed too few. Are not more genes required for a human body? More recently it has been discovered that we make up for that small number of genes with alternative splicing schemes. Most of our genes may undergo such editing, and the result can be a completely different function for the resulting protein.
We have an enormous alternative splicing program in our cells, far more than chimps have. And this is another inconsistency with evolutionary theory.
Given the high similarity between the chimp and human genomes, and the relatively few beneficial mutations in protein-coding genes (discussed above), evolutionists have considered the possibility of evolution by splicing. In other words, our enormous alternative splicing program may have been an important factor in our evolving from a small, primitive ape.
But there are many thousands of these gene-splicing changes that would have to evolve. And unlike bacteria whose populations are large and generation times are short, our gene splicing changes would have to evolve in smaller populations with longer generation times.
It is difficult to see how evolution would have the resources to make this happen. The problem quickly becomes astronomically improbable if groups of genes would need to implement their new splicing logic together. And how could that not be the case?
In fact, even if only the order of implementing splicing for a small number of genes is important, the problem quickly becomes astronomically improbable. And again, how could that not be the case?
But this is only the beginning. In addition to the fact that the evolution of our enormous gene splicing changes is unlikely, it also represents an enormous serendipity problem. We would have to say that random mutations constructed complicated genes, with exons and introns and splicing codes, and the incredible splicing machinery, which, it would just so happen, would luckily be just what was needed to evolve humans.
It is even worse than this when one considers the exons themselves. Those random mutations would have divided the genetic instructions into so many exons, and it just so happened that they would be the right building blocks that, when rearranged, would lead to humans. The serendipity is astronomical here.
Imagine if you were building a tricycle and your friend modified each part you had crafted (not adding anything), and now the parts fit together to construct the space shuttle rocket motor.
The Kangaroo-Human Genomes
In my previous article I explained that, in addition to striking differences in otherwise allied species, striking similarities in otherwise distant species are also inconsistent with evolution. This problem arises also with the human genome. Consider the kangaroo genome, which turned out to be similar to the human genome. As one evolutionist explained:

There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. Which really surprised us, we thought they'd be completely scrambled, but they're not, there's great chunks of the human genome which is sitting right there in the kangaroo genome.

It was a surprise because under evolution humans and kangaroos must be quite distant relatives. Evolutionists believe a small mouse-like species split into two lineages -- the marsupials and the placentals -- about 150 million years ago. And according to evolutionists that mouse-like species eventually evolved by random mutations into, among other things, a kangaroo in the one lineage and into a human in the other. With that much evolutionary distance the kangaroo and human genomes should have evolved substantial differences.
Conclusion
The genomes of primates do not support evolutionary theory. As we have discussed, there are always speculations for whatever evidence is discovered. Perhaps evolution did this, perhaps it did that. But that does not change the fact that the primate genomes do not "strongly support the hypothesis that our species arose through an evolutionary process," as Venema and fellow evolutionists claim. There are a wide variety of substantial contradictions and problems with this theory.

A clash of Titans XIX

File under "Well said" XXVII

A man should be upright, not be kept upright. 
Marcus Aurelius

Neanderthals continue to prove more human than convenient for Darwinists.

Neanderthals Built Mysterious Stone Circles

Rings of stalagmites found in a cave in France suggest that our ancient relatives were surprisingly skilled builders.

By Nadia Drake

Once illuminated by the flickering fires of prehistoric builders, an array of mysterious stone circles hid in darkness for millennia, tucked into the recesses of a cave in France. Now, these ancient structures are again emerging from the shadows.

The strange rings are crafted from stalagmites and are roughly 176,000 years old, scientists report today in Nature. And if the rings were built by a bipedal species, as archaeologists suspect, then they could only be the work of Neanderthals, ancient human relatives that are proving to be much more “human” than anticipated.

“This discovery provides clear evidence that Neanderthals had fully human capabilities in the planning and the construction of ‘stone’ structures, and that some of them penetrated deep into caves, where artificial lighting would have been essential,” says paleoanthropologist Chris Stringer of the Natural History Museum in London.

However, why Neanderthals ventured deep into the darkness and constructed such elaborate structures is an enigma, at least for now.

Time Capsule

Sealed since the Pleistocene, Bruniquel Cave is located in southwest France, in a region littered with decorated caves and other Paleolithic sites. In 1990, spelunkers excavated its entrance and squeezed through, finding signs of long-vanished cave bears and other extinct megafauna just inside.

But the cave’s real treasure lay in a damp chamber more than 1,000 feet (330 meters) from the entrance. There, several large, layered ring-like structures protruded from the cave floor, the seemingly unmistakable craftwork of builders with a purpose.

“All visitors have noticed the presence of these structures, from the first speleologists,” says Jacques Jaubert of the University of Bordeaux, a coauthor of the study describing the finding.

It would take decades for scientists to begin deciphering the enigmatic circles, an endeavor slowed by restricted access to the cave and the untimely death of the archaeologist who began work on the site in the 1990s.

In 2013, Jaubert and his team were finally able to bring Bruniquel’s secrets into the light.

“The cave was very well preserved, with very few visits, almost none,” he says, noting that the site is on private property and is regulated by the French government. “The structures are spectacular and have virtually no equivalent for that period, and even for more recent periods.”

Stony Mysteries

The mysterious structures are built from nearly 400 stalagmites—the cone-shaped rock formations that rise from cave floors as dripping, mineral-rich water accumulates over time.

Hewn to roughly the same length, some of the stalagmites were crafted into a large circular structure measuring nearly 22 feet (6.7 meters) across. Others were aligned in a smaller semicircle, and the rest were stacked in heaps.

Cracked areas of red and black discoloration indicate that fires had been lit atop the stalagmites, and charred bits of bone, including the burnt bone of a bear or large herbivore, were found near the smaller circle.

Even to a trained eye, the scene looked like it could be the work of early modern humans, who first appeared in Europe about 40,000 years ago. But uranium dating of the stalagmites, as well as dates for a mineral cloak that had grown over them and the bone bits, revealed an age the team didn’t expect.

At around 176,000 years old, the structures vastly predate the arrival of Homo sapiens, not just by a smidge, but by more than 100,000 years.

“These must have been made by early Neanderthals, the only known human inhabitants of Europe at this time.” Stringer says.

Neanderthal Behavior

Neanderthals thrived for 300,000 years, coexisting with and occasionally breeding with modern humans. Like us, they were big-brained and clever, with a mastery of fire. But scientists argue about how similar the two species really were, and debate whether Neanderthals were capable of symbolic thought and ritual behaviors.

Unlike us, Neanderthals didn’t survive, and the reasons why they vanished from the landscape some 30,000 to 40,000 years ago are still a source of contention.

Until now, anthropologists had thought it unlikely that Neanderthals had mastered the art of subterranean living, which is a bit trickier than traipsing around above ground. The Bruniquel cave could prove otherwise.

“The find is solid, and it is an important documentation of the advanced behaviors of the Neanderthals,” says paleoanthropologist Erik Trinkaus of Washington University in St. Louis.

To craft those enormous stone rings, Jaubert and his colleagues argue, the cave’s occupants needed a reliable source of illumination, some kind of social organization, and the ability to conceive of and construct the patterns, which are made from more than two tons of stalagmites.

“This requires the mobilization of people who choose, who lead, who advise, manufacture—and with continuous light,” he says. “All this indicates a structured society.”

Clan or Cave Bears?

That’s one interpretation, but some scientists say it’s too soon to draw these kinds of conclusions about the site. To begin with, it’s not yet clear how widespread such complex behavior may have been among Neanderthals, or if the structures were built by one person or many.

“We don’t know how many people were involved, if the structures were done in one event or during several events, by one person or by several,” says anthropologist Marie Soressi of Leiden University. “I don’t know what to expect, because such a discovery is very unusual.”

Other scientists question the presumed human origin for the structures and instead suggest they could be the work of hibernating cave bears.

“Who in their right minds builds structures 300 meters underground inside of a cave? Seeking refuge in a cave is a way of avoiding having to make an artificial structure,” says paleoanthropologist John Shea of Stony Brook University. “When bears settle in for the winter hibernation, they push all kinds of litter to the side. This looks like a place where cave bears settled in for a nice nap over and over through time.”

But bear dens are generally smaller than the largest ring, Soressi says, and the animals don’t stack stalagmites so much as excavate hollows and brush things aside. Plus, Jaubert notes, “bears do not make fire.”

Subterranean Secrets

If the structures are indeed the work of Neanderthals and not cave bears, their purpose is still a mystery. No one knows what the Neanderthals might have been doing in that cave, or how long they used it. Jaubert and his colleagues refuse to speculate about the structures’ purpose until further work at the site tells more of the story.

In the meantime, it’s hard to resist wondering what our ancient relatives were doing deep inside that cavern, with their fire-lit rings of stone.

“The complex Bruniquel structures are well-dated to within a long cold glacial stage, and at that time the cave might have provided a temporary, more temperate refuge,” Stringer says.

“If there is still-buried debris from occupation, it would help us to determine whether this was a functional refuge or shelter, perhaps roofed using wood and skins, or something which had more symbolic or ritual significance.”

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.