Biological variation is, in part, transmitted from parent to progeny. Tall individuals tend to have tall offspring, fast individuals tend to have fast offspring, and so forth. This transmission process is key to the action of natural selection. Those trait variations that are successful in transmitting themselves to the next generation, by definition, survived while those that failed would disappear from the population. So long as traits are transmitted, evolutionists argue that natural selection is inevitable.

In other words, whatever it is that determines your traits is also transmitted to your offspring. Therefore, if you have evolutionarily successful traits then you will have more offspring, and they will receive your successful traits.

But how are the traits defined and transmitted? Darwin didn’t quite know how but in the twentieth century it seemed obvious—via the genes. According to the merger of modern genetics and evolution, it was all in the genes. They determined your traits and they were passed on to your offspring. This view fit evolutionary theory and was quickly accepted as an unquestionable scientific fact.

There is only one problem: it is false.

The fact that our genes are practically identical with the chimpanzees genes should have been a sign to evolutionists that their gene-centric view was problematic. How could the chimp and human be so different if their genes are so similar? Nonetheless, evolutionists proclaimed the great similarity as evidence that there must be an evolutionary relationship between humans and chimps.

In fact the biological evidence is clear: genes are only part of a far more complicated story than what evolution envisioned. As Stuart Newman explains:

Genes, which are composed of DNA, directly specify the sequences of RNA molecules and indirectly, the amino acid sequences of proteins. Before there were multicellular forms, single-celled organisms evolved for as much as two billion years driven, in part, by genetic change, as well as by establishment of persistent symbiotic relationships among simpler cells. During this entire period no cellular structure or function was specified exclusively by a cell’s genes. The protein and RNA molecules produced by cells associate with each other in a context-dependent fashion or, in many cases, catalyze chemical reactions (generating lipids, polysaccharides and other molecules), whose rates depend on the temperature and composition of the external environment. So the population of molecules inside the cell can vary extensively even if the genes do not.

It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true—the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous influence over their functions.

The deployment of information in the genes, moreover, is itself dependent on the presence of certain RNA and protein molecules in the cell. Since, as described above, the composition of the cell’s interior and the activity of many of its proteins depend on more than just the genes, the portion of the genes’ information content that is actually used by the cell is determined, in part, by non-genetic factors. So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent.

As Newman explains, the gene is nothing close to how evolution envisioned it. The gene myth is yet another example of evolution’s failed expectations. It seems that inevitably evolution’s interpretations turn out to be wrong as it has produced a steady stream of false predictions. Evolution is certainly the best counter indicator in the life sciences.

We continue to examine the work of authors George Johnson and Jonathan Losos in their biology textbook, The Living World ((Fifth Edition, McGraw Hill, 2008). In their chapter on evolution and natural selection, these accomplished evolutionists begin by (1) misrepresenting the relationship between microevolution and macroevolution and biological variation here, (2) making a non scientific, metaphysical, truth claim that mandates the truth of evolution here, (3) making the false statement that the fossils themselves are a factual observation that macroevolution has occurred here and here, and (4) making a series of misrepresentations by carefully selecting the evidence to provide to the student and protecting it with circular reasoning here.

Johnson and Losos’ next move is to distort the molecular evidence. They write:

A series of evolutionary changes thus implies a continual accumulation of genetic changes in the DNA. From this you can see that evolutionary theory makes a clear prediction: organisms that are more distantly related should have accumulated a greater number of evolutionary differences than two species that are more closely related.

But how are species judged to be “distantly related”? By what measure are species compared? The answer, of course, is by the similarities and differences in their visible anatomy. So what exactly is this powerful evolutionary prediction? It is that genetic differences between species are proportional to the differences in their visible anatomy. If two species look alike, then their genomes should be similar. If they look very different, then their genomes should be very different. This is by no means a heroic prediction.

There is, however, another problem with this prediction. Aside from not being heroic, it is false. By now the authors have established a trend of misrepresentation and distortion, and predictably the trend continues:

This prediction is now subject to direct test. Recent DNA research, referred to in section 15.3, allows us to directly compare the genomes of different organisms. The result is clear: for a broad array of vertebrates, the more distantly related two organisms are, the greater their genomic difference.

Here the distortion is mainly one of omission. Like saying that geocentrism’s prediction that the planets should travel across the sky is true without mentioning retrograde motion, Johnson and Losos fail to mention important deviations from this pattern that have even evolutionists acknowledging the evolutionary expectation has failed.

Yes, there is a broad pattern of correlation between visible anatomy and molecular sequences, but there are inescapable and significant deviations which are far outside evolution’s “noise” level. If evolution predicts that “organisms that are more distantly related should have accumulated a greater number of evolutionary differences than two species that are more closely related” then evolution is false, end of story.

The authors next discuss the protein evidence, and in like manner continue their distortion:

This same pattern of divergence can be clearly seen at the protein level. Comparing the hemoglobin amino acid sequence of different species with the human sequence in figure 17.7, you can see that species more closely related to humans have fewer differences in the amino acid structure of their hemoglobin. … Again, the prediction of evolutionary theory is strongly confirmed.

Again, this prediction is not only not “strongly confirmed,” it is in fact false. Yes, hemoglobin and many other proteins fall into the non heroic pattern, but other proteins do not. These are well known to scientists, but evolution has unfortunately compromised science.

Johnson and Losos end this misleading section on the molecular evidence for evolution with yet another fallacious icon of evolution, the molecular clock.

In science theory evaluation is a critical skill. It is crucial to take a neutral, unbiased perspective and be willing to acknowledge both pros and cons of even one’s cherished theories. Unfortunately evolutionists don’t follow this scientific dictum. Yes there is plenty of evidence for evolution, but there are problems as well. But one would never know it from reading the evolution genre. Don’t count on evolutionists to give a scientifically accurate evaluation of their theory. Religion drives science, and it matters.

You probably learned in high school biology class that the new DNA data has powerfully confirmed evolution. Take any gene and it reveals differences between the species exactly as we would expect. And this sentiment is not limited to high school textbooks. As the Chair of a university Biology department once wrote to me, “DNA sequences provide an absolute and irrefutable record” that evolution is a fact. “Virtually every single gene sequence we examine,” he explained, “can be seen to be represented in closely related species and in more distantly related species with increasing numbers of nucleotide changes as we look at more distant species.” It was, he concluded, “absolute proof, in hard copy, reiterated in every single gene of every single organism.” That is an unfortunately common misrepresentation of the data but the story doesn’t end there. The DNA evidence has falsified several other evolutionary predictions.

Vast stretches of identical DNA segments are found in distant species. Multitudes of differences are found in the DNA of cousin species. Retroviruses that were so often considered to be junk now must be viewed crucial to evolutionary history if Darwin was right. These are some obvious surprises that DNA offered up to evolutionists, but there are more subtle contradictions. One of them, which shows up repeatedly, is the way DNA interacts with proteins.

Consider a recent study of how transcription factor binding is not conserved between mice and men. Transcription factors are proteins that bind to DNA and influence which genes are expressed (transcribed). You may recall that proteins are created by first transcribing genes. So in this complex regulatory network, genes are transcribed to create transcription factor which then return to regulate gene expression.

Evolutionists believe their theory is crucial to biology. Nothing in biology makes sense, they say, except in the light of evolution. We know what questions to ask and where to look only because we have Darwin’s powerful ideas guiding and motivating our research. But transcription factors in the mouse and human do not follow the evolutionary pattern.

Not only do these transcription factors often bind to retrovirus sections of DNA—which evolutionists so often considered to be nothing more than worthless junk—they also usually do not bind in the same DNA locations in spite of their importance. As one commentary explained:

Remarkably, they find that the genomic locations of binding sites for two key regulatory proteins (OCT4 and NANOG) are poorly conserved across species, despite their functional importance in mammalian embryonic stem cell biology. […]

Unexpectedly, only ~5% of binding sites for the two transcription factors OCT4 and NANOG were found in orthologous positions in human and mouse ES cells, suggesting major differences in genome-wide binding profiles between species.

And the story becomes even more contradictory with many of the binding sites were found in non conserved junk DNA:

Remarkably, many of these RABS [repeat-associated binding sites] were found in lineage-specific repeat elements that are absent in the comparison species, suggesting that large numbers of binding sites arose more recently in evolution and may have rewired the regulatory architecture in embryonic stem cells on a substantial scale.

Furthermore, even those genes with conserved transcription factor binding often revealed more detailed differences in the particular binding location:

However, among genes whose OCT4 dependence was conserved between human and mouse, most of the OCT4 binding sites identified were not directly conserved. Instead, the disappearance of a binding site in one species was compensated for by the emergence of a new binding site for the same transcription factor nearby.

The commentary concludes that these findings are consistent with other recent lineage-specific findings:

The notion that some regulatory networks have substantially changed in evolution is also supported by recent independent observations of lineage-specific network rewiring in vertebrate preimplantation embryos and adult liver tissue.

Of course there have been no observations of "network rewiring," lineage-specific or otherwise. This is yet another unfortunate misrepresentation of science. Yes, the new findings are consistent with other recent findings that species differ in subtle yet dramatic ways. But none of this was expected by evolutionary theory. As the paper explains:

Together, these results suggest that many genes have been rewired into the core regulatory network of human embryonic stem cells following the insertion of transposable elements.

So species-specific studies are required:

In contrast, OCT4 and NANOG have very different binding profiles in human and mouse embryonic stem cells, with only ~5% of their sites being homologously occupied. The fact that there is also a limited concordance between regions experimentally observed to be bound and conserved elements, as determined from multispecies sequence alignments, implies that in vivo maps in the relevant species will be important in the study of many mammalian systems. Moreover, to help explain the vast occupancy differences, we showed that species-specific transposable elements have been an important source of new sites in both species.

In other words, evolution doesn’t help explain the findings. What is remarkable is how evolutionists are able to fit even contradictory evidence into their thinking:

we were also able to identify a group of human-specific target genes that show evidence of having been added to the core regulatory network of human embryonic stem cells via the insertion of transposable elements. Although we do not expect all binding events to directly influence gene expression, this data adds important support to a seminal hypothesis on the impact of repeats on the evolution of transcription regulation.

A seminal hypothesis? That is how evolutionists describe unfounded speculation that invokes serendipity to explain unexpected findings.

Genes added to the core regulatory network via the insertion of transposable elements? This is a remarkable example of how evolution has compromised both science and the peer review process. They conclude:

Our results reveal the striking plasticity of the core regulatory network of mammalian embryonic stem cells and the importance that transposable elements have had in facilitating this functional turnover.

This is what happens when evolution is mandated as true. Religion drives science and it matters.

In its never ending tales of serendipity, evolutionary theory now exalts the once lowly virus as crucial to the evolutionary process itself. It seems that those pockmarked sequences of ancient retroviruses tend to show up in important DNA binding sites where regulatory proteins perch and control which genes are expressed. As one science writer explained:

Surprisingly, the infected hosts and their primate descendants also appear to have benefited from this genetic invasion, new evidence suggests. The ancient retroviruses … helped a gene called p53 become an important “master gene regulator” in primates, …

The advent of gene regulatory networks allowed for greater control over gene expression in higher vertebrates. With tightly controlled variations in gene expression, species that had very similar genetic codes—for instance, humans and chimpanzees—could nevertheless exhibit striking differences.

Amazing how viruses can help create humans. We must be living in the right universe. The tale continues:

Scientists have long wondered how a master regulator such as p53 gained the ability to turn on and off a broad range of other genes related to cell division, DNA repair, and programmed cell death. How did p53 build its complex and powerful empire, so to speak?

Using the tools of computational genomics, the UCSC team gathered compelling evidence that retroviruses helped out. ERVs jumped into new positions throughout the human genome and spread numerous copies of repetitive DNA sequences that allowed p53 to regulate many other genes, the team contends.

Compelling evidence that viruses allowed p53 to regulate many other genes? Of course there is no such compelling evidence. The findings revealed that p53 binding sites sometimes fall within the ancient virus sequences. But for the evolutionary faithful this has profound, if idiotic, implications.

"This would have provided a mechanism to quickly establish a gene regulatory network in a very short evolutionary time frame," said Ting Wang, a post-doctoral researcher at UCSC and lead author of the paper.

Thus, p53 was crowned "guardian of the genome," as biologists now call it. …

Moreover, the team has proposed a new mechanism for evolutionary change. Conventional wisdom says that evolution is driven by small changes--point mutations--to the genetic code. If a change is beneficial, the mutation is passed onto future generations.

Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression. If such a change in gene regulation is beneficial, it is passed onto future generations.

You cannot make this stuff up. Retroviruses insert DNA sequences and bingo, new amazing designs rapidly appear. It all happens automagically. Junk religion breeds junk science.

One of reasons evolutionists find their theory to be so compelling is the so-called “shared error” evidence. Designs that are shared between species are evidence for evolution, but junk that is shared between species are veritable proofs for evolution. This evolutionary interpretation of shared junk is yet another example the religious foundation of evolutionary thought. We might say it is another example of evolution’s junk religion.

Similarities between species are evidence for evolution, but the evidence is decidedly mixed. While there are similarities that support the evolution expectation, there are others that contradict the pattern. But erroneous similarities are particularly persuasive for evolutionists.

For example broken genes, referred to as pseudogenes, are sometimes found to be disabled by identical mutations in cousin species. As evolutionist Jerry Coyne concludes in his book Why Evolution is True, “Only evolution and common ancestry can explain these facts.” [68]

That of course is the sort of non scientific, metaphysical, IF-AND-ONLY-IF claim which is fundamental to evolution. Coyne summarizes this important finding:

But if you believe that primates and guinea pigs were specially created, these facts don't make sense. Why would a creator put a pathway for making vitamin C in all these species, and then inactivate it? Wouldn’t it be easier simply to omit the whole pathway from the beginning? Why would the same inactivating mutation be present in all primates, and a different one in guinea pigs? Why would the sequences of the dead gene exactly mirror the pattern of resemblance predicted from the known ancestry of these species? And why do humans have thousands of pseudogenes in the first place? [69]

Should we laugh or cry? The evolution genre is loaded with such trash posing as science, yet I am still struck by the astonishing banality of evolutionary thought.

Of course Coyne omits the scientific details. He omits the findings of non randomness of mutations. And he omits the examples of pseudogenes that don’t fit the pattern, which require even evolutionists to admit to convergent mutations. He omits the fact that evolution fails to explain how the protein synthesis machine, including the genes, arose in the first place.

But can these omissions be at all serious when Coyne and the evolutionists know evolution must be true? After all, they know what a creator would and would not do, and obviously said creator would not have created these pseudogene patterns. Indeed, he wouldn’t have created pseudogenes at all. The evolutionist’s anti intellectualism is exceeded only by his certainty.

The fact that evolution struggles with the evidence is of little consequence—it is true by virtue of creation being false. So what if pseudogenes do not always cooperate. Elliot Sober calls this Darwin’s Principle.

This naïve and facile dorm room argument reveals the astonishing level of anti intellectualism at the heart of evolutionary thought. It is the junk religion behind the junk science. Religion drives science, and it matters.

Evolution was claimed to be an undeniable fact in the nineteenth century so today new proofs hardly seem necessary. But science continues to offer them up, say evolutionists, as we probe the depths of biology. These days a common source of such proofs is the genomic data which exploded onto the scene in recent decades. But are the new data really undeniable confirmations of Enlightenment speculation or are the new data merely interpreted according to the same old metaphysics?

The genomic revolution has taught us that genomes contain far more than an inventory of genes. Included is a genomic cast of characters, including viruses, pseudogenes, and LINEs and SINEs (long and short interspersed elements, respectively), to name a few. Evolutionists were quick to find that such intruders were not only useless junk but in accordance with common descent—they appear in the same genetic location in cousin species. Such evidence, according to evolutionists, proved their theory yet again, and once and for all.

The molecular revolution was providing the usual evidence of dysteleology, but it was coupled with commonality across species. The so-called shared error evidence, like identical typos in homework assignments from different students, provided the ultimate proof text of a common source. There could no longer be any doubt, evolution was mandated by the evidence.

Evidential Problems

Indeed there is much evidence here that supports evolution. But there are problems as well. Occasionally, for instance, this genomic junk does not align with the pattern required by common descent but instead mysteriously appears where it shouldn’t (such as in distant species rather than close cousins) or is absent from where it should be (such as in a particular species among many).

Such anomalies can be explained by various mechanisms. Perhaps junk occasionally goes missing because it failed to become fixed in the population, though it succeeded in cousin species. Or perhaps DNA repair processes sometimes erase the junk repeatedly and independently in cousin species. Or perhaps insertion site preferences cause the same pattern to appear in distant species.

Aside from speculation, we don’t know how evolution created such mechanisms. But given their existence and utility in explaining anomalous patterns, this means that evolutionists can explain a wide variety of patterns. And that means the particular pattern we do observe is less compelling evidence for evolution.

The Finding of Function and Theory-Dependent Interpretations of Evidence

Another problem altogether is the failure of the evolutionary expectation (and triumphant proclamation) that these genomic intruders are nothing more than junk. In fact this so-called junk has occasionally been discovered to perform various functions, such as in embryonic development and gene regulation. Indeed evolutionists have had to conclude that this junk actually played an important role in, yes, evolution itself.

But if you already believe that all of biology just happened to arise by itself, then it is hardly a challenge to believe that retro viruses and the like could have serendipitously played important roles in the narrative. Philosophers refer to this as theory-dependent observations. The evolutionist’s credulous interpretation is a consequence of the fact that they are evolutionists to begin with.

From a theory-neutral perspective these functions cast a long shadow on evolution. Are we simply and automatically to believe that evolution just happened to create retro viruses which then, in turn, just happened to play crucial roles in the evolution of the species?

The Religion in Evolution

Given these conundrums one might think evolutionists would go easy on these evidences. There certainly is plenty of supporting evidence, but there are complicating questions. The complicating questions, however, have to do with the details of evolutionary history. How could this happen and how could that happen?

Those are merely the details of evolutionary theory, and evolutionary theory never was motivated by the liklihood of evolution. Evolutionary theory is, and always has been, motivated by the mandate for naturalistic explanation. As so many Christians have argued, naturalism is required for both philosophy and theology. Both man and god need a natural history, for anything less is bad science and bad religion.

In this case, it is obvious that god never would have designed or created pseudogenes, viruses and the rest of the genomic malcontents. We would have to believe, as Ken Miller explains, that the designer made serious errors, wasting millions of bases of DNA on a blueprint full of junk and scribbles. As Elliot Sober has pointed out, this is the Darwinian principle—it is not that the probability of the evidence is so high on evolution, but that it is so low on creation.

Whether the pattern always fits, or whether unlikely functions are discovered, is altogether irrelevant. Yes, they reduce the probability of the evidence on evolution, but so what? What’s the difference between 0.1/0 and 0.01/0? Either way evolution wins.

This is evolutionary thinking. Darwin and evolutionists before and after, evaluate the evidence on creation and find it wanting. Furthermore naturalistic explanation is necessary for good science. Evolutionary theory is unlikely, but necessarily true, for the alternatives are both false and not allowed anyway.

Yes there is evidence for evolution in the genome. It is complicated but any objective analysis would tally points for Darwin. But those points would have to be compared to the many other evidences, both for and against the theory. The problematic evidences are formidable and evolution would not emerge unscathed. The genomic evidence in particular, and the totality of evidence in general, do not bode well for evolution, whichever version one favors. The idea from Kent certainly would not qualify for anything close to the status of fact. Unless, that is, the idea had to be true. Religion drives science and it matters.

You may have been taught in your high school biology class that DNA point mutations provide the raw material for evolution. Such mutations can cause biological variation which might lead to improved reproductive rates. In those cases such mutations would likely be selected, and evolution would have taken yet another small step. You may have wondered how such unguided point mutations could ever produce the wonders we find in biology. The answer, evolutionists will tell you, is that point mutations are only the beginning of the story. In fact there are a variety of mechanisms, many far more complex than a DNA point mutation, that can produce biological variation. For instance, new research has found that so-called jumping genes, or transposons, provide for even more biological variation than previously thought. As one evolutionist remarked, “This movement of genetic material provides the raw material of genetic evolution.” There’s only one problem: transposons aren’t free.

The advantage of DNA point mutations is they are simple. Given some organic compounds in a warm little pond, and of course the all important sunlight that makes evolution possible, and some sort of reproduction cycle, and … . Well the story does become far-fetched rather quickly, but if you will go with me this far, it is not too heroic to imagine the occurrence of point mutations, of some sort. In other words, point mutations are conceivably free. They just happen, courtesy of nature and the available ingredients that are lying around.

Not so for the many more sophisticated mechanisms in biology that produce variation and are claimed as evolutionary fuel. Consider the retrotransposons that, in addition to its promoter sequence that helps initiate the copying of its DNA into an single-stranded RNA molecule, carries its own handy reverse transcriptase gene which encodes the protein machine that copies the RNA back into a DNA molecule, for later insertion into the genome. This can certainly cause biological variation, but it is anything but free.

With evolution we must believe that so many of the sophisticated biological variation mechanisms, such as in retrotransposons, were produced by evolution. Do you see the problem? In this circular tale that even Hans Christian Andersen could never have imagined, evolution produces the intricate mechanisms that produce evolution.

Evolutionists insist that there is no problem because none of this is impossible. Why can’t evolution produce mechanisms that produce evolution? Unless one can prove this is impossible, evolution wins (an argument that goes back to the sage of Kent himself). Though the evidence fails to prove evolution, it nonetheless must be a fact. In this Alice-in-Wonderland world, that which is not false is a fact (if it is evolution, that is).

Because similar species are thought to share a relatively recent common ancestor, they are assumed to have not had much time to evolve differences between them. That explains why they are similar, and it also predicts that such species do not have significant differences. Their genome differences should be minor. This is because evolution is limited by the rate at which genetic variations can appear and subsequently spread throughout the respective lineages. But we now know of significant numbers of unique genes between allied species and even between different variants within the same species.

Evolutionist Ian Musgrave has the explanation for this unexpected finding. Illustrating the bend-but-don’t-break property of evolution, Musgrave explains that those truly unique genes that we find are actually de novo genes.

Of course, I should have thought of that—de novo genes.

But wait, isn’t that the point? Aren’t de novo genes an unexpected finding? Of course they are. They arise entirely too fast, and those de novo genes for whose origin which we have some understanding reveal anything but evolution. Indeed, there is compelling evidence that new genes can be manufactured in response to environmental pressures. You can read more here.

You’ve probably heard that evolution has not been falsified. That’s true—it is the predictions of evolution that have been falsified. Evolution is a fact.

What good is a compass that is never right? Evolution certainly is not that bad, but it is telling how often Darwin’s idea, mandated to be a fact, is so far off base. Consider for example 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 turned 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. Sometimes evolution gets it right but often the theory, which evolutionists claim is mandatory for making sense of all of biology, just looks foolish.

DNA damage repair is a fascinating topic in cell biology. Fascinating because the cell's repair mechanisms are so incredible. What's more the mechanisms are coordinated in a sophisticated control network. As one researcher put it, "it’s almost as if cells have something akin to a computer program that becomes activated by DNA damage, and that program enables the cells to respond very quickly."

Now a new mechanism has been discovered which repairs DNA alkylation damage (the erroneous addition of carbon groups to DNA bases). The new mechanism links two previously known mechanisms. Here is how one science writer describes these two mechanisms:

The DNA repair process that removes such toxic "lesions" is known as base repair, and uses a protein called AGT (O6-alkylguanine DNA-alkytransferase) to remove the alkyl group before DNA replicates. The protein essentially sticks a chemical finger inside the DNA to flip the damaged [base] out from the DNA helix structure so that its adduct is exposed and can be transferred from the [base] to a part of its protein structure. The [base] is now repaired and can rejoin cytosine with three hydrogen bonds linking them.

AGT is believed to act alone, but there is another, unrelated repair process—nucleotide excision repair (NER)—that uses lots of proteins in its pathway. This repair occurs when bulky adducts stuck to bases distort the sleek shape of the DNA helix. Then a whole group of proteins come in and remove a patch of bases that includes the adduct, and DNA polymerase follows and fills in the patch while adding the correct base back.

The new mechanism uses alkyltransferase-like proteins (ATLs) which are similar to the AGT protein. Like AGT, ATL attacks the DNA base that has suffered alkylation damage. But the ATL protein distorts the DNA structure significantly, and thus triggers the nucleotide excision repair (NER) mechanism.

This sophisticated and coordinated repair sequence was found in all three domains of life (prokaryotes, eukaryotes and archaea). For evolutionists this forces the absurd conclusion that such a sophisticated DNA repair interaction evolved early on. Before there was so much as an amoeba, evolution had worked wonders. The earliest crude cells must not have been so crude after all. Evolution incredibly worked miracles in those heady days of early life. As the researchers write:

Our analysis of lesion-binding site conservation identifies new ATLs in sea anemone and ancestral archaea, indicating that ATL interactions are ancestral to present-day repair pathways in all domains of life.

This conclusion that complexity comes early is often forced on evolutionists, in spite of the evolutionary expectations to the contrary.

It is well known that the genetic code translates DNA genes into proteins. But the process is immensely complex and new research is revealing some fascinating and challenging details. This process of protein synthesis begins with the unwinding of the DNA double helix. The two strands are separated and an incredible protein machine makes a copy of one of the strands. The copy contains the appropriate gene and, after some editing, the copy is sent to the ribosome where it provides the needed instructions.

The copy of the DNA strand is simply a sequence of nucleotides glued together. At the ribosome the nucleotides are read three at a time. Each triplet of nucleotides is called a codon because it codes for one of the 20 amino acids, according to the genetic code. There are four different nucleotides, so a codon has 64 different possible sequences of the three nucleotides. Since there are only 20 amino acids, several codons code for the same amino acid. In other words, the genetic code is degenerate.

At the ribosome there is a small army of molecular machines, called tRNAs, that read the codons and supply the appropriate amino acid, as per the genetic code. These tRNAs have a codon reader on one end and the corresponding amino acid glued to the other end. (The amino acids are glued onto the tRNAs by an army of proteins--the masters of the genetic code).

The tRNA machines are not always restricted to reading a particular codon, and in general there is not a one-to-one relationship between the codons and the tRNAs. For instance, a particular type of tRNA may read two of the six different codons that code for the serine amino acid. Also, the different tRNA machines are not in equal abundance. Instead, some are common and others are more rare.

One consequence of all this is that a given amino acid sequence (to be used in a protein) can be coded for by many different sequences of codons, which in turn could be read by different tRNAs. Therefore, a given amino acid sequence can use very different tRNAs, depending on the codon sequence used.

It has long been known that the different possible codons, which code for an amino acid, are not merely used at random in gene sequences. Instead, there are patterns though they vary across different genes and different organisms.

For instance, some codons appear more often than others, and genes that are used frequently tend to show a marked preference for the more common codons. And of course this means that certain tRNAs tend to be in greater demand.

The new research has now found another pattern: correlations in the sequence of codons used for a given amino acid along the protein sequence. For instance, consider all the serine amino acids in a protein sequence. What codons are used to code for those different serines?

The research found that the particular codon used for one of the serines, to stay with our example, influences the codon used at the next serine in the sequence. And what is this influence? The two codons tend to be either identical or, if not identical, they tend to be two codons that are read by a common tRNA machine. In other words, gene sequences tend to use the same tRNA machine for successive occurrences of an amino acid--tRNAs tend to be conserved.

This influence tends to wane as the distance between the two codons grows, in the protein sequence. And, as usual, the correlation is by no means consistent across genes or organisms. But the correlation is statistically significant, and the researchers showed that is is not merely a consequence of the well known codon bias.

Indeed, the correlation seems to be stronger in genes that need to be expressed quickly, such as those contributing to rapid growth or to acute stress responses. And finally, the researchers found this pattern of tRNA conservation is strongest for rare tRNAs, particularly in highly expressed genes.

Though many questions remain, all of this makes sense for enhancing the speed and fidelity of protein synthesis. What doesn't make a great deal of sense, as usual, is evolution. With evolution we must imagine a micro world of profound complexity--which we still do not fully understand--just happened to emerge.

The threats to the DNA in our cells are incredible. Radiation, carcinogens and even chemicals produced within the cell attack the DNA thousands of time every day. What is more incredible though is the cell’s DNA repair system, which you can read more about here and here. The worst kind of DNA damage is the so-called double-strand break where both strands of the double helix break. In response the cell mounts a swift and sophisticated response which new research is helping to elucidate.

One of the key proteins involved in this DNA repair, known as CtIP, has a 49 amino acid DNA-binding segment that has an important role in the repair job. Interestingly, this segment appears to be normally buried within the interior of CtIP. It is exposed when chemical signals indicating DNA damage modify the CtIP structure. The tool is now flipped open and ready to do its job.

Obviously this repair kit wouldn’t work without the CtIP protein. But it also wouldn’t work without the chemical signal that opens it up. Remove either one and the repair kit doesn’t work very well. Of course CtIP needs to have a binding site for the chemical signal, and CtIP needs to undergo just the right conformational change under the influence of the binding.

This is only the beginning of the repair kit’s complexity. There are several more important players in the choreography, without which the repair job would suffer. Nothing in biology makes sense in the light of evolution.

Katherine Pollard's Scientific American article from last year, about what makes humans different from chimpanzees, is an unfortunate example of the banality of evolution. Charles Darwin's theory, updated to account for a variety of surprise evidences, is taken as fact and this leads to a remarkable level of credulity. Whatever we find in biology, it must be the product of evolution. This leads evolutionists away from a whole range of possible investigations and interesting questions. Instead, they drone on with the same, tired, evolutionary explanations that are so predictable. Here are a few passages of note from Pollard's article:

Six years ago I jumped at an opportunity to join the international team that was identifying the sequence of DNA bases, or “letters,” in the genome of the common chimpanzee (Pan troglodytes). As a biostatistician with a long-standing interest in human origins, I was eager to line up the human DNA sequence next to that of our closest living relative and take stock. A humbling truth emerged: our DNA blueprints are nearly 99 percent identical to theirs. That is, of the three billion letters that make up the human genome, only 15 million of them—less than 1 percent—have changed in the six million years or so since the human and chimp lineages diverged.

Humbling? Why is Pollard humbled? Did the brain evolve the feeling of humility to be activated upon learning of similarities with other species? If you think this is sarcasm check out what evolutionists have had to do to explain human behavior. It isn't your Daddy's evolution anymore. It seemed that evolution was as silly as could be. It was story telling on steroids. But then came the updated version of the theory, and evolutionists became their own best parody.

Evolutionary theory holds that the vast majority of these changes had little or no effect on our biology. But somewhere among those roughly 15 million bases lay the differences that made us human. I was determined to find them. Since then, I and others have made tantalizing progress in identifying a number of DNA sequences that set us apart from chimps.

Tantalizing progress? You've got to be kidding me. This "progress" is based on yet another evolutionary fumble; namely, an extreme over emphasis on DNA. In evolution-dom, DNA is king. Long ago evolutionists latched onto DNA as a Hail Mary explanation of how the information for macro evolution could be stored and passed on. Ever since then DNA has been viewed as the blueprint for biological design. Like a computer program, DNA was forced into the role of the biological "program" that determines the nature of an organism. The other parts of the organism, as with the computer, are viewed as merely mechanically performing tasks and following instructions.

Evolutionists need DNA to fulfill this role because they need unguided change to be heritable. Such change was viewed as created by DNA mutations, which could then be passed on to offspring. Scientific problems with this dogma are mounting, but evolutionists will be slow to adjust and reconcile such a fundamental failure.

Until recently the DNA dogma was even more narrow, as evolutionists viewed only the genes within the DNA as important. The remainder of the DNA (the vast majority) was often thought of as useless junk. Now that science, no thanks to evolution, is discovering that "junk" DNA can actually be important, evolutionists changed their view to include more of the DNA.

Now science is taking the next step, again no thanks to evolution, in finding that the nature of an organism may be influenced by players outside the exalted DNA. One obvious suggestion for this comes from precisely the data Pollard analyzes: the human and chimp DNA which are so similar. But Pollard's story is firmly rooted in the DNA dogma. Evolutionists make the absurd claim that a handful of genes, which stand out in humans, are the source of so much of the human-chimp difference.

Because most random genetic mutations neither benefit nor harm an organism, they accumulate at a steady rate that reflects the amount of time that has passed since two living species had a common forebear (this rate of change is often
spoken of as the “ticking of the molecular clock”).

Except that the "molecular clock" doesn't actually work. It is yet another false prediction that goes unmentioned.

Acceleration in that rate of change in some part of the genome, in contrast, is a hallmark of positive selection, in which mutations that help an organism survive and reproduce are more likely to be passed on to future generations. In other words, those parts of the code that have undergone the most modification since the chimp-human split are the sequences that most likely shaped humankind.

Do we really need evolution to tell us that the DNA segments with the most differences between the human and chimp are more important in understanding the sources of the human-chimp difference? Here we see the banality of evolution.

The fact that HAR1 was essentially frozen in time through hundreds of millions of years indicates that it does something very important; that it then underwent abrupt revision in humans suggests that this function was significantly modified in our lineage.

More banality. The gene is significantly different in humans as compared to a wide range of other species. So yes, this suggests its function is significantly different in humans. This conclusion is obvious and we don't need evolution to figure it out. The evolutionary wrapping is superfluous. The talk of how the gene is "frozen in time" and that it "underwent abrupt revision in humans" is gratuitous story telling. Science gives the important findings and evolution gives the meaningless extras.

In fact, what evolutionists do not mention is that HAR1 is yet another example of genome differences between species that are larger than evolution predicted. The human-chimp differences are more than an order of magnitude greater than what evolution predicts. Fortunately, this freak barrage of typos just happened to hit the mark, providing quantum leaps in design improvement leading to the human brain.

Furthermore, these typos simultaneously must have altered two other genes which overlap with HAR1. That's right, HAR1 lies in a region of overlapping genes. Imagine typing a paragraph which contains one message when read normally and a different message when read backward. Not only must evolution have created all of biology's genetic information, but it composed the information in overlapping prose. Someday evolutionists will figure out how.

It might seem surprising that no one paid attention to these amazing 118 bases of the human genome earlier. But in the absence of technology for readily comparing whole genomes, researchers had no way of knowing that HAR1 was more than just another piece of junk DNA.

It was technology, not evolution, that was needed.

The way to evolve a human from a chimp-human ancestor is not to speed the ticking of the molecular clock as a whole. Rather the secret is to have rapid change occur in sites where those changes make an important difference in an organism’s functioning. HAR1 is certainly such a place. So, too, is the FOXP2 gene, which contains another of the fast-changing sequences I identified and is known to be involved in speech.

I wish Charles Darwin could see the new levels of banality he has given us. The "fact" of his theory now underwrites the ascribing anything and everything to evolution, no matter how ludicrous. Evolution has become a tautology. Whatever we find in biology is simply chalked up to evolution's amazing powers. A core tenet of evolution is that the biological variation, upon which natural selection operates, is independent of need. This view has been falsified so many times that evolutionists such as Pollard no longer skip a beat when reporting on evolution's "secret" miracles. In this case, evolution's secret is to focus the multiple mutations where they are needed to construct jaw-dropping designs.

The heroics of the cell's DNA repair system are well known, but new research is adding yet another incredible facet to the story. Experimentalists tagged DNA repair proteins with nanocrystals that light up. They then observed how they interact with DNA molecules. As reported:

They watched while UvrA proteins randomly jumped from one DNA molecule to the next, holding on to one spot for about seven seconds before hopping to another site. But when UvrA formed a complex with two UvrB molecules (UvrAB), a new and more efficient search technique emerged: the complex slid along the DNA tightrope for as long as 40 seconds before detaching itself and jumping to another molecule. ... In addition to random jumping and sliding, the researchers also observed what they called "paused motion," in which UvrAB's motion seemed slower and purposeful.

Proteins certainly do perform remarkable functions. As one researcher explained:

How this system works is an important unanswered question in this field. It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It's akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.

It would be extremely unlikely for blind variations to stumble upon such protein designs. With evolution we must believe that such proteins just happened to arise and then were selected because they helped in the DNA repair system. If you believe that then I have a bridge to sell you.

Here is another "junk DNA" claim that needs to be junked. And this time in rather dramatic fashion. The headline reads "Research team finds important role for junk DNA." That's putting it mildly. The "junk" DNA genes "spur an almost acrobatic rearrangement of the entire genome" of the humble protozoan, Oxytricha.

Early discoveries of "junk" DNA function were a bit more mundane. For instance, some segments were found to have a structural role. To be sure, structural roles actually are complex, and it is not good science to think mutations constructed such a marvel. Later, the "junk" DNA was found to be responsible for massive, sophisticated gene regulation. Pretty amazing. But now we have the rearranging of the entire genome. Biology doesn't seem to understand evolution. But evolutionists don't give up easily--after all, it's a fact.

Penguins have always been a problem for evolution. Their flippers, for instance, are supposed to be the vestiges of wings. "Say again ...?" you say? That's right, according to evolution penguins are supposed to have evolved from an earlier bird with wings. The bird morphed into a penguin and the wings morphed into the penguin's flippers. Anyone who has seen a penguin swim knows its flippers are not just a happenstance design. The penguin is an incredible swimmer and the last thing that comes to mind is that its flippers somehow evolved from a wing. Of course for evolutionists this transition is a fact, even though they don't know how it happened.

Now penguins have been discovered to defy the much touted molecular clock. The molecular clock is simply a measure of the time that two species diverged from their common ancestor, as determined by their genetic differences. In other words, like the ticking of a clock, the steady stream of mutations, which help drive evolutionary change, accumulate and can be measured. Sometimes evolutionists have an idea of the supposed time since divergence from the fossil record. They use such cases to compute the rate at which the mutations accumulate, and once they know the rate they can use it in cases in which only the genetic data are available.

Evolutionists have been using this concept of the molecular clock for almost fifty years. But the clock is consistently wrong and the concept is becoming increasingly suspect. As with the steady ticking of a clock, problems with the molecular clock concept have slowly but surely continued to mount. Indeed, molecular clock predictions have been falsified many times over. Here's one example of many.

Early on it was found that the molecular clock varies dramatically depending on context. It would be like the clock in the kitchen running twice as fast as the clock in the living room. For instance, if evolution is true then we must believe that this molecular clock varies dramatically for different types of proteins. The histone IV protein, for example, shows only a few changes

Evolutionists concluded that histone IV must have a highly constrained design. Histone IV is involved in DNA packing, and surely that role is too important to monkey with. As evolutionist Thomas Jukes wrote:

... the histones are a class of proteins that are bound to DNA in cells that possess a nucleus. They take part in the formation of nucleosomes. Any change in histones could therefore have a destructive effect on the integrity of the cell.

Jukes had no empirical evidence for this claim. It was based solely on the assumption that evolution is true. It is one example of many of how evolution corrupts science. In this case, laboratory research showed that cells sustain histone IV changes with fewer problems than expected. And the other histones sustain changes even more readily.

It was yet another example of evolution interfering with scientific progress in general, and of a molecular clock failure in particular. Now we are learning of dramatic failures of the molecular clock in penguins. These data are interesting because they are from penguin remains as old as 44,000 years. These remains allow for empirical comparison of old and current genomes (mitochondrial in this case), and the differences are several times off the molecular clock prediction.

Religion drives science and it matters.

If you scramble about 90% of a protein sequence—randomly replacing amino acids with different ones—would the protein still work? That is what evolutionists are implying in order to make sense of their theory. The problem is that evolution’s explanations for de novo genes are unlikely and very unlikely. In the case of the T-urf13 de novo gene, the two choices seem to be (i) a one in ten million shot that protein coding sequences just happened to be lying around waiting for use or (ii) only about 10% of the T-urf13 sequence really matters and you can scramble the rest with no effect.

Background

An obvious problem with evolution is that it calls for vast banks of biological programs to arise on their own. One example of this is the protein coding genes within DNA. Evolutionists usually say that these resulted from the reuse of existing protein coding genes. For instance, we are able to see in color because the photocells in our retina contain different proteins that are sensitive to different colors of light.

And how did the genes for these different proteins arise? Easy, take one such gene, duplicate it and throw in a few mutations to modify the color sensitivity. Of course there are massive problems with this narrative which evolutionists fail to recognize, but that’s another story.

Also, there is the question of from where did the first such gene come? If new genes come from pre existing genes, then from where did the first gene come? Ever since David Hume, evolutionists have argued against an infinite regress of causation so they have to have a starting point. But they have no explanation for such massive complexity beyond vague speculation which amounts to “See, poof, it happened.”

In an effort to bridge this enormous gap, evolutionists have constructed a new narrative based on de novo genes. These are genes that were not predicted but now, amazingly, evolutionists are using them as proof that evolution can indeed create new protein coding genes.

That is the argument evolutionists use for the de novo gene T-urf13 which was found in the mitochondrial genome of certain varieties of corn. The problem is that T-urf13 provides no such evidence. Indeed, if anything, it is yet another de novo gene that contradicts evolutionary theory. Let’s have a look.

Two choices: Unlikely and very unlikely

The T-urf13 gene sequence appears to come from two separate sequences already residing in the mitochondrial genome. The two sequences are in, and flanking, an RNA gene. In other words, it appears that two sequences came together, along with a short unidentified segment, to form this new gene.

But the story is more complicated than the mere reuse of pre existing coding sequences. Under the theory of evolution, the RNA and flanking sequences are not designed to have a role in coding for proteins. Evolution does not have the foresight, for instance, to imbed secondary functions for future use in the DNA information.

Evolutionists therefore cannot say the T-urf13 gene arose from the duplication of an existing protein gene. They could say that T-urf13 is a lucky strike—that the RNA and flanking sequences just happened to have protein coding properties even though they were not designed or used as such. As explained elsewhere this is unlikely (probably far worse than a one in ten million shot).

Or evolutionists can agree that, yes, the RNA and flanking sequences were not originally protein-coding like segments, but mutations evolved them into a protein coding sequence. The problem here is that we don’t find very many mutations at work. This is a difficult argument for evolutionists to make because there is so little sequence information added to the sequence. What we find is a couple dozen point mutations out of about 340 nucleotides (about 93% of the nucleotides are conserved), along with several insertions and deletions.

This second option is probably worse than the first option. For evolutionists would have to say that a sequence that has no protein-coding properties—that was not designed or selected for such information and therefore is no better than a random sequence insofar as protein-coding is concerned—can be converted into a protein-coding gene by swapping only a relatively few nucleotides. The resulting protein would have only a few percent of the amino acids modified, along with some insertions and deletions.

One way to test this evolutionary hypothesis would be to introduce mutations at those T-urf13 nucleotide sites that share identity with the original RNA and flanking sequences. In other words, scramble the majority of the T-urf13 gene. While we cannot know for sure, certainly our current knowledge suggests the resulting gene would be junk. You cannot scramble ninety percent of a gene and reasonably expect a folding, functioning, fitness-adding protein.

And if the mutated gene is junk, then we would conclude that T-urf13 owes its protein-coding abilities, probably in large part, to those original RNA and flanking sequences and that the evolutionary hypothesis makes little sense.

Summary

Evolution is not well supported by the scientific evidence. Yet evolutionists continue to reinterpret the evidence in creative ways to prop up the theory. In the case of the T-urf13 gene evolutionists have claimed that, in spite of the science, the gene is a result of a routine evolutionary capability to produce new genes.

On a day when President Obama once again called for civility and unity I am reminded how difficult this is to achieve in the origins debate. Intellectual discussions with evolutionists are about as likely as intellectual discussions with the Wizard of Oz. Rarely have I been able to cajole an evolutionist into reasoned discussion of the scientific evidence. Instead the evolutionist mischaracterizes science and deploys metaphysical justifications while accusing the skeptic of all manner of misdeeds. This infinite loop was replayed again last week on an evolutionary blog when Nick Matzke criticized recent posts here, here and here on T-urf13. I explained that the de novo gene T-urf13 is unlikely to have blindly evolved. I concluded the chances of that occurring are substantially worse than one in ten million. In return I received several pages of bizarre and irrelevant vitriol which managed to avoid the science at hand.

This is a genre that evolutionists seemed to have honed, and I was quickly reminded of it in Matzke's opening where he labelled me as a "young-earth creationist." Not only am I not a young-earth creationist, I have never even written about the topic. But accuracy and truth are not prominent in this genre.

For evolutionists the "young-earth creationist" label carries immense rhetorical value which outweighs any loss of credibility that may result. After all, the evolutionist can always respond to correction with taunts of secrecy, denial, and so forth. Indeed, I am routinely labelled as a "closet young-earth creationist."

And if I am hiding a secret religious belief then, of course, whatever I have to say in response to such charges is nothing more than a tired cover-up to which no one should pay heed. The verdict has been rendered: The evolution skeptic is an unscientific, religious zealot and therefore evolution remains a scientific fact. As Matzke pronounces:

as with many creationists, Hunter thinks his ridiculous little trope is actually a silver bullet that can be used to effortlessly kill any evolutionary evidence, thus saving his tender innocent brain the trauma of actually having to come up with a better explanation than the evolutionary one.

So much for truth and accuracy. And of course the fact of evolution stands firm:

Well, how does Hunter react to this empirical evidence on the origin of a new gene? He simply ignores the overwhelming sequence evidence right in front of him, and instead claims, based on typical creationist “it must have come together all at once from completely random sequence” assumptions, that the natural origin of T-urf13 is too improbable to be believed.

Matzke misrepresents both the science and my points. Far from ignoring the sequence evidence, it is precisely that evidence that is problematic for evolution. Protein coding sequences are extremely unlikely but here we find a significant part of one in a non-coding region.

And Matzke's quote is a silly and fictitious strawman. Of course the de novo gene arose from the pre existing sequences rather than "all at once from completely random sequence." The problem is that evolutionists are now claiming from unclear evidence that evolution is clearly capable of producing de novo genes.

Yes, some sequences came together to form a new gene. But that does not automatically demonstrate evolution any more than would a population responding to an environmental shift. Sure we can imagine how these sequences came together, but the elephant in the room is "how do lengthy protein coding sequences arise in non coding regions?"

Evolution predicts this should not happen and does not explain it. We may find an answer to this question, but for now it is not immediately obvious. At best it appears that evolution will be left with the usual "new proteins arise from the cutting, copying and pasting of pre existing proteins, with a few mutations thrown in here or there." But that hardly makes a de novo gene, such as T-urf13, evidence that evolution creates new proteins.

We have been discussing the de novo gene T-urf13 found in the mitochondrial genome of certain varieties of corn. Readers have asked about the evolutionary claim that the gene arose via blind evolution, and in particular about the role of mutations. Let's have a look.

First, the time frame over which T-urf13 arose is too short for mutations to play a significant role. The evolutionary explanation is that existing, non proteins coding, DNA sequences in the corn mitochondrial genome provided the raw material for the new protein-coding gene, T-urf13.

Under evolution non protein coding DNA sequences are not supposed to carry a pre-planned protein coding information layer. Such information layers are common. For instance, in a communication system it is possible to transmit multiple messages simultaneously. Several telephone conversations or Internet users could, for example, share a single wire. In other words, there can be multiple messages superimposed on a signal.

And just as multiple messages can be transmitted in a wire, so too there can be multiple messages, or layers of information, in a DNA sequence. Of course evolution expected no such level of cleverness. Hence the surprise when overlapping genes were discovered in DNA. In recent years DNA has been found to contain several layers of information.

Could it be that there is another such layer of information that the cell uses to create new genes? Apparently so, for we now find de novo genes such as T-urf13. But because evolution dogmatically rejects any possibility of design, it does not allow non protein coding DNA sequences to carry a preplanned protein coding information layer.

Instead, such protein coding information must exist only by random chance. And when chance rearrangements occur, and a complete protein sequence just happens to form, then de novo genes can appear. A sophisticated protein such as URF13 may appear to be designed, but such an appearance must be deceptive. Such events must occur by chance, not by design.

And what are the chances of this occurring? The corn mitochondrial genome is about half a million base pairs in length. That is enough room to contain about 2,000 T-urf13 sized genes. This number can be increased by accounting for DNA's six different reading frames, and decreased by accounting for the fact that only part of the corn mitochondrial genome is available. It can also be increased by allowing for some overlap in the hidden genes.

Let's be conservative and say there is room for 100,000 such genes in the corn mitochondrial genome. Nonetheless this is seven orders of magnitude shy of the million million sequences needed for any hope of obtaining a functioning gene, as found in one experiment. And even that estimate was conservative because only the minor function of ATP binding was required.

In contrast, the URF13 protein is a far more complex, cleverly designed machine. It is designed such that several copies fit together to form a protein machine. And that machine fits into the inner mitochondria membrane, a very complex environment. And the machine provides a channel that allows only certain types of chemicals to pass through the membrane. And did I mention the channel is gated, with a molecular switch to open the gate?

The URF13 protein design dwarfs the experimentally screened function of ATP binding. And yet, even in that simple case, and with conservative assumptions, we find the probabilities of the T-urf13 de novo gene arising via blind evolution to be one in ten million (that is, 1 in 10,000,000). The real number undoubtedly has many more zeroes.

This is the story of evolutionary probabilities. Over and over we come up with so many zeros. In design after design, and species after species, evolution repeatedly draws upon unlikely events to create its marvels. Evolutionists now contemplate a multiverse--a super universe containing an untold number of unseen universes toiling away through the ages--in order to beat the odds. Sure these designs would never appear if there was just one universe, but what if there was a near infinity of universes? Surely one of them would get lucky.

Evolutionists do not worry that their story is unlikely. They insist de novo genes must, one way or another, be simply the result of blind processes. This is a good example of the absurdity of evolution. Like a robot that hits a wall but just keeps on trying, evolution cannot adjust to the scientific data. This is because evolution is not, at bottom, a scientific theory. It is driven by the metaphysical mandate that matter and motion must explain everything, regardless of the evidence. This mandate has arisen from a long history of thought in science, philosophy and theology. Religion drives science and it matters.

Science can be wrong about some things and still make great discoveries and inventions. One can believe the earth is flat or that electrons are nothing more than tiny billiard balls and still make progress. The history of science is a fascinating story of erroneous theories and beliefs intertwined with remarkable progress. And even today’s life science research journals are full of asinine statements, arising from a belief in evolution, mingled with perfectly good scientific research. Most scientists can distinguish between the hard data gathered in the laboratory and the obligatory evolutionary framework into which the data are forced and presented. You focus on the former in order to make progress and tolerate the latter in order to get funded. Such are the practical realities of working in science.

But the origins debate is different. Here the evolution paradigm itself is questioned. That evolutionary framework and filter through which all data and hypotheses must fit is up for debate. Perhaps evolution, or at least core parts of the framework, are not true.

One may scorn at such folly and remain within the paradigm. Or one may argue against such folly. But one may not do both. It makes no sense to interpret the evidence from within the paradigm, and then argue that such interpretations prove the paradigm. In order to defend evolution as true, one must examine the evidence from a theory-neutral perspective.

Here is a simple example: A new horse fossil is discovered and evolutionists decide where it fits best amongst the already known fossils. It may not fit perfectly, and the evolutionists may be unsure about which twig in the evolutionary bush is right for this new fossil (or if perhaps a new twig should be hypothesized). But they believe evolution is true and so the fossil must fit somewhere. They announce to the world that horse evolution is now better understood and apologists then use the finding as an example of powerful evidence for evolution. After all, the evolution of the horse has been revealed.

But of course the fossil revealed no such evolutionary step—it was interpreted as an evolutionary step. Unfortunately this sophistry is common. All the time I see evolutionists making just this sort of argument. Arthur Hunt, for instance, uses de novo genes in just such an argument. Genes that are found in only one or a few allied species are sometimes thought to be newly evolved. Hunt realizes the evolution of such genes might seem “difficult to some” as there are “judicious” events that must have occurred.

Now from within the evolution paradigm, there is the question of whether such genes really are de novo. Could they not have evolved via some other mechanisms, such as lateral gene transfer. Evolutionists investigate such options, and sometimes can find none that work. In these instances they conclude a gene must be newly evolved. Hunt explains these issues and then erroneously argues that since the other evolutionary options have been eliminated for these genes, therefore they must be de novo genes, and therefore de novo genes do not pose a problem for evolution. He writes:

I would encourage readers to read the paper … This is the best way to appreciate that this one pillar of [design] thought, that new protein-coding genes cannot arise by “natural” means, is an illusion.

Design can occur by natural means but that is another story. What is even more problematic than this caricature of design is Hunt’s argument for evolution according to its own assumptions.

The paper, of course, provides no compelling explanation for the blind evolution of de novo genes. As usual the paper presupposes that such blind evolution must have occurred. Therefore the paper’s conclusions must be carefully weighed rather than simply employed as evidence for blind evolution. This logical fallacy is, unfortunately, pervasive in the origins discussion.