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.

I once met a fellow who was an aficionado of, believe it or not, flashlights. It seemed rather mundane until I saw all the neat designs using LEDs (light emitting diodes). These semiconductor devices have been greatly improved in recent years and are finding a wide range of uses. But as is so often the case, these technological advancements were there all along in the biological world. In this case, certain butterfly species have their own elaborate optical emission system in their wings. As one researcher put it, “Who knows how much time could have been saved if we'd seen this butterfly structure 10 years ago.”

Up until a few years ago the problem with LEDs was that most of the light was not emitted. This inefficiency was resolved with two-dimensional crystals and layered reflectors called distributed Bragg reflectors (DBRs). And like these high-emission LEDs, scales on the wings of African Swallowtail butterflies make up a two-dimensional photonic crystal enhanced by a three-layer, cuticle-based DBR. The photonic crystal is infused with highly fluorescent pigment and contains an array of hollow air cylinders arranged in a pattern of triangular symmetry. As one paper further explains:

As in ultra–high-efficiency LEDs, these Butterflies’ DBRs support a spectral stop band that matches the peak emission from the structure above it. The DBRs reflect upwardly the downward-emitted fluorescence concurrently with non absorbed longer wavelengths pass through the PCS. The spatial separation between the DBR and PCS minimizes losses via coupling to guided modes in the DBR. Excitation for this fluorescent material appears to be optimized for the radiance from blue skylight, which peaks around 420 nm. Additionally, because the alpha-absorbance band of rhodopsin dominates the green wavelength photosensitivity of Papilio vision, the spectral form of this absorption is ideally placed for stimulation by fluorescence from conspecific wings. As with some shrimps and birds, this enhances signaling, because absorption of visually less productive short wavelengths leads to the emission of longer wavelengths that trigger photoreception.

As the passage explains, the butterfly’s optical emission system is tuned to use sunlight and to maximize visibility. Here is a less technical description of the system:

The trouble with this mechanism is that while half the fluorescent light radiates away from the butterfly, the other half radiates into the wing structure. That half of the light would be lost were it not for the extraordinary structure of the scales.

Vukusic discovered that the base of each scale is a highly efficient three-layered mirror—a structure known as a distributed Bragg reflector. Light from the pigment bounces between these layers, interferes constructively, and then escapes in the direction it came from.

Distributed Bragg reflectors are not perfect, however; some light always becomes trapped on the surface of the reflector and is lost. But the butterfly has another neat trick to get around this. Vukusic and his colleague Ian Hooper discovered that in each scale, sitting just above the mirror, is a slab of material filled with hollow cylinders of air that run perpendicular to the mirror. These cylindrical holes channel the light away from the reflector, preventing it from getting trapped. The slab, says Vukusic, is what optical physicists call a photonic crystal.

The end result is a highly specialized structure that converts skylight into blue-green light, captures this light, and finally channels it out to act like plumage to attract female butterflies.

Was this remarkable system constructed by the blind interplay of natural processes? Evolutionists think so. In fact they are certain it was, though beyond vague speculation they don’t know how.

Evolutionists speculate that perhaps these marvels happened to arise luckily via random mutations. Or perhaps self-assembly and mechanical processes such as buckling, cracking and splitting are important factors. In fact, perhaps pre existing cellular structures serendipitously provide a manufacturing framework. Could it be that “the highly complex inverse opal-type structures could appear ‘suddenly’ in evolutionary time (without having to evolve stepwise)”? Amazingly this is what one finds in evolutionary theory--unfounded speculation underwritten by dogmatic certainty.

Perhaps flashlights also appeared suddenly. Religion drives science, and it matters.

In your idiotic ideas file you no longer have to go back to the ancient myths, or even to centuries-old folly such as bloodletting, for we now have evolution--an idea that is promoted at this very time. One of the many inanities of evolution is its serendipity. If evolution is true, then we must believe that all manner of complex biological structures and machinery evolved (somehow) for one function, only then to enable new, revolutionary advancements to occur. Call it evolution's Law of Unintended Consequences.

Consider multicellularity. According to evolutionists, unicellular organisms aggregated and ultimately formed multicellular species. This would not have occurred without certain machines already present in the unicellular organisms. For instance, unicellular organisms have complex machines that secrete proteins whose function have nothing to do with working with other cells. But in multicellular aggregates such machines, according to evolutionary theory, were "recruited" (a favorite word in the evolutionist's lexicon) to fulfill an entirely new mission. Here is how Stuart Newman describes it:

Certain unicellular proteins and other molecules mobilize physical effects in the multicellular context that were unanticipated during their earlier evolution. To take a simple example, all single-celled organisms can secrete protein molecules into the environment around them. These molecules will generally float away, but they may serve to attract prey, repel predators, and so forth. When the external environment consists of other cells, as is the case in a multicellular cluster, the secreted molecule can form a distributed signal – a “morphogen” gradient – that can cause one end of the cluster to be different from another. The gene involved simply specifies the sequence of the secreted protein. What function the protein comes to assume in the new multicellular context has nothing to do with the evolutionary history of that gene, or the selection to which it had been subject. We have called such developmentally efficacious associations of ancient gene products with the physical effects they mobilize in multicellular aggregates “dynamical patterning modules” (DPMs). There are many other such examples.

It is another example of serendipity gone wild in evolutionary theory, but for evolutionist's it is just another event in a long Alice-in-Wonderland history of make believe events.