Autonomous air vehicles are finding increasing use and the Air Force is interested micro versions:

Micro Air Vehicles (MAVs) typically UAVs with wingspan on the order of 15cm or less are fast becoming commonplace for meeting a wide range of current and future military missions.

But there are tremendous technical challenges:

A typical sensor suite for a MAV consists of GPS, MEMs-based linear accelerometers, angular rate sensors, magnetometers, and barometric-altimeters. While this is adequate for waypoint navigation, the potential of MAVs to replicate the flight agility of natural fliers (e.g., birds, bats, insects) remains elusive, especially in complex terrain such as city streets or forests.

For hints at how to solve such problems designers are looking at nature’s solutions:

The desire to engineer the agility of natural fliers has led researchers to the study of flying organisms to learn how animals combine sensory input with control output to achieve flight maneuverability. Biologists are beginning to understand how visual information is integrated with mechanosensory information in biological systems for flight stabilization, landing, and prey/mate pursuit. Studies are also underway to discover how proprioceptive sensory feedback is used for fine-scale control the movement of wings, legs, etc. during aggressive maneuvers (e.g., obstacle or collision avoidance). These sensory modalities are combined with olfactory or auditory information for predator avoidance and prey/mate pursuit.

Fortunately evolution has created highly advanced flight systems:

The fact that animals such as fruit flies exhibit such remarkable flight agility with many sensory inputs and modest onboard processing suggests a particular kind of coupling between sensing, control and dynamics altogether qualitatively different from that of engineered systems. Advancements in flow control have made it possible to control the separation of flow around wings, either to inhibit separation for higher cruise lift-to-drag ratios or to promote it for large transients in aerodynamics loading for aggressive maneuvers. Natural flyers have anatomic features which probably act as flow control devices (e.g., covert flaps) and may act as aerodynamic sensors.

But understanding evolution’s marvels remains a research challenge:

Rigorous system modeling that can accurately capture the vehicle dynamics, sufficiently accounting for uncertainties in aerodynamic and structural models, remains primitive even for engineered vehicles, let alone for natural flyers. Uncertainty arises both in the veracity of particular models in describing a given flow or dynamics phenomenon, and in unknowns in the inputs, such as wind gusts and their time-dependent effect on the vehicle. While on-going research efforts are addressing some of the critical limitations in this area, significant uncertainties in the dynamics models of MAVs are unlikely to be completely eliminated.

How do random mutations produce such brilliant designs? Answering such questions is, of course, what science is all about. As Darwin explained, evolution opens up wide areas of scientific research. But now we know it also gives top scientists hints to their toughest problems.

The fossil record cannot usually tell us about the soft body parts or the behavior of its specimens. For these, we look to the extant species. But now a clever finding reveals an odd behavior in carpenter ants from the distant past.

Nature is full of designs and behaviors not easily preserved in the fossils. Consider the bat, certain types of which map out objects around it as small as a mosquito by sensing the echoes of its own squeaks—a system known as echolocation. The bat emits a high-pitch squeak, well beyond the range of human hearing, up to 2,000 times per second. Next it determines both range and direction to the tiny mosquito by sensing the echo while filtering out echoes from the squeaks of nearby bats. Or consider fish that use underwater electric fields either passively or actively to sense objects around them, including other fish.

It is difficult to determine such details from the fossil record, but they reveal how unlikely is the theory of evolution. Anyone familiar with today’s sonar or radar systems knows the immense complexity involved with such systems: the problems of sensing the echo in the presence of the transmitted signal which can be billions of times stronger, of filtering out spurious signals such as echoes of older transmissions, of combining the echo information with knowledge of your own motion, and so forth. Yet the bat’s detection abilities are superior to those of the best electronic sonar equipment.

It is also difficult to determine complex behaviors from the fossil record. Consider certain Hydra species, a small underwater creature, that develop nematocysts—stinging cells which eject a tiny poisoned hair. A planarian worm known as the Microstomum, consumes Hydra but passes the nematocysts through its digestive system and positions them on its surface. The Hydra meal serves to arm the Microstomum, and when fully equipped the Microstomum omits the Hydra from its diet, resuming again after discharging its ill-gotten arsenal.

For evolution to have formed this system, certain Microstomum must have happened to have selectively digested the Hydra, leaving the nematocysts untouched. Then they also happened to have vectored the nematocysts to the surface and positioned it there. Then certain Microstomum happened to have a feedback loop installed to regulate its diet.

Or consider a sheep parasite known as the brainworm:

The brain worm that reproduces in sheep uses ants to get back into a sheep. The worms get into ants by infecting snails that eat sheep feces. The snails expel tiny worm larvae in a mucus that ants enjoy, and some dozens of worms take up residence in an ant. But this would do them no good if the ant behaved normally; too few ants would be eaten by sheep. Consequently, while most of the worms make themselves at home in an ant’s abdomen, one finds its way to the ants brain and causes the ant to climb up a grass stem and wait to be eaten by a sheep. Ironically, the worm that programs the ant is cheated of happiness in the sheep’s intestine; it becomes encysted and dies.

The whole procedure seems unnecessary. Why do the worm eggs defecated by the sheep not simply hatch and climb up the grass stem to await being eaten by a sheep instead of making the hazardous trip through snail and ant? How could they become adapted to being carried by the ant unless the ant were already programmed to make itself available to be eaten by a sheep?

The list, of course, goes on and on. There is the decoy-fish with its detachable dorsal fin that mimics a smaller fish complete with a dark spot resembling an eye and notch resembling a mouth. The decoy-fish becomes motionless except for the decoy which moves from side to side, causing the “mouth” to open and close. And there is the owl with ears tuned to different frequencies, to better track its prey, and the rattlesnake with heat-sensitive (infrared) sensors to image its prey at night.

Now, a new fossil finding shows just how persistent nature's odd behaviors can be. A carpenter ant (Camponotus leonardi) can be infected by the fungus Ophiocordyceps. Sensitive to the forest temperature and humidity, the fungus must be up off the ground but lower than the forest canopy. It arrives at the desired height by taking over the ant it infects:

The fungus cannot grow high up in the canopy or on the forest floor, but infected ants often die on leaves midway between the two, where the humidity and temperature suit the fungus. Once an ant has died, the fungus sprouts from its head and produces a pod of spores, which are fired at night on to the forest floor, where they can infect other ants.

Scientists led by Hughes noticed that ants infected with the fungus, Ophiocordyceps unilateralis, bit into leaves with so much force they left a lasting mark. The holes created by their mandibles either side of the leaf vein are bordered by scar tissue, producing an unmistakable dumb-bell shape.

It is another fascinating parasitic action that, it would seem, could never be found in the fossil record. But a team of intrepid researchers found a way:

Writing in the journal, Biology Letters, the team describes how they trawled a database of images that document leaf damage by insects, fungi and other organisms. They found one image of a 48m-year-old leaf from the Messel pit that showed the distinctive "death grip" markings of an infected ant. At the time, the Messel area was thick with subtropical forests.

"We now present it as the first example of behavioural manipulation and probably the only one which can be found. In most cases, this kind of control is spectacular but ephemeral and doesn't leave any permanent trace," Hughes said.

And how did evolution design such a Rube Goldberg device? Who knows:

"The question now is, what are the triggers that push a parasite not just to kill its host, but to take over its brain and muscles and then kill it."

He added: "Of all the parasitic organisms, only a few have evolved this trick of manipulating their host's behaviour.

Evolution is truly amazing. It creates in ways we cannot even figure out.

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.

Like engineers carefully blowing up a bridge, cells have intricate, programmed suicide mechanisms. The signal is sent and an apparatus of destruction is activated. But suicide hardly fits the evolutionary narrative. Wasn’t this all about survival, reproductive advantages and leaving more offspring? Why would a cell evolve intricate and complex suicide machinery?

The answer is that suicide at the cellular level doesn’t kill the whole organism. Such self destruction serves a range of purposes, from guiding development to keeping cancer at bay. In short, cell death in a multicellular organism can be a good thing.

But if cell suicide in multicellular organisms passes the evolutionary test, what about recent findings of suicide in unicellular organisms? New genome data from the Great Barrier Reef demosponge (Amphimedon queenslandica) reveals high levels of unexpected complexity, for this lowly sponge has an impressive complement of genes. As one evolutionist put it, “This flies in the face of what we think of early metazoan evolution.”

Another evolutionist asked perhaps an even more telling question. “What I want to know now,” he asked, “is what were all these genes doing prior to the advent of sponge?”

That’s a good question because some of those genes are for programmed suicide. What this sponge genome apparently tells us is that programmed cell death would have to have arisen in single-cell organisms. Suicide at the cellular level did kill the whole organism—and that doesn’t make evolutionary sense.

With evolution what we must believe is that programmed cell death did not arise in multicellular species, but in unicellular species. In other words, an intricate, highly complex, set of tools and signals somehow arose and, rather than leading to enhanced survival as evolution calls for, they led to destruction. Evolutionists will need yet another one of their just-so stories to rationalize this.

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 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.

The genome of Ectocarpus siliculosus, a brown algae, has been sequenced and analyzed. As usual the evolutionary model fits about as well as the flat earth theory. Evolutionists claim their theory is crucial for predicting the contents of such newly sequenced genomes. But in practice we see a different story. Most obvious are the many differences found between allied species. The E. siliculosus genome is no different in this regard:

Analysis of the Ectocarpus genome failed to detect homologues of many of the enzymes that are known, from other organisms, to have roles in alginate biosynthesis and in the remodelling of alginates, fucans and cellulose, indicating that brown algae have independently evolved enzymes to carry out many of these processes.

[…]

For example there are several additional membrane-localized proteins of interest, including three integrin related proteins. Integrins have an important role in cell adhesion in animals but integrin genes are absent from all the previously sequenced stramenopile genomes. The Ectocarpus genome also encodes a large number of ion channels, compared to other stramenopile genomes. These include several channels that are likely to be involved in calcium signalling such as an inositol triphosphate/ ryanodine type receptor (IP3R/RyR), four 4-domain voltage-gated calcium channels, and an expanded family of 18 transient receptor potential channels. Members of all these classes are found in animal genomes but are absent from the genomes of land plants. No IP3R genes have been identified in the sequenced diatom and oomycete genomes, but the presence of an IP3R in Ectocarpus is consistent with the demonstration of ‘animal-like’ fast calcium waves and inositolphosphate-induced calcium release in embryos of the brown alga Fucus serratus.

In all E. siliculosus has close to ten thousand ORFans, something evolutionary theory predicted did not exist. But beyond these massive differences between cousins, The E. siliculosus genome further elucidates evolution’s tale of multicellularity.

Instead of the expectation that multicellularity arose once and then proliferated, evolutionists now must say it arose independently several times. And instead of a sort of primitive multicellularity emerging and then undergoing evolutionary refinement, we must believe evolution first produced profoundly unlikely molecular machines, which then in turn enabled multicellularity.

Animal tyrosine and green plant serine/threonine receptor kinases form two separate monophyletic clades, indicating that these two families evolved independently, and in both lineages the emergence of receptor kinases is thought to have been a key event in the evolution of multicellularity. The Ectocarpus receptor kinases also form a monophyletic clade, discrete from those of animal and green plant receptor kinases, indicating that the brown algal family also evolved independently.

In other words, evolution just happened to evolve intricate machines that then were crucial in evolving a major new innovation—multicellularity. I guess we’re living in the right multiverse.

The fossil record reveals a history of life characterized by the abrupt appearance of new species followed by no change and eventual extinction in most cases. Needless to say, abrupt appearances and no change is not exactly what evolution expected. Much of this was known in Darwin's time and he figured that the fossil record was incomplete. Today such speculation doesn't work anymore. The evidence reveals even more clearly this pattern of abrupt appearances followed by stasis. As one recent paper explained:

Beginning some 555 million years ago the Earth’s biota changed in profound and fundamental ways, going from an essentially static system billions of years in existence to the one we find today, a dynamic and awesomely complex system whose origin seems to defy explanation. Part of the intrigue with the Cambrian explosion is that numerous animal phyla with very distinct body plans arrive on the scene in a geological blink of the eye, with little or no warning of what is to come in rocks that predate this interval of time.

As in Darwin's day, the fossil record does not match evolutionary expectations and evolutionists have been trying to solve the riddle. How can the empirical scientific data be explained by evolution? One new idea is to have the recently discovered microRNAs do the heavy lifting.

MicroRNAs are short snippets of DNA, about 20 nucleotides long, that help regulate protein production. The idea is that:

miRNAs might be instrumental in canalizing development such that phenotypic variation decreases through geologic time at the cost of increasing developmental precision, allowing for subsequent increases in morphological complexity.

The big words hide the fact that there is no substance to the proposal. Here is the proposal in English (my translation):

New forms abruptly appeared because evolution somehow created them. In fact, there was an abundance of these new forms, representing dozens of different designs, and many variations on each design. As luck would have it, evolution began creating microRNAs which suppressed much of that variation because, after all, microRNAs regulate protein production. So microRNAs explain the reductions in variation that follow the explosions. And, oh by the way, microRNAs also helped evolution create new wonders, not that it couldn't already, but you know, they helped.

This is the usual just-add-water view of science that prevails courtesy of evolution. Incredibly complex organisms which defy our understanding just appear now and then. They might give rise to more incredible creations, or maybe not. Meanwhile, the details of what actually happened remain a complete mystery.

For instance, the notion that microRNAs just began to proliferate on their own is absurd. They are one part of a mind-boggling regulation network. Indeed, the microRNAs themselves (which regulate protein production remember) are regulated by proteins. As new research is gradually elucidating, "MicroRNAs control the translation of mRNAs into proteins, and proteins in turn regulate the microRNAs at various levels.”

Not only is the production of microRNAs tightly controlled, but they are carefully removed from action as well, as a consequence of "a dense network of regulatory mechanisms."

But for a moment let's set all the problems aside. Let's give evolution every break and consider that this fanciful story may really be not the creation myth it appears to be, but the real thing. Taking this narrative at face value, it would mean that evolution produced the elaborate mechanisms and machinery (and sequences) of microRNAs, so that evolution then could really take off. It would be the ultimate Rube Goldberg device. Evolutionists, who are not the least abashed at presenting such tripe, are seriously telling each other that evolution created evolution. This is truly astonishing.

With each new failed expectation and each new unfounded absurd speculation, evolutionists are digging themselves deeper and deeper in their hole. Religion drives science, and it matters.

Every biology student learns of two massive machines that operate on the DNA molecule. There is the transcription machine that makes a single-stranded copy of a gene, and there is the replication machine that makes a double-stranded copy of the DNA double helix. The former is the first step in the protein synthesis process while the latter is part of the cell division process. But what happens when these different machines meet as they operate on the same stretch of DNA? What are the rules of the DNA road?

New research suggests that the highly intricate replication process is not destabilized by head-on collisions wth the transcription machine, but merely pauses while it displaces the intruder. To do this it uses a protein that otherwise helps with transcription repair. As the paper explains:

These findings demonstrate the intrinsic stability of the replication apparatus and a previously unknown role for the transcription-coupled repair pathway in promoting replication past a RNAP [replisome and RNA polymerase] block.

It is research that is both important and interesting. And, as with any new finding, it may be relevant to the question of evolution. For instance, perhaps the theory of evolution had led us to predict this finding. Or, almost as good, perhaps the finding is reasonably inferred from the theory.

In this case a such a retrodiction would go something like this: If evolution is true then we would expect the replication machine to oust the transcription machine because random mutations could lead to such a design, but not to other conceivable designs.

But what if, on the other hand, evolution did not favor such a design? What if there was no such prediction, or retrodiction? Then it would be more difficult to enlist the design as support for evolution. In fact, what if evolution has no plausible explanation for the design?

In this case, perhaps the replication and transcription machines successfully negotiating their way in the crowded environment, resolving head-on collisions, and having an established “rules-of-the-road” is not likely given evolution’s random biological variation under the winnowing hand of natural selection. Here we would have a finding which does not fit evolutionary explanation, and the evidence shifts over from the plus column to the minus column.

What is interesting is how evolutionists routinely react to such findings. When presented with such designs, evolutionists almost invariably erect a series of fallacious roadblocks. You can see these same roadblocks used repeatedly, and they speak volumes about evolutionary thought.

One such fallacious roadblock is that placing such evidence in the minus column amounts to an argument from incredulity. “You can’t imagine how evolution could possibly have created such a design,” say evolutionists, “and so you think it is evidence against evolution.” It is a strange argument that places the burden on the one evaluating a theory also to defend the theory.

In fact anyone can “imagine” how evolution might have constructed the design, but what is needed is a plausible explanation. Evolutionists want us simply to accept an empty narrative. The problem is not incredulity on the part of the evaluator but credulity on the part of the evolutionist. “Don’t worry, it evolved” is not a plausible explanation.

This fallacious complaint of evolutionists also is another sign of the protectionism that runs through evolutionary thought. If findings that a theory does not explain are not allowed in the minus column, then what could possibly harm the theory? It is the ultimate form of unfalsifiability. Evidences that the theory explains make it a fact and DNA rules-of-the-road don’t count because that would be an argument from incredulity.

What do bacterial resistance to antibiotic drugs and the universal genetic code have in common? They both have been explained by horizontal gene transfer, a mechanism that evolutionists are increasingly using to explain the origin of the species. And what’s wrong with that? First, it makes evolution superfluous and second, it makes evolution ridiculous.

In the last century widespread use of antibiotics led to widespread resistance to antibiotics. Sometimes the resistance was rapid and so indicated a transfer of resistance between bacteria rather than independent adaptations. We now understand that bacteria, as well as higher organisms, can trade genetic material via several different mechanisms collectively referred to as horizontal gene transfer. As one science writer put it:

This seems to be a crude analogue of social learning, in which one species can learn the good tricks already discovered by another … the apparent ubiquity of horizontal gene transfer implies that microorganisms have an impressive capacity to actively alter their genomes in response to environmental stresses or opportunities.

This provides evolutionists with a convenient explanatory device for the many instances where the genetic sequence data do not cooperate with evolutionary expectations. Various studies have found that bacterial sequences often do not form the predicted evolutionary tree, and in such cases horizontal gene transfer is the typical explanation.

But while such explanations make sense, they also make evolution vulnerable to Occam’s razor. For when evolutionary predictions fail, as they often do, we find scientific explanations that are independent of evolution. Organisms intelligently adapt to environmental challenges and genes show up in the wrong place. We now understand that epigenetic and horizontal gene transfer mechanisms, respectively, often account for such phenomena. And while evolution requires such mechanisms to save it from its failures, those mechanisms do not need evolution. As we increasingly explain life with empirically observed, non evolutionary, mechanisms, why do we drag along with them the unwieldy nineteenth century Victorian doctrine?

The least of its problems

But horizontal gene transfer’s making evolution superfluous is the least of its problems. For in order for the evolutionary story to make sense, we must believe that evolution created horizontal gene transfer. This mechanism, increasingly understood to be a crucial player in adaptation, is not simple. Unlike the bumper sticker’s reminder, horizontal gene transfer is not something that just happens. It is a consequence of various complex mechanisms for which evolution has no explanation beyond the usual speculation.

So we must believe that evolution, sans horizontal gene transfer, somehow happened upon such a facility which then allowed for more evolution. Apparently we are living in the right multiverse.

This incredible level of serendipity has evolutionary theory looking increasingly ridiculous. Recently this reached a fever pitch when horizontal gene transfer was employed to explain the universal genetic code. The code is essentially the same across all species and yet it is profoundly robust and efficient. Compared to randomly selected codes the actual code is a standout. Now, to account for the codes “universality and optimality,” recent evolutionary speculation calls for a massive level of horizontal gene transfer which was “likely to be present in early communal life” and led to “innovation-sharing protocols.”

And how do we know such a world was “likely”? Because it is needed to evolve the genetic code. The evolutionists explain that traditional evolutionary theory doesn’t account for how the code could have arisen. Amazingly, following Francis Crick, evolutionists have often ascribed such marvels as the genetic code to accidents of history. But if that is excessive serendipity, so is the new idea.

The researchers set up a virtual world to rerun history multiple times and test out different ideas. As one report explained:

Starting with a random initial population of codes being used by different organisms - all using the same DNA bases but with different associations of codons and amino acids - they first explored how the code might evolve in ordinary Darwinian evolution. While the ability of the code to withstand errors improves with time, they found that the results were inconsistent with the pattern we actually see in two ways. First, the code never became shared among all organisms - a number of distinct codes remained in use no matter how long the team ran their simulations. Second, in none of their runs did any of the codes evolve to reach the optimal structure of the actual code. “With vertical, Darwinian evolution,” says Goldenfeld, “we found that the code evolution gets stuck and does not find the true optimum.”

The results were very different when they allowed horizontal gene transfer between different organisms. Now, with advantageous genetic innovations able to flow horizontally across the entire system the code readily discovered the overall optimal structure and came to be universal among all organisms. "In some sense," says Woese, "the genetic code is a fossil or perhaps an echo of the origin of life, just as the cosmic microwave background is a sort of echo of the big bang. And its form points to a process very different from today's Darwinian evolution." For the researchers the conclusion is inescapable: the genetic code must have arisen in an earlier evolutionary phase dominated by horizontal gene transfer.

In other words, a population of organisms that just happened to arise, also just happened to develop advanced genetic codes--a large number of codes. And they then just happened to trades parts of their codes with each other, taking the good and leaving off the bad. This all just happened to happen. And fortunately incredible horizontal transfer mechanisms just happened to arise, to facilitate all this.

Evolutionists are now making the Greek myth makers appear downright sober. In an all-time understatement they do admit that pinning down the details of that early process remains a difficult task. This work augments the already rampant evolutionary serendipity with absurdity. Evolutionary theory is not merely superfluous, it is ridiculous.

About twenty five years ago Lars Olov Bygren discovered that feast and famine years can affect not only those who endure them, but their progeny as well. Bygren was not the first to observe that environmental influences can be transmitted to subsequent generations. And as with the earlier discoveries, even in recent decades such empirical findings have not been welcomed by evolutionists. Why? Because such findings go against evolutionary theory. As a recent Time magazine article explained:

Could parents’ experiences early in their lives somehow change the traits they passed to their offspring?

It was a heretical idea. After all, we have had a long-standing deal with biology: whatever choices we make during our lives might ruin our short-term memory or make us fat or hasten death, but they won’t change our genes — our actual DNA. Which meant that when we had kids of our own, the genetic slate would be wiped clean.

What’s more, any such effects of nurture (environment) on a species’ nature (genes) were not supposed to happen so quickly. Charles Darwin, whose On the Origin of Species celebrated its 150th anniversary in November, taught us that evolutionary changes take place over many generations and through millions of years of natural selection. But Bygren and other scientists have now amassed historical evidence suggesting that powerful environmental conditions (near death from starvation, for instance) can somehow leave an imprint on the genetic material in eggs and sperm. These genetic imprints can short-circuit evolution and pass along new traits in a single generation.

Such imprinting is the subject of epigenetics—the study of changes in gene activity that do not involve changes to the DNA yet in some cases may be passed down to successive generations. And although various epigenetic phenomena have been observed for over a century, and even the molecular details have been outlined for several decades, basic and applied research in the field has been slow to progress. Only in recent years have epigenetic-based therapeutics begun to appear. As the article explains:

Geneticists are quietly acknowledging that we may have too easily dismissed an early naturalist who anticipated modern epigenetics—and whom Darwinists have long disparaged. Jean-Baptiste Lamarck (1744-1829) argued that evolution could occur within a generation or two. He posited that animals acquired certain traits during their lifetimes because of their environment and choices. The most famous Lamarckian example: giraffes acquired their long necks because their recent ancestors had stretched to reach high, nutrient-rich leaves.

In contrast, Darwin argued that evolution works not through the fire of effort but through cold, impartial selection. By Darwinist thinking, giraffes got their long necks over millennia because genes for long necks had, very slowly, gained advantage. Darwin, who was 84 years younger than Lamarck, was the better scientist, and he won the day. Lamarckian evolution came to be seen as a scientific blunder. Yet epigenetics is now forcing scientists to re-evaluate Lamarck’s ideas.

Though in decades past evolutionists ridiculed scientists who dared suggest this heresy, at this point the evidence is undeniable. Through a great variety of complex mechanisms, organisms not only respond intelligently to the environment, they can pass response information on to their progeny. Evolutionists long since resisted such findings, for aside from their immense complexity, such mechanisms mean that evolution somehow created response mechanisms with future environments in mind. Not exactly the stuff of unguided mutations. It is yet another falsification of a fundamental expectation of evolutionary theory.

Now, in spite of evolution, science is pursuing the epigenome—the map of how the genome is marked, modified and influenced in response to the environment. As the article explains:

Remember the Human Genome Project? Completed in March 2000, the project found that the human genome contains something like 25,000 genes; it took $3 billion to map them all. The human epigenome contains an as yet unknowable number of patterns of epigenetic marks, a number so big that Ecker won't even speculate on it. The number is certainly in the millions. A full epigenome map will require major advances in computing power. When completed, the Human Epigenome Project (already under way in Europe) will make the Human Genome Project look like homework that 15th century kids did with an abacus.

But the potential is staggering. For decades, we have stumbled around massive Darwinian roadblocks. DNA, we thought, was an ironclad code that we and our children and their children had to live by. Now we can imagine a world in which we can tinker with DNA, bend it to our will. It will take geneticists and ethicists many years to work out all the implications, but be assured: the age of epigenetics has arrived.

Epigenetics has become, as past Director of the National Institutes of Health Elias Zerhouni recently remarked, “a central issue in biology.” It seems that the long-standing claim of evolutionists, that “nothing makes sense in biology except in the light of evolution,” needs to be revised.

Male crickets attract females with their chirping, but some males are incapable of chirping. Now, new research shows that those silent males are affected by their singing comrades. Specifically, silent males that develop in the presence of abundant male song tend to be larger, with more reproductive potential, than male crickets growing up in a silent environment. Insects are more complicated than thought. As one researcher explained:

people often think of insects, especially the non-social insects, as mindless automatons, pre-programmed to carry out simple procedures throughout their lives

Of course, after all they simply happened to evolve.

Our research shows quite the opposite, and demonstrates how even small, inconspicuous animals respond to the vagaries of their social environment by capitalizing on conspicuous signals that are intended for a different receiver.

So now we know that a blind mutation made the crickets sensitive to the songs in their environment. And another blind mutation connected that sensitivity to increased growth and reproductive potential. This research demonstrates the power of evolutionary change.

Once again evolution has come up with an ingenious design, this time a multilayered protective material with a range of potential applications. The material was discovered in the shell of a deep-sea snail, Crysomallon squamiferum, which is able to withstand powerful crab attacks. Here is the summary of the new findings:

Biological exoskeletons, in particular those with unusually robust and multifunctional properties, hold enormous potential for the development of improved load-bearing and protective engineering materials. Here, we report new materials and mechanical design principles of the iron-plated multilayered structure of the natural armor of Crysomallon squamiferum, a recently discovered gastropod mollusc from the Kairei Indian hydrothermal vent field, which is unlike any other known natural or synthetic engineered armor. We have determined through nanoscale experiments and computational simulations of a predatory attack that the specific combination of different materials, microstructures, interfacial geometries, gradation, and layering are advantageous for penetration resistance, energy dissipation, mitigation of fracture and crack arrest, reduction of back deflections, and resistance to bending and tensile loads. The structure-property-performance relationships described are expected to be of technological interest for a variety of civilian and defense applications.

C. squamiferum’s shell is truly an evolutionary breakthrough providing material science with several new concepts for protective armoring. As one report explains:

the snail employs some unique tricks to protect itself. For example, the shell's outermost layer consists of strong particles of iron sulphide created in the hydrothermal vents, each around 20 nanometres across, embedded in a soft organic matrix secreted by the snail. This structure is designed to crack when hit, but in a way that absorbs energy.

Cracks spread only by fanning out around the iron sulphide particles. This "microcracking" not only absorbs energy, it also ensures that larger cracks do not form. What's more, the particles of iron sulphide may blunt and deform intruding claws …

A thick, spongy middle layer acts as padding to dissipate further the energy of the blow. This makes it less likely that the mollusc's brittle inner shell, which is made of calcium carbonate, will crack. …

Helmets, motorbikes and Arctic pipelines that collide with icebergs, leading to costly oil spills, could also benefit ...

C. squamiferum’s revolutionary shell design is yet another reason why evolution is so important to science as a whole.

The DNA code, which translates DNA sequences into protein sequences, has always been claimed as extremely compelling evidence for evolution. The code was first described in the mid twentieth century and, among other things, was found to be universal, or nearly so. The same DNA code is used in the cells in your brain and your big toe. The same DNA code is used in different species. The same DNA code is even used across the major kingdoms. All tissues, all species use the same code? Surely they were not independently created—they must have evolved. And if the code varied, on the other hand, evolution would surely be falsified. In one fell swoop, the DNA code not only is another compelling evidence for evolution, it also demonstrates that evolution is falsifiable, a badge that is crucial for evolutionists who seek to distinguish themselves from those religious rascals. But now a new code has been discovered and, believe it or not, it is not universal.

Most people understand that genes are sections of DNA that code for molecular machines such as proteins. But what is less familiar is that in higher organisms many of the genes are broken up into expressed regions, or exons, which are separated by intervening regions, or introns. After the gene is copied the transcript is edited, splicing out the introns and glueing together the exons. Not only is it a fantastically complex process, it also adds tremendous versatility to how genes are used. A given gene may be spliced into alternate sets of exons, resulting in different protein machines. There are three genes, for example, that generate over 3,000 different spliced products to help control the neuron designs of the brain.

But how does the splicing machinery know where to cut and paste? The answer is that there is an elaborate code that exciting new research is helping to elucidate. The new massive study systematically analyzed how genes are alternatively spliced in four different types of mouse tissue: central nervous system tissue, muscle tissue, digestive system tissue, and whole embryos.

The study found significant signals that the splicing machinery seem to use to decide how to do its splicing. This splicing code is extremely complicated, using not only sequence patterns in the DNA transcript, but also the shape of transcript, as well as other factors.

What is also complex about the new code is that it varies substantially across the four tissue types. There is still much to learn, but there certainly is no question that this is no universal code. Is evolution still falsifiable?

In his evolution apologetic, Science on Trial, Douglas Futuyma argued that the idea that the species were created is obviously false because they not well designed. Evolution, concluded Futuyma, must be true. For instance, Futuyma pointed out that photosynthesis is immensely useful, yet no higher animals have this mechanism. But new research is finding just that. The green sea slug, it seems, is part animal and part plant. As one report explained:

Pierce emphasized that this green slug goes far beyond animals such as corals that host live-in microbes that share the bounties of their photosynthesis. Most of those hosts tuck in the partner cells whole in crevices or pockets among host cells. Pierce’s slug, however, takes just parts of cells, the little green photosynthetic organelles called chloroplasts, from the algae it eats. The slug’s highly branched gut network engulfs these stolen bits and holds them inside slug cells.

Some related slugs also engulf chloroplasts but E. chlorotica alone preserves the organelles in working order for a whole slug lifetime of nearly a year. The slug readily sucks the innards out of algal filaments whenever they’re available, but in good light, multiple meals aren’t essential. Scientists have shown that once a young slug has slurped its first chloroplast meal from one of its few favored species of Vaucheria algae, the slug does not have to eat again for the rest of its life. All it has to do is sunbathe.

In fact the slug comes pre equipped with the necessary equipment to synthesize its own chlorophyll, the machine that captures energy from sunlight and makes plants green, and run the captured chloroplasts. As one researcher put it, “This could be a fusion of a plant and an animal—that’s just cool.” It certainly is, and for evolution it is bizarre. As one evolutionist put it, “Steps in evolution can be more creative than I ever imagined.”

Evolutionists are always pointing out that evolution is a lousy process. Our aching backs, useless wisdom teeth, and backward wiring in our retinas are, they say, consequences of evolution's ineptitude. It is hardly the sort of thing that a designer would want to copy. Would you want to fly on an aircraft if its design was inspired by such a haphazard process? Of course not. And who can argue with the evolutionist’s logic. If life is the result of the random interplay of the laws of thermodynamics, motion, electromagnetism, gravity and so forth, then we would hardly expect anything that works very well, if at all. But if all this is true, then what about nature’s dazzling designs? If evolution is a lousy designer, then what can we say about biology’s many intricacies? In fact biology’s designs are not only incredibly complex (so much so we’re still trying to figure them out), they often are quite useful.

Biology is yielding a wealth of designs and structures that find a variety of practical applications. In today's engineering fields there is an emphasis on biologically-inspired designs. Courses, textbooks and conferences increasingly look to biology for design ideas and synergies.

Military researchers, for instance, have been on to this for years. If the bat's biosonar can perform ranging measurements several times more accurately than our best military equipment, then let's find out how they do it. Likewise, if bats can perform synthetic aperture imaging in a few seconds and simultaneously solve complex geometrical equations to optimally intercept their prey, then it is no surprise that the military is interested.

In fact biology offers a wealth of such high-tech productions. Consider the fly's advanced image processing capabilities. As one writer explained, the "pesky fly's eyes hold an important blueprint for creating better video cameras, military target-detection systems, and surveillance equipment." The potential applications are significant and include commercial (e.g., cameras and video cameras), security (e.g., improved detection of movements in shadows), and military (e.g., improved target detection and tracking).

Evolutionists say that evolution created the many biological marvels such as the bat's biosonar and the fly's vision system. They say that a lousy, undirected and haphazard process just happened to outwit the best scientists and engineers in the world—time and time again. According to Darwinists, biological structures with unknown function are useless and an obvious sign of an inept, undirected process. But biological structures with awesome designs are, on the other hand, also supposed to be the product of undirected biological change, such as mutations.

Claiming that the bat's biosonar or the fly's vision system is the result of evolution is more speculation than explanation. In fact, that is putting is nicely. How silly it would be to unequivocally claim that the most advanced, complex designs must have arisen as a consequence undirected biological change. A sequence of mutations just happened to produce the most accurate sonar system known to humanity.

This is so silly, in fact, that Darwinists usually refrain from saying this. It is their theory, but more often than not Darwinists use the less ridiculous-sounding Lamarckian language. The designs, they say, arose as a consequence of selection pressure. This explanation violates their own principle that biological change must not be initiated or crafted in response to need. According to evolution, biological change must be undirected. Selection must play a role only after the biological change occurs, not before.

Nor is gradualism a remedy to the problem. Construction of biosonar and advanced image processing, one undirected mutation at a time, is no better than all at once. In both cases the undirected biological change must hit upon the same phenomenal design. Gradualism, however, has the added burden that there must exist a very long sequence of finely graded useful intermediates, leading to the final design. We know of no such sequence, but we must believe it exists. All very amazing for such a lousy process.

In 1831 Charles Darwin boarded the HMS Beagle to gather biological information from around the world. It was a wonderful opportunity for the young naturalist, and Darwin saw many fascinating wonders. The voyage is best known for its stop at the Galápagos Islands off the coast of Ecuador. There Darwin observed finches, mockingbirds and tortoises that varied distinctly from island to island. Some finches lived in coastal areas on the ground, others lived in forest trees, yet another lived in bushes. And the diet of these varieties varied considerably. One of the species ate buds and fruit, another prickly pear, others ate seeds and others were insectivores. And one of the insectivores even used a twig to fish out insects from crevices in the tree bark. Nicholas Lawson, the vice-governor who entertained Darwin over dinner claimed that so distinct were the tortoises from island to island that given the tortoise shell he could identify the island of origin.

Since then the Galápagos Finches in particular have become a celebrated icon of evolution. From academic dissertations and research papers to award-winning books and documentaries, they have been watched, dissected, analyzed, and praised. As science writer Jonathan Weiner put it, the changes in the beaks of the finches show us “Darwin’s process in action.” There’s only one problem: How did evolution create the process?

After Darwin, the twentieth century revealed the details of what should have been obvious. If Darwin’s evolutionary change brought about those different Galápagos Finches, it was driven by a profoundly complex process of chromosomes, genes and an army of molecular machines. We’re still learning about what Weiner calls “Darwin’s process” and it shows no sign of having evolved.

Consider the curious case of Carpodacus mexicanus (house finches) which began spreading throughout the United States in the 1940s from Mexico and the southwest. The beaks of these birds adapted to their new environments with great speed. Within a decade or so their beaks had adjusted to the new habitats. How could this occur to rapidly? Certainly not by evolution’s random mutations and natural selection. It was, as one science writer put it:

a complex interplay of processes … Interacting embryonic processes result in an initial level of phenotypic variation greater than what would be predicted from underlying genotypic variation alone.

In other words, complex embryonic machinery produce biological variation that responds to the environmental challenge far more efficiently and rapidly than evolution’s random mutation plus natural selection ever could. And that’s good because otherwise the birds would have failed in their new environments—evolution doesn’t work, but nature’s built-in adaptation machine does.

But in spite of this non evolutionary story of adaptation, evolutionists claim adaptation as proof of their idea. According to Ernst Mayr, “evolutionary change is also simply a fact owing to the changes in the content of gene pools from generation to generation.” Likewise, Isaac Asimov claimed that the peppered moth’s adaptation to industrial pollution proves evolution. And Steve Jones informed his readers that the changes observed in HIV (the human immunodeficiency virus) contain Darwin’s “entire argument.”

Such claims persist and even today evolutionists routinely claim examples of adaptation, from bacteria to birds, as evidence or even proof of evolution. It is another example of how vulnerable science is to simple and straightforward blunders in our thinking. This is not a complex scientific miscalculation or a clever logical fallacy. This is a blunder that is striking not for its subtly but for its transparency. Evolutionists cannot drop their theory though the science doesn’t support it, so they are driven to reprehensible reasoning. Religion drives science, and it matters.

Fascinating new research suggests that the mere sight of a sick person can trigger an immune response. When test subjects viewed photos showing symptoms of infectious disease, their immune systems responded more aggressively compared to test subjects who viewed other types of photos (including photos of people bearing firearms). It is the first hard evidence that visual cues alone can influence the immune system. Evolutionists have no difficulty explaining this new finding, but that may not be a good sign for Darwin’s theory.

Biological designs that appear to be inefficient or useless are, not surprisingly, explained by evolutionists as a consequence of the blind, happenstance process of evolution. But it is also easy for evolutionists to explain profound designs and complexity, such as the immune response discovered by this new research.

This immune response begins with the viewing and processing of symptoms of infectious disease. These are complex visual scenes that easily can be confused with scenes having nothing to do with disease, infectious or otherwise. Other research suggests that persistent priming of the immune system is not good, so this visual processing needs to be reasonably accurate.

Next in line is a link to the immune system. Once the visual processing identifies a scene as containing signs of infectious disease, then signals need to be sent to the immune system to trigger an appropriate response. Of course, the response should not be too aggressive.

Certainly this immune response to the sight of sickness is not a trivial design. But divining an evolutionary explanation is a simple matter. Why? Because the design works. And anything that works is said to be a consequence of selection, for if it works, then of course it would be selected. Useless junk is due to evolution’s ineptitude—profound designs are due to evolution’s efficiency. As one science writer put it:

Having this immune response may have had its advantages in the days of early humans - even though they may have recoiled at the sight of other sick people too, their immune responses would have helped them live in proximity with others.

There you have it—evolution happens. But such facile explanations are too easy. For while it certainly seems obvious that selection would select what works, it is not obvious how what works arises in the first place. This is the elephant in the room that is so often conveniently ignored in evolutionary just-so stories.

In fact, there is no scientific reason to think that this incredible physiological response would just happen to arise occasionally, and then patiently await selection’s nod. But scientific reasoning is not the driving force.

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.

In the dense tropical rainforest of Borneo live species unknown to science. One new find is Ibycus rachelae, a slug that, like the mythological Cupid, shoots its mate with an arrow of love. The dart injects an amorous hormone into its reluctant partner to liven things up.

And how does evolution explain this suave strategy? It would be something like this. First, the hormone happened to evolve and somehow served some purpose in the hapless slug. But the hormone also happened to work wonders when the lights were low. On those rare occasions when the slug was lucky, the hormone might somehow transfer to its partner when there was physical contact.

But this occurred rarely and so didn't help too much. That is, until the randomly designed slug happened to develop an arrow. The arrow worked wonders when it happened to fire at a prospective partner, and it happened to be armed with the hormone. That slug's wild success would proliferate into generations of gigolos.

That's how evolution works. Things that work luckily arise sometimes, and they are then selected.

This slug-turned-Cupid tale is typical of evolutionary storytelling. Stories such as these are told over and over. From textbooks to peer reviewed journals, just-so stories, as with the process of evolution, arise and persist.

But don't evolutionists ever tire of absurdity? Don't they ever think twice about their silliness? Or are they just winking at each other while taxpayers fund their imaginations? Either way, who needs Cupid, evolution is our new mythology.