Finally, the Details of How Proteins Evolve

A Step-By-Step Description

How did proteins evolve? It is a difficult question because, setting aside many other problems, the very starting point—the protein-coding gene—is highly complex. A large number of random mutations would seem to be required before you have a functional protein that helps the organism. Too often such problems are solved with vague accounts of “adaptations” and “selection pressure” doing the job. But this week researchers at the University of Illinois announced ground-breaking research that provides a step-by-step, detailed, description of the evolution of a new protein-coding gene and associated regulatory DNA sequences. The protein in question is a so-called “antifreeze” protein that keeps the blood of Arctic codfish from freezing, and the new research provides the specific sequence of mutations, leading to the new gene. It would be difficult to underestimate the importance of this research. It finally provides scientific details answering the age-old question of how nature’s massive complexity could have arisen. As the paper triumphantly declares, “Here, we report clear evidence and a detailed molecular mechanism for the de novo formation of the northern gadid (codfish) antifreeze glycoprotein (AFGP) gene from a minimal noncoding sequence.” Or as lead researcher, professor Christina Cheng, explained, “This paper explains how the antifreeze protein in the northern codfish evolved.” This is a monumental finding. Having the scientific details, down to the level of specific mutations, of how a new protein-coding gene evolved—not from a related gene but from non-coding DNA—is something evolutionists could only dream of only a few short years ago. There’s only one problem: it is all junk science.

The first problem is that this new “research” is, in actuality, a just-so story:

In science and philosophy, a just-so story is an unverifiable narrative explanation for a cultural practice, a biological trait, or behavior of humans or other animals. The pejorative nature of the expression is an implicit criticism that reminds the hearer of the essentially fictional and unprovable nature of such an explanation. Such tales are common in folklore and mythology.

For example, the antifreeze protein is of relatively low complexity chiefly consisting a repeating sequence of three amino acids (threonine-alanine-alanine), and the evolutionists claim that these repeating sequences “strongly suggest” that the protein-coding gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.”

Why is that true?

Why does a repeating genetic sequence “strongly suggest” that it “evolved from repeated duplications?” What experiment revealed this truth? What evidence gives us this profound principle? The answer, of course, is that there is none. Nowhere do the evolutionists justify this claim because there is no empirical justification.

There is no scientific evidence for it. Zero.

The paper continues with yet more non-empirical claims. Those nine nucleotides “likely originated within a pair of conserved 27-nucleotide” segments that flank each side of the repetitive region. And these four 27-nucleotide segments are similar to each other, “indicating they resulted from the duplication of an initial copy.” As the paper concludes, “chance duplications” of an ancestral 27-nucleotide segment “produced four tandem copies.”

But why are those claims true? Why do such similarities imply an origin via evolutionary mechanisms? The problem is, they don’t. There is no empirical evidence for any of this. This is completely evidence-free.

The evolutionists next explain that the 9-nucleotide segment duplicated a large number of times because it worked well:

We hypothesize that, upon the onset of selective pressure from cold polar marine conditions, duplications of a 9-nt ancestral element in the midst of the four GCA-rich duplicates occurred.

The above quote is an example of the non-empirical, teleology that pervades evolutionary thought. It was upon the onset of cold conditions that the needed genetic duplications occurred. This is not empirical; this is story-telling.

The paper continues with a series of one-time, contingent events crucial to their story and non-empirical claims. The genetic sequence “was appropriately delimited by an existing in-frame termination codon.”

Appropriately delimited?

The presence of a region in two of the species “indicates that it existed in the gadid ancestor before the emergence of the AFGP.” The absence of a thymine nucleotide at a location in some of the species “very likely resulted from a deletion event,” causing a fortuitous frameshift which supplied the crucial signal peptide segment, telling cellular machinery that the protein should be secreted to the bloodstream. As the paper concludes, “the emerging AFGP gene was thus endowed with the necessary secretory signal.”

Endowed with the necessary signal?

There is no empirical evidence for any of this.

Another problem with this just-so account, is the substantial level of serendipity required. The new antifreeze protein did not arise from some random DNA sequence, but rather from crucial, preexisting segments of DNA that just happened to be lying around. In other words, the fish were facing a colder environment, they needed some antifreeze in their blood, and the pieces needed for such an antifreeze gene were fortuitously available.

The authors hint at this serendipity when they conclude that their story of how this protein evolved is an example of “evolutionary ingenuity.”

Evolutionary ingenuity?

The press release is even more revealing. Cheng admits that the evolution of this gene “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.”

The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”

Even the evolutionists admit to the rampant serendipity. Nonetheless they are triumphant, for “the findings offer fresh insights into how a cell can invent ‘a new, functional gene from scratch.’”

Fresh insights?

In actuality the findings arose from a series of non-empirical claims.

Religion drives science, and it matters.

Brochosome Proteins Encoded By Orphan Genes

A Pattern Problem

A few years ago Paul Nelson debated Joel Velasco on the topic of design and evolution. Nelson masterfully demonstrated design in nature. For his part Velasco also provided an excellent defense of evolution. But the Epicurean claim that the world arose via random chance is not easy to defend, and Velasco’s task would be challenging. Consider, for example, the orphans which Nelson explained are a good example of taxonomically-restricted designs. Such designs make no sense on evolution, and though Velasco responded with many rebuttals, none were very convincing. Since that debate the orphan problem has become worse, as highlighted by a new study of brochosomes.

Background

The term orphan refers to a DNA open reading frame, or ORF, without any known similar sequence in other species or lineages, and hence ORFan or “orphan.” Since orphans are unique to a particular species or lineage, they contradict common ancestry’s much celebrated nested hierarchy model.

The Nelson-Valasco Debate

Velasco addressed the orphan problem with several arguments. First, Velasco reassured the audience that there isn’t much to be concerned with here because “Every other puzzle we’ve ever encountered in the last 150 years has made us even more certain of a fact that we already knew, that we’re all related.”

Second, Velasco argued that the whole orphan problem is contrived, as it is nothing more than a semantic misunderstanding—a confusion of terms. These are nothing more than open reading frames without significant similarity to any known sequence.

Third, Velasco argued that many of the orphans are so categorized merely because the search for similar sequence is done only in “very distantly related” species.

Furthermore, and fourth, Velasco argued that orphans are really nothing more than a gap in our knowledge. For the more we know about a species, the more the orphan problem goes away. And which species do we know the most about? Ourselves of course. And we have no orphans: “Well what about humans, we know a lot about humans. How many orphan genes are in humans? What do you think? Zero.”

In fact, and fifth, Velasco argued that while new orphans are discovered with each new genome that is decoded, the trend is slowing and is suggestive that in the long run relatives for these orphans will be found: “In fact if you trend the absolute number going up, as opposed to the percentage of orphan genes in organisms, that number is going down.”

So to summarize Velasco’s position, the orphan problem will be solved so don’t worry about, but actually orphans are not a problem at all but rather a semantic misunderstanding, but on the other hand the orphan problem is a consequence of incomplete genomic data, but actually on the other hand the problem is a consequence of insufficient knowledge about the species, and in any case even though the number of known orphans keeps on rising, they will eventually go away because the orphans, as a percentage of the overall genomic data (which has been exploding exponentially) is going down.

This string of evolution arguments reminds us of the classic dog-owner’s defense: He’s not my dog, he didn’t bite you, and besides you hit the dog first anyway. Not surprisingly, each of Velasco’s arguments fails, as I explained here.

In fact, there are many orphans, and while function can be difficult to identify, it has been found for many orphans. As science writer Helen Pilcher explained:

In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.

Up to a third of genomes have been found have been found to be unique, as this review explains:

Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes. 

And this is yet another failed prediction of evolution, as this paper explains:

The frequency of de novo creation of proteins has been debated. Early it was assumed that de novo creation should be extremely rare and that the vast majority of all protein coding genes were created in early history of life. However, the early genomics era lead to the insight that protein coding genes do appear to be lineage-specific. Today, with thousands of completely sequenced genomes, this impression remains.

Why then was Velasco so confident and almost nonchalant in his argumentation? Why was he so assured that, one way or another, the orphan problem was not a problem? And why did he believe there are zero orphans in humans, and so it merely is a matter of studying biology, and the orphans will go away?

Lander Orphan Study

It could be due to a significant 2007 study from Eric Lander’s group which rejected most of the large number (several thousands) of orphans that had been tentatively identified in the human genome. The study confidently concluded that “the vast majority” of the orphans were “spurious”:

The analysis here addresses an important challenge in genomics— determining whether an ORF truly encodes a protein. We show that the vast majority of ORFs without cross-species counterparts [i.e., orphans] are simply random occurrences. The exceptions appear to represent a sufficiently small fraction that the best course is would be [sic] consider such ORFs as noncoding in the absence of direct experimental evidence.

The authors went on to propose that “it is time to undertake a thorough revision of the
human gene catalogs by applying this principle to filter the entries.”

That peer-reviewed paper, in a leading journal, was well received (e.g., Larry Moran called it an “excellent study”) and it certainly appeared to be authoritative. So it is not surprising that Velasco would be confident about orphans. For all appearances, they really were no problem for evolution.

There was just one problem. This was all wrong.

There was no scientific evidence that those human sequences, identified as orphans, were “spurious.” The methods used in the Lander study were full of evolutionary assumptions. The results entirely hinged on evolution. Although the paper did not explicitly state this, without the assumption of evolution no such conclusions could have been made.

This is what philosophers refer to as theory-ladenness. Although the paper authoritatively concluded the vast majority of the orphans in the human genome were spurious, this was not an empirical observation or inference, as it might seem to some readers. Their data (and proposed revisions to human gene catalogs), methods, and conclusions were all laden, at their foundation, with the theory of evolution.

So Velasco’s argument was circular. To defend evolution he claimed there were zero orphans in the human genome, but that “fact” was a consequence of assuming evolution is true in the first place. If the assumption of evolution is dropped, then there is no evidence for that conclusion.

Brochosomes

Since the Nelson-Velasco debate the orphan problem has just gotten worse. Consider, for example, brochosomes which are intricate, symmetric, secretory granules forming super-oily coatings on the integuments of leafhoppers. Brochosomes develop in glandular segments of the leafhopper’s Malpighian tubules.

The main component of brochosomes, as shown in a recent paper, is proteins. And these constituent proteins, as well as brochosome-associated proteins, are mostly encoded by orphan genes.

As the paper explains, most of these proteins “appear to be restricted to the superfamily Membracoidea, adding to the growing list of cases where taxonomically restricted genes, also called orphans, encode important taxon-specific traits.”

And how did all these orphan genes arise so rapidly? The paper hypothesizes that “It is possible that secreta exported from the organism may evolve especially rapidly because they are not strongly constrained by interactions with other traits.”

That evolutionists can so easily reach for just-so stories, such as this, is yet another example of how false predictions have no consequence for evolutionary theory. Ever since Darwin evolutionists have proclaimed how important it is that the species fall into the common descent pattern. This has especially been celebrated at the molecular level.

But of course the species fall into no such pattern, and when obvious examples present themselves, such as the brochosome proteins, evolutionists do not miss a step.

There is no empirical content to this theory. Predictions hailed as great successes and confirmations of the truth of evolution suddenly mean nothing and have no consequence when the falsification becomes unavoidable.

Religion drives science, and it matters.

h/t: El Hombre

But, But, But, … The Origin Of Life Was All But Solved!

“The origin of life is among the greatest open problems in science”

With everyone from the National Academy of Sciences to science writers such as Carl Zimmer proclaiming that the origin of life problem has essentially been solved, we wonder why we continue to find researchers, this time Yehuda Zeiri at Ben-Gurion University, admitting that:

Despite decades of research, how life began on Earth remains one of the most challenging scientific conundrums facing modern science.

and Sara Walker resorting to hope and luck:

The origins of life stands among the great open scientific questions of our time. While a number of proposals exist for possible starting points in the pathway from non-living to living matter, these have so far not achieved states of complexity that are anywhere near that of even the simplest living systems. A key challenge is identifying the properties of living matter that might distinguish living and non-living physical systems such that we might build new life in the lab. This review is geared towards covering major viewpoints on the origin of life for those new to the origin of life field, with a forward look towards considering what it might take for a physical theory that universally explains the phenomenon of life to arise from the seemingly disconnected array of ideas proposed thus far. The hope is that a theory akin to our other theories in fundamental physics might one day emerge to explain the phenomenon of life, and in turn finally permit solving its origins. […] If we are so lucky as to stumble on new fundamental understanding of life that allows us to solve our origins, it could be such a radical departure from what we know now that it might be left to the next generation of physicists to reconcile the unification of life with other domains of physics, as we are now struggling to accomplish with unifying general relativity and quantum theory a century after those theories were first developed.

But “hope” is not a good science strategy.

One sign of this problem is the proliferation of hypotheses, indicating, as we have pointed out many times, the lack of any good solution. Or as Alex Berezow a bit more bluntly puts it:

The origin of life is a profound mystery. Once life arose, natural selection and evolution took over, but the question of how a mixture of various gases created life-giving molecules that arranged into structures capable of reproducing themselves remains unanswered. Many theories have been proposed, some of which are popular (e.g., RNA World), and some of which are a far-fetched (e.g., aliens). Unlike politics, more ideas are not necessarily better; in science, a diversity of theories tends to betray the reality that scientists have no idea what's going on.

No idea what’s going on? It must be time for Jeremy England to find another Ilya Prigogine idea.

Human Evolution: Missing Link Still Missing

The Need For Theory Evaluation

The evolution of humans is, in many ways, similar to evolutionary theory on the whole. As Colin Barras reveals in his recent article at the BBC, There are conflicting evidences, a lack of details, opposing hypotheses held with great confidence, and a wide range of explanatory mechanisms that are routinely used as needed. That much is obvious. What is a bit more subtle, and arguably even more important, is the absence of a serious evaluation of the theories at hand.

Barras’ article is a good summary, from TH Huxley and Darwin up to today, of how evolutionists have viewed human evolution. What is humanity’s phylogenetic neighbor, our so-called sister species, and what is our most recent common ancestor?

Following Huxley, gorillas or chimpanzees were typically held by early evolutionists as both our sister species and representative of the common ancestor, which swung from branch to branch and rambled along on all fours. But some evolutionists held that monkey’s were our closest evolutionary neighbor.

With the rise of molecular biology came genetic comparisons and the firm conclusion that chimpanzees and bonobos are our sister species. Huxley, it seemed, was right. Students were told, in no uncertain terms, that the chimp was our sister species—after all, we shared something like 99% of our DNA in common.

But then new evidences arose, questioning this seemingly incontrovertible truth. Subtle differences between gorillas and chimps suggested independent evolution, rather than inheritance via a common ancestor, of certain traits. Furthermore, a new fossil species, Ardipithecus ramidus, as well as anatomical and behavioral comparisons, called into question the accepted human-chimp relationship.

All of this leaves evolutionists today contemplating a range of explanations for human evolution. One common theme of all the different explanations, however, is their lack of detail. The explanations do not provide any sort of detailed account of the rise of the many unique traits and capabilities in humans.

And where detailed evidence does exist, such as in the chimp, gorilla, and human DNA data, it makes little sense (see here, here, and here, for example).

The theoretical problems and lack of detail with human evolution, and evolution in general, raise the question of how good these theories are. Evolutionists repeatedly state that evolution is a fact, just as much as gravity, heliocentrism, and the roundness of the Earth are facts. There is no question about it.

But the science does not support this claim. What we need is a legitimate, serious evaluation of the theories at hand.

The Real Problem With Convergence

Worse Than Lightning Striking Twice

Biology is full of convergence—repeated designs in distant species. Marsupials and placentals, for instance, are mammals with different reproductive designs (placentals have significant growth in the embryonic stage attached to the nutrient-rich placenta whereas marsupials have no placenta and experience significant development after birth) but otherwise with many similar species. The marsupial flying phalanger and placental flying squirrel, for example, have distinctive similarities, including their coats that extend from the wrist to the ankle giving them the ability to glide long distances. But evolutionists must believe that these distinctive similarities evolved separately and independently because one is a marsupial and the other is a placental, and those two groups must have divided much earlier in evolutionary history. Simply put, evolution’s random mutations must have duplicated dozens of designs in these two groups. Isn’t that kind of like lightning striking twice?

It is kind of like lightning striking twice but for evolutionists—who already have accepted the idea that squirrels, and all other species for that matter, arose by chance mutations—this is not difficult to believe. It simply happened twice rather than once (or several times, in the cases of a great many convergences).

What is often not understood however, by both evolutionists and their critics, is that convergence poses a completely different theoretical problem. Simply put, a fundamental evidence and motivation for evolution is the pattern of similarities and differences between the different species. According to evolutionary theory, the species fall into an evolutionary pattern with great precision. Species on the same branch in the evolutionary tree of life share a close relationship via common descent. Therefore they share similarities with each other much more consistently than with species on other branches.

This is a very specific pattern, and it can be used to predict differences and similarities between species given a knowledge of where they are in the evolutionary tree.

Convergence violates this pattern. Convergence reveals striking similarities across different branches. This leaves evolutionists struggling to figure out how the proverbial lightning could strike twice, as illustrated in a recent symposium:

Does convergence primarily indicate adaptation or constraint? How often should convergence be expected? Are there general principles that would allow us to predict where and when and by what mechanisms convergent evolution should occur? What role does natural history play in advancing our understanding of general evolutionary principles?

It is not a good sign that here in the twenty first century evolutionists are still befuddled by convergence, which is rampant in biology, and how it could occur. This certainly is a problem for the theory.

But a more fundamental problem, which evolutionists have not reckoned with, is that convergence violates the evolutionary pattern. Regardless of adaptation versus constraint explanations, and any other mechanisms evolutionists can or will imagine, the basic fact remains: a fundamental evidence and prediction of evolution is falsified.

The species do not fall into the expected evolutionary pattern.

The failure of fundamental predictions—and this is a hard failure—is fatal for scientific theories. It leaves evolution not as a scientific theory but as an ad hoc, story-telling, procedure. The species reveal the expected evolutionary pattern—except when they don’t. In those cases, they reveal some other pattern.

So regardless of where you position yourself in this debate, please understand that attempts to explain convergence under evolutionary theory, while important in normal science, do nothing to remedy the underlying theoretical problem, which is devastating.

Religion drives science, and it matters.

New Evolution Book: Echolocation Solved

Just Add Water

We have seen that a new evolution book co-authored by evolutionist Dennis Venema is influenced by the mythical Warfare Thesis (here and here) and makes erroneous arguments that the fossil evidence supports evolution (here). Regarding the Warfare Thesis the book propagates the false history that the basic issue of the seventeenth century Galileo Affair was “the veracity of the new science, and its perceived threat to biblical authority.” As we saw, this is the false, evolutionary rendition of history. The Warfare Thesis is a myth, and the Galileo Affair is perhaps the favorite example for evolutionists. Regarding the fossil evidence (which reveals species appearing abruptly in the strata), the book makes two erroneous arguments: that evolution is needed for science to work at all (the “intellectual necessity” philosophical argument) and the use of random design as the alternative to evolution (a theological argument). Now we move on to another topic: echolocation. This was of particular interest to me since I have used echolocation as an example of how evolution fails, and fails badly. When I saw that Venema appealed to echolocation to argue for evolution I was interested to see what he had to say. I am always looking for good arguments for evolution, but I did not find one here. Below I summarize the five different reasons why echolocation destroys evolution. Finally, I turn to Venema’s argument, if it can be called that. What we will see is that his argument utterly fails. Venema fails to address any of the problems with echolocation, and he fails to present any kind of a positive case that might be used to overcome the many problems. In short, it is a complete disaster.

Complexity: The original sonar technology

Most people are familiar with the concept of radar and sonar. Simply put, a reflected signal is used to track a target. But what most people are less familiar with are the many details and complications any radar or sonar system must reckon with. For example, the transmitted pulse must be very strong because it will weaken as the square of the distance it travels, and only a tiny fraction of it will be reflected. Ultimately, the return signal is very weak, so while the receiver is exposed to the very powerful transmitted signal, it must then detect a return signal many orders of magnitude weaker. Think of shouting as loud as you can, and then listening for the echo off of a mosquito.

This is just the beginning of the many sonar design issues. The pulse rate, duration, intensity, pitch are all design parameters that influence how small a target can be detected, how far away it can be detected, how accurately it can be tracked and resolved, and so forth. An advanced sonar design can vary these parameters to optimize the tracking.

Sonar design must also consider how to compensate for target motion and the resulting Doppler effect, erroneous reflections from clutter in the environment, and how to guide toward a moving target. There is also the possibility of imaging to determine what type of target it is.

Not surprisingly, there are many different sonar design strategies. Depending on the clutter environment, typical types of targets, and so forth, various design strategies might work better.

All of this is what we find in nature’s echolocation designs. Whales and bats have incredibly efficient and accurate tracking capabilities. We have developed sonar, but nature had it all along—the original sonar technology. In fact nature’s designs are better than our military equipment. Which is one reason why they are studied so closely.

Complexity at the molecular level

We have seen how complicated echolocation can be. Not surprisingly the molecular machines that help to make it happen are also highly complex. Prestin, a protein important in mammalian hearing, is a transmembrane protein in the outer hair cells of the cochlea. It serves as a frequency-selective amplifier in a sound system that works something like this.

As sound enters the ear, it deflects the outer hair causing tiny amounts of stretching or compression in the outer hair cells. There are channel proteins that sit in the membrane of these cells which are sensitive to such mechanical strain. These proteins provide a tunnel (or channel) across the membrane so that ions can easily cross, and the mechanical strain can cause the channels to open.

These channels are precisely designed to allow only certain types of ions to cross. For example, some channels allow the positively charged potassium ion to cross but not the positively charged sodium ion, and vice-versa.

When a channel opens, ions usually tend to cross through the membrane (either into the cell or out of the cell) because the ion concentration is not uniform, and because there is a voltage, across the membrane. Such differences in concentrations across the membrane, and the voltage, are actively maintained by the cell. They serve as a sort of battery whose energy can be tapped at any time by opening membrane channels.

When the incoming sound causes certain channels to open, the ions that cross cause a change in the membrane voltage. In the outer hair cells, this voltage change encourages negatively charged chlorine ions to exit the cell. They interact with the prestin protein, in the membrane, to cause a mechanical deformation resulting in the elongation of the cell.

In other words, the incoming sound, that caused the hair to move, ends up causing yet more hair movement, and this serves precisely to amplify the incoming sound. This amplification is greater at low sound levels, as it should be.

One of the interesting features of this system is the speed at which it operates. Obviously in order to amplify sound you need to respond as fast as the changes in sound occur. Protein motors often use chemical energy (such as the splitting of the ATP molecule) but that would be too slow for the ear's sound system. Instead, prestin uses the membrane's voltage. This electrical energy can be used much faster and prestin operates at microsecond rates. Here is how one paper summarized the system:

The exquisitely high sensitivity and frequency selectivity of the mammalian hearing organ originates from a mechanical amplification mechanism that resides in the organ of Corti, the sense organ of hearing in mammals. The gain provided by this amplification can reach as high as a thousandfold; it is highest at low sound levels and progressively diminishes with increasing sound energy.

Evolution has no explanation for the origin of this system beyond unfounded speculation, and this is only the beginning of the many molecular machines behind the echolocation systems found in nature.

Echolocation designs incongruent with evolutionary tree

It does not appear that random mutations are the cause of systems such as echolocation in bats and whales. Although this is an enormous problem for evolutionary theory, it is not the only one. As discussed above, there are many different types of echolocation designs. Evolution would predict that species that are thought to be close neighbors on the evolutionary tree would share similar echolocation designs. In other words, the echolocation designs should be congruent with the evolutionary tree. But they are not.

Whereas Darwin argued that the evolutionary tree explained nature’s designs rather than habitat, nature’s echolocation designs follow the exact opposite rule. Here is how one paper described it:

the animal’s habitat is often more important in shaping its call design than is its evolutionary history.

This is an enormous falsification of a key prediction of evolutionary theory.

Convergence at the morphological level

One consequence of this falsification is that evolutionists must construct highly complicated narratives for the origin of echolocation. For example, if evolution is true, then we must believe that the incredible echolocation ability found in some bats arose multiple times, by evolving independently. That’s not easy for evolutionists to explain. How could such uncanny design details repeat themselves via blind biological variation (no, natural selection doesn’t help)?

But this convergence problem goes far beyond the bats. Whales and bats share some uncanny similarities in how they track their prey. But if evolution is true, we would have to believe that their common ancestor had none of these capabilities. So in completely different parts of the world, in completely different environments, random mutations in these different species must have independently constructed the same ultra complex designs. As one report explained:

Though they evolved separately over millions of years in different worlds of darkness, bats and toothed whales use surprisingly similar acoustic behavior to locate, track, and capture prey using echolocation, the biological equivalent of sonar. Now a team of Danish researchers has shown that the acoustic behavior of these two types of animals while hunting is eerily similar.

If evolution is true then bats and whales would have been evolving independently for millions of years. And yet they both constructed a sonar capability which involves transmitting loud signals while receiving incredibly weak signals, adjusting the signal parameters in real time, processing the received signals, and so forth. They even share the same range of ultrasonic frequencies:

Bats and toothed whales (which include dolphins and porpoises) had many opportunities to evolve echolocation techniques that differ from each other, since their nearest common ancestor was incapable of echolocation. Nevertheless – as scientists have known for years – bats and toothed whales rely on the same range of ultrasonic frequencies, between 15 to 200 kilohertz, to hunt their prey.

And that similarity is in spite of the different environments:

This overlap in frequencies is surprising because sound travels about five times faster in water than in air, giving toothed whales an order of magnitude more time than bats to make a choice about whether to intercept a potential meal.

But that is not all. The bat and whale also use similar strategies for adjusting their signals while homing in on prey:

Bats increase the number of calls per second (what researchers call a “buzz rate”) while in pursuit of prey. Whales were thought to maintain a steady rate of calls or clicks no matter how far they were from a target. But the new research shows that wild whales also increase their rate of calls or clicks during a kill – and that whales’ buzz rates are nearly identical to that of bats, at about 500 calls or clicks per second.

It is another example of a complex design evolution can only speculate about, and once again the evolutionary tree fails to predict its pattern.

Convergence at the molecular level

Not only is incredible echolocation convergence evident at the morphological level, it is also seen at the molecular level. For instance, the prestin proteins in certain bat and whale species are more similar than evolution would expect. The massive prestin protein has too many amino acids that match up between these species. If one were to construct an evolutionary tree on the basis of prestin comparisons alone, then the bat and whale would be grouped together, and that cannot be correct.

This fact alone need not be a problem for evolutionists. They simply say that prestin is under the influence of strong selection. In other words, there are strong functional constraints on prestin that require more similarity, even between distant species, than we typically find in proteins.

In particular, researchers identified nine amino acids in prestin that seem to be responsible for the overly-consistent whale-bat matchup. Those nine amino acids must be under very strong selection. If one of them mutated then the biosonar system would not work well. The bat or whale would not survive, and that is why we don’t observe such changes. That is how natural selection works.

But if all nine amino acids are required, how did evolution stumble onto the design in the first place? It would be highly unlikely for the right nine amino acids to arise via blind mutations, at the same time.

But the convergence of molecular machines behind echolocation goes far beyond prestin. As one paper explains, “convergence is not a rare process restricted to several loci but is instead widespread”.

As one evolutionist admitted, “These results imply that convergent molecular evolution is much more widespread than previously recognized”. And another admitted that the results are astonishing:

We had expected to find identical changes in maybe a dozen or so genes but to see nearly 200 is incredible. We know natural selection is a potent driver of gene sequence evolution, but identifying so many examples where it produces nearly identical results in the genetic sequences of totally unrelated animals is astonishing.

Astonishing.

Venema’s argument for why echolocation is not a problem

This brings us to Venema’s argument for why echolocation is not a problem. Given the enormous problems briefly reviewed above, how exactly does Venema find echolocation to be evolution-friendly? We have looked at the problem of complexity of echolocation, including at the molecular level, the problem that echolocation designs are incongruent with the evolutionary tree and, as an example, the problem of convergence at both the morphological and molecular levels. Surely no objective scientist would find evidence for evolution in nature’s echolocation designs.

Would they?

Believe it or not, here is what Venema writes:

If you’ve ever stumbled through a pitch-black room and pulled yourself up short just before colliding with a wall or other object, you have employed your (very rudimentary) sense of echolocation. What you detected (though you might not have even consciously perceived it) was that sound waves were reflecting off the object in your way. All mammals can do this, but most (like us) do it very poorly. We need to be very close to the object in question before it is even possible for us to notice reflected sound, and more likely than not we won’t, and we’ll stub our toe or worse.

As it turns out, cetacean echolocation is a specifically tuned sense of hearing that is based on the same genes used for hearing in other mammals. One key gene used for hearing in all mammals is called the “prestin” gene, a protein involved with the specialized structures in the mammalian ear that vibrate in response to sound waves. In whales, the prestin gene is tuned to the ultrasonic frequencies that are better suited to echolocation. This tuning required only a few amino acid changes within the protein—an amount of change easily within the reach of the sort of molecular tinkering we saw for the insulin gene in various mammals. This tinkering within the prestin gene to tune it for echolocation was so easy to achieve, it would seem, that nearly identical changes occurred independently in the lineage leading to modern bats, who also use a prestin tuned to ultrasonic frequencies for echolocation. So even echolocation is not “new”—it too is remodeled from a standard mammalian sense of hearing.

This is a complete disaster. Venema’s equating of echolocation with his imagined ability to avoid a wall in a dark room, his transforming convergence to a virtue, his casting of echolocation as “easy to achieve” and the result of mere “tinkering,” and nothing new but rather simply a remodel of “standard mammalian sense of hearing,” is all standard evolutionary pretzel logic.

This is the evolutionary “just add water” view of biology where you add a couple of mutations and, poof, you have echolocation. But as we saw above, echolocation is not at all comparable to “standard mammalian” hearing. It doesn’t fit the evolutionary tree, and the convergence is astonishing and utterly unexpected and unexplained.

Venema’s attempt to explain away echolocation as a standard result of evolution is not even wrong.

When I saw that this new book had a section on echolocation I was keen to read it over. I have followed the echolocation research for years. I write about it, and often include it in presentations. I discuss the various ways the echolocation evidence contradicts evolution. So why would there be a section on this subject in this book promoting evolution? Have I missed something? Is there some fundamental aspect of echolocation I have missed? Is there a new paper I have missed, overturning the large body of research?

But as I read the section, I quickly realized it was nothing more than the usual evolutionary just-so story. A wholesale ignoring of well-established science, an embracing of imagined thought experiments that make no sense, and an utterly unscientific conclusion.

It isn’t even wrong.

Brand New Study on the Evolution of Photosynthesis

A “Very Advanced Capability”

How exactly is evolution a fact when, as the number two science journal in the world put it, “How and when Cyanobacteria evolved the ability to produce oxygen through photosynthesis is poorly understood”? Or as evolutionist Robert Blankenship admitted, “The whole question of the origin of cyanobacteria has long been a mystery because they kind of just appeared out of the tree of life with this very advanced capability to do oxygenic photosynthesis without any apparent forebears.”

If the cyanobacteria that do photosynthesis “just appeared” with this “very advanced capability” and “without any apparent forebears,” and if how and when they evolved photosynthesis “is poorly understood,” then just how is it that evolutionists are so certain that evolution is a fact?

What am I missing here?

It is not as though photosynthesis is a tangential capability or a minor event in the so-called “evolutionary history” of life. As the leading science writer Charles Q. Choi put it, “One of the most pivotal moments in Earth’s history was the evolution of the photosynthetic life that suffused air with the oxygen on which virtually all complex life on the planet now depends.”

Nor is it as though photosynthesis is a simple capability, in no need of explanation for how it possibly could have arisen by random mutations. Anyone who has studied photosynthesis even superficially knows it is incredibly complex. And for those who have studied in greater detail, it only gets worse. The molecular machines and their exquisite, finely-tuned, functions are truly amazing. It doesn’t “just happen.”

Even evolutionists, who are always trying to explain how easy it would be for biology’s wonders to arise by happenstance, admit to the complexity of photosynthesis. As Blankenship put it, photosynthesis is a “very advanced capability.” Similarly, Woodward Fischer agreed that the evolution of photosynthesis would be “very challenging”:

It took a substantial unfolding of evolutionary time before oxygenic photosynthesis developed, perhaps because, as we know, it was a very challenging biochemistry to develop.

Nor is it as though the evidence we do have suggests any kind of a straightforward evolutionary development of photosynthesis.

If evolution is true, then we must fire up fresh rounds of evolution’s fake news, including incredible convergences and massive horizontal, or lateral, gene transfer and fusion. Round up the usual suspects:

The phylogenetic relationships of these prokaryotes suggest that the evolution of aerobic respiration likely occurred multiple times. This, along with evidence that the modern photosynthetic system apparently arose through the lateral gene transfer and fusion of two photosynthetic systems

This is absurd. Convergence, horizontal gene transfer, and fusion are all made up mechanisms to fix the problem that the scientific evidence contradicts evolutionary theory. This isn’t making sense.

But it gets worse.

Not only are evolutionists forced to draw from their army of phony explanatory mechanisms, but they are left with the proverbial “missing link.” The problem is, from where did the photosynthesis come? It couldn’t have come from the purported common ancestor via descent, and it “just appeared” with this “very advanced capability.”  So evolutionists have to usher in their horizontal gene transfer story.

But from where?

From where did the incredible battery of genes—that would just happen to team up and create the all-time incredible capability of photosynthesis—come? Conveniently for evolutionists—and here’s one of the beauties of being an evolutionist—they can never know. Like Flew’s gardener, evolutionists are certain that some “missing link” organism somehow had photosynthesis up and running, or just happened to have the crucial genes just lying around, but we likely will never observe that organism because it has long since become extinct.

Oh how convenient. Some mysterious organism did it. We’ll never know just how photosynthesis evolved because the organism where it happened has long since gone extinct, billions of years ago. Since then, it just luckily passed the technology around for other organisms to have, such as the cyanobacteria. Choi and Fischer explain:

The fact that Oxyphotobacteria possess the complex apparatus for oxygenic photosynthesis while their closest relatives do not suggests that Oxyphotobacteria may have imported the genes for photosynthesis from another organism via a process known as lateral gene transfer. It remains a mystery what the source of these genes was, “and because it happened long ago, it's pretty likely that the group may actually have gone extinct,” Fischer said.

Can I be an evolutionist too?

Photosynthesis is crucial to life and incredibly complex, evolutionists haven’t a clue how it could have evolved, it doesn’t fit the evolutionary common descent model and “just appeared” without a hint of where it came from, evolutionists are forced to make up a long just-so story to try to explain it, their story can’t be falsified because the origin of photosynthesis has long since disappeared, and on top of all this, evolutionists insist their theory is a fact, beyond all reasonable doubt.

This is hilarious. It is like something out of a Monte Python skit. Evolution loses every battle, but manages to win the war because, after all, it’s right.

Religion drives science, and it matters.

Here’s That Paper on MicroRNAs in Brown Algae

“No evidence of conservation”

MicroRNAs are small RNA gene products, typically consisting of 20-24 nucleotides, which help to regulate protein synthesis, for example by pausing or halting the ribosome translation process. Like the small drill bit which is inserted into the much larger drill tool, the small microRNAs are attached to a much larger molecular machine that performs the regulation. The microRNA role is to help the molecular machine recognize the correct RNA target. In other words, instead of the cell having to construct a large quantity of different molecular machines to perform the regulatory role on a large quantity of RNA targets, the cell can construct a more generic type of molecular machine, and then simply attach the instructions—the microRNA—as needed. This design approach requires the existence of these two entities: the big molecular machine and its little instruction set. Remove either entity, and this particular regulatory process isn’t going to happen. That does not fit the evolutionary narrative. According to evolution you need a slow, gradual buildup of designs, not all-or-none scenarios. But not surprisingly biology is chocked full of the latter, and so with evolution we must say that the different parts just happened to arise, perhaps serving some other roles, and then just luckily they worked fantastically together to achieve a new function. MicroRNAs are yet another finding that must be force-fit into evolutionary theory. But this irreducible complexity is only the beginning of the problem. With microRNAs, it only gets worse.

A completely different problem that microRNAs pose for evolutionary “theory” is that microRNAs do not fit the common descent pattern. As a recent paper admitted:

There is no evidence of conservation of miRNAs between the phylogenetic groups, indicating that miRNA systems evolved independently in each lineage

Evolved independently?

In other words, microRNAs do not fit the evolution model. The evidence contradicts the theory. Of course one can always make up an explanation. In this case, we say that the microRNAs “evolved independently.”

There you go, problem solved.

But let’s be honest—this is not indicated by the evidence. When the paper states that there is no evidence of conservation of miRNAs between the phylogenetic groups, thus “indicating” that miRNA systems evolved independently, it is simply misrepresenting the science.

There is precisely zero scientific evidence that microRNAs “evolved independently.”

Zero.

That is not my opinion. That is not conjecture. That is scientific fact.

Evolutionists talk a lot about scientific “fact.” They insist evolution is a scientific “fact.” But let’s just be honest. What is a scientific fact here is not evolution, but rather the exact opposite. The “fact” is the microRNAs show “no evidence of conservation.”

That fact does not “indicate” evolution, it contradicts evolution.

Let’s just be honest. For once.

The paper finds yet another example of this failure in the microRNAs in brown algae. The study investigated the microRNAs in the species, Saccharina japonica, and compared them to previously investigated microRNAs, including those in a different brown algae species. Their findings were, as usual, “surprising.” The microRNAs in the two brown algae species were different.

Completely different.

There was not a single pair of microRNAs, between the two species, that showed any sign of statistically significant sequence similarity.

Interestingly, the microRNAs in the two species did generally share some structural and genomic features. So the evolutionists had to conclude that the microRNAs in the two species evolved from a common ancestor, but then their respective sequences evolved like crazy, leaving zero trace of sequence similarity.

This. Makes. No. Sense.

Here how the paper spun the results:

Surprisingly, none of the S. japonica miRNAs share significant sequence similarity with the Ectocarpus sp. miRNAs. However, the miRNA repertoires of the two species share a number of structural and genomic features indicating that they were generated by similar evolutionary processes and therefore probably evolved within the context of a common, ancestral miRNA system. This lack of sequence similarity suggests that miRNAs evolve rapidly in the brown algae (the two species are separated by ∼95 Myr of evolution). The sets of predicted targets of miRNAs in the two species were also very different suggesting that the divergence of the miRNAs may have had significant consequences for miRNA function.

“Probably evolved within the context of a common, ancestral miRNA system”? So what does “within the context” mean?

The answer is this is a meaningless cover phrase that masks the fact that the evidence contradicts the theory. It is evo-speak for “We don’t know what we’re talking about.” A more polite description is “hand-waving.”

A less polite, and more accurate description won’t be repeated here.

I will now consider the elephant in the room: Why is evolution being used to interpret the results in the first place? The theory is superfluous. It is redundant. It is vacuous. It is non-parsimonious. It is meaningless.

The theory does nothing to help us understand, interpret, elucidate, guide, or formulate meaningful predictions. Its only justification is itself.

We use the theory of evolution to interpret the results because the theory is true. And how do we know it is true? Because it is true?

The theory is self-referential. It is circular. It is famous for being famous.

It is a hold-over from the Epicureans of antiquity, the schoolmen of the Middle Ages, the rationalists of the seventeenth century, and the Darwinists today, and it has made a mockery of science.

Religion drives science, and it matters.

h/t: The Man

About Those Placental Regulatory Genes

Evolution Recruits and Deploys Genes

Last time we noted the teleological ideas and language used to describe the hypothetical evolution of several genes that are expressed for a mere few hours, in the early development stages of many placental mammals. And by early we mean when we consist of only 8-16 cells. The teleology is not a mere slip-up. As we have documented many times, it is a common thread running throughout the genre of evolutionary literature. It is needed to make sense of the data, because evolution doesn’t.

That teleological language appeared in an article about the research. Not too surprisingly, teleological language also appears in the research journal paper as well. To wit:

A small number of lineage-specific tandem gene duplications have occurred, and these raise questions concerning how evolutionarily young homeobox genes are recruited to new regulatory roles. For example, divergent tandem duplicates of the Hox3 gene have been recruited for extra-embryonic membrane specification and patterning in dipteran and lepidopteran insects, a large expansion of the Rhox homeobox gene family is deployed in reproductive tissues of mouse, and duplicates of TALE class genes are expressed in early development of molluscs.

Two of the evolutionists’ favorite words are “recruited” and “deployed.” They sound so active. What better way to obviate the rather awkward problem that, if evolution is true, all biological variation must be random with respect to fitness (a claim which, by the way, has been falsified so many times we stopped counting). Evolutionists nonetheless continue to spread this fake news.

And no teleological idea would be complete with the mandatory infinitive form (“for … specification and patterning”). Religion drives science and it matters.

The Sea Anemone: A Proverbial Precambrian Rabbit

A Contradiction of Another “Widely Held Belief”

When asked what evidence would disprove evolution, the famous 20th century evolutionist J.B.S. Haldane is famously said to have responded “a fossil rabbit in the preCambrian.” In other words, a fossil rabbit would have to be found in strata dating to long before rabbits, or mammals for that matter, are normally found. And by “long,” we’re talking about somewhere between roughly one-half a billion years to several billion years. It was an exercise in what philosophers refer to as theory protectionism—erecting insurmountable protective barriers around a theory. The fossil record was sufficiently understood in Haldane’s day to know that such as finding was highly unlikely. And it was also known that much less astounding, and more feasible, fossil findings would (or at least should) pose serious problems for evolutionary theory. In fact there are many such contradictions in the rocks, but if a rabbit in the preCambrian is the evidential standard, then evolution is comfortably safe. Haldane’s preCambrian rabbit response was also an exercise in naïve falsificationism—the thinking that a single finding is going to take down a theory so deeply imbedded in our thinking, and so confidently held to be true. In fact evolutionary theory has survived myriad contradictory evidences of at least as much severity as a preCambrian rabbit without so much as skipping a beat. Consider, for example, the genome of the starlet sea anemone, Nematostella vectensis. Here is how one report summarized it:

The genome of the sea anemone, one of the oldest living animal species on Earth, shares a surprising degree of similarity with the genome of vertebrates, researchers report in this week's Science. The study also found that these similarities were absent from fruit fly and nematode genomes, contradicting the widely held belief that organisms become more complex through evolution. The findings suggest that the ancestral animal genome was quite complex, and fly and worm genomes lost some of that intricacy as they evolved.

In other words, it was the genomic equivalent of Haldane’s preCambrian rabbit—a preCambrian genome had, err, all the complexity of species to come hundreds of millions of years later. In other cases it has more complexity than species such as worms and flies which, according to evolution, must have lost enormous amounts of genetic complexity.

The lead author of the sea anemone study explained that “We have this basic toolkit now for the whole animal kingdom.” Of course the idea of foresight is contradictory to evolutionary theory. As one evolutionist admitted, it is surprising to find such a “high level of genomic complexity in a supposedly primitive animal such as the sea anemone.” It implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.”

Or as another evolutionist put it:

It is commonly believed that complex organisms arose from simple ones. Yet analyses of genomes and of their transcribed genes in various organisms reveal that, as far as protein-coding genes are concerned, the repertoire of a sea anemone — a rather simple, evolutionarily basal animal — is almost as complex as that of a human.

None of this makes any sense on evolutionary theory. Of course it is “commonly believed” by evolutionists “that complex organisms arose from simple ones.” That would be rather fundamental to the theory. And yet we repeatedly find early complexity. This is another example of how resistant evolution is to testing and falsification.

The science contradicts the theory.

Graur and Martin Explain Monumental Failure in Molecular Clock Uncertainty Estimate

Mirages Contain No Water

The scientific evidence contradicts evolutionary theory. Consider, for example, the problem of tracing out the mammalian evolutionary tree. According to evolution similar species should be neighbors on the evolutionary tree. For example, the flying squirrel and sugar glide certainly are similar—they both sport distinctive “wings” stretching from arm to leg. Shouldn’t they be neighboring species? The problem is that, while they have incredible similarities, they also have big differences. Most notably, the flying squirrel is a placental and the sugar glider is a marsupial. So they must be placed far apart in the mammalian evolutionary tree. The problem in this example is that different characters, across the two species, are not congruent. Here is how evolutionists rationalize the contradiction:

Flying squirrels and sugar gliders are only distantly related. So why do they look so similar then? Their gliding "wings" and big eyes are analogous structures. Natural selection independently adapted both lineages for similar lifestyles: leaping from treetops (hence, the gliding "wings") and foraging at night (hence, the big eyes).

This is a good example of how contradictory evidence drives evolutionists to use irrational just-so stories. Natural selection cannot “adapt” anything. Natural selection kills off the bad designs. It cannot influence the random mutations which must, somehow, come up with such amazing designs. This is the hard reality, but in order to rationalize the evidence, evolutionists must resort to this sort of teleological language, personifying and endowing natural selection with impossible powers. As usual, the infinitive form (“for similar lifestyles”) is a dead giveaway. Natural selection becomes a designer.

This example is by no means exceptional. In fact, this sort of incongruence is rampant in biology. Evolutionists have attempted to deny it in the past, but it is undeniable. It is the rule rather than the exception. As one recent paper, entitled “Mammal madness: is the mammal tree of life not yet resolved?” admitted:

Despite the keen interest in mammals, the evolutionary history of this clade has been and remains at the center of heated scientific debates. In part, these controversies stem from the widespread occurrence of convergent morphological characters in mammals.

In addition to the morphological characters, evolutionists make extensive use of molecular sequence data using the so-called molecular clock method. The molecular clock method, however, has a long history of problems. You can see here and here how the molecular clock method has failed, but an entirely different problem is the non-scientific, misuse, of this approach. Consider how evolutionists have misused it in the mammalian evolutionary tree problem:

Two articles in this issue address one such node, the root of the tree of living placental mammals, and come to different conclusions. The timing of the splitting event—approximately 100 Ma based on molecular clocks—is not in debate, at least among molecular evolutionists. Rather the question is the branching order of the three major lineages: afrotherians (e.g., elephants, manatees, hyraxes, elephant shrews, aardvarks, and tenrecs), xenarthrans (sloths, anteaters, and armadillos), and boreoeutherians (all other placentals; fig. 1).

Such overly optimistic interpretation of the molecular clock results unfortunately has a long history. Dan Graur and William Martin have showed how such over confidence became common in evolutionary studies. They write:

We will relate a dating saga of ballooning inapplicability and snowballing error through which molecular equivalents of the 23rd October 4004 BC date have been mass-produced in the most prestigious biology journals.

Graur and Martin chronicle how a massive uncertainty was converted to, err, zero, via a sequence of machinations, including the arbitrary filtering out of data simply because they do not fit the theory:

A solution to the single-calibration conundrum would be to use multiple primary calibrations because such practices yield better results than those obtained by relying on a single point. Indeed, it was stated that “the use of multiple calibration points from the fossil record would be desirable if they were all close to the actual time of divergence.” However, because no calibrations other than the 310 +/- 0 MYA value were ever used in this saga, the authors must have concluded that none exists. This is not true. Moreover, deciding whether a certain fossil is “close to the actual time of divergence” presupposes a prior knowledge of the time of divergence, which in turn will make the fossil superfluous for dating purposes.

Not only are uncooperative data discarded, but tests are altogether dropped if they don’t produce the right answer:

The results indicated that 25% of the homologous protein sets in birds and mammals failed the first part of the consistency test, that is, in one out of four cases the data yielded divergence times between rodents and primates that were older than those obtained for the divergence between synapsids and diapsids. One protein yielded the absurd estimate of 2333 MYA for the human–chicken divergence event, and as an extreme outlier was discarded. For the remaining proteins, the mean bird–mammalian divergence estimate was 393 MYA with a 95% confidence interval of 471-315 MYA. In other words, the 310 MYA landmark was not recovered. Because neither condition of the consistency test was met, it was concluded that the use of the secondary calibration is unjustified.

In one example, a monumental dating uncertainty, roughly equal to the age of the universe, is magically reduced by a factor of 40:

Were calibration and derivation uncertainties taken into proper consideration, the 95% confidence interval would have turned out to be at least 40 times larger (~14.2 billion years).

Now of course there is little question that evolutionists will resolve their evolutionary tree problems. A combination of filtering the data, selecting the right method, and, of course, deciding there is nothing at all improbable about natural selection “adapting” designs in all manner of ways, can solve any problem. But at what cost? As the paper concludes, “Unfortunately, no matter how great our thirst for glimpses of the past might be, mirages contain no water.”

What Are They Teaching at Washington University? S. Joshua Swamidass and the Chimp-Human Divergence

Stunning Evidence For Common Ancestry

I once had a rare and valuable baseball card I wanted to sell. I placed an ad and was shortly contacted by a collector. But to my dismay he wasn’t interested. He had probably looked at hundreds of baseball cards and it only required one look for him to know that my treasured card held no value for him. He did not attempt any negotiating tricks, just a polite “thank you” and off he went. I would have felt better about the encounter if he had tried to haggle down the price. For I would have had the comfort of knowing my card held at least some value. Instead, there was no price discovery—apparently the card was worthless.

I too am a collector of sorts. And like that baseball card collector I have looked at hundreds of specimens. No matter how unlikely the source or the venue, I will go there and have a look. And in short order, I will know exactly what I am looking at, and if there is any value there. But unlike the baseball card collector, my subject is not something you can touch. What I am interested in are the arguments and evidences for evolution. Ever since Darwin, evolutionists have insisted that their idea is undeniable—beyond all reasonable doubt. I find that complete certainty to be fascinating. So I search, find, analyze and categorize every justification and explanation for that conclusion that I can find.

My goal is to find the strongest, most powerful, such arguments and evidences, and to understand how we can have such certainty. This brings us to S. Joshua Swamidass’s recent article, Evidence and Evolution where Swamidass explains, in typical fashion, that the evidence for evolution is powerful and compelling. Swamidass describes the evidence as stunning. As a professor in the Genomic Medicine Division at Washington University, Swamidass deserves to be listened to. This is definitely a specimen I want to have a look at.

In his article, Swamidass’ focus is human evolution. Evolutionists believe that we humans evolved from a small ape-like creature and that our closest relative on the evolutionary tree is the chimpanzee. The chimpanzee must be our closest relative, they reason, because the chimp’s genome is closest to ours, and according to evolution, genetic mutations are the fuel behind evolutionary change.

The problem with this reasoning is that the chimpanzee is not very similar to humans according to many other measures. There are enormous differences between the two species. Simply put, from an evolutionary perspective the genetic data are not congruent with the other data. Swamidass’ evidence will need to overcome this obvious problem.

But that’s not all.

The basic idea of humans arising via a long series of genetic mutations is, itself, not indicated by the science and unlikely to say the least. Remember, the mutations have to be random. According to evolution, you can’t have mutations occurring for some purpose, such as creating a design. And natural selection doesn’t help—it cannot induce or coax the right mutations to occur. This makes the evolution of even a single protein, let alone humans, statistically impossible. So this is another enormous problem Swamidass’ evidence will need to overcome.

But that’s not all.

The incredible designs in the human body are not the only thing those random mutations have to create—they will also have to create human consciousness. Evolutionists may try to explain consciousness as an “emergent” property that just luckily arose when our brain somehow evolved. Or they may try to explain that consciousness is really no more than an illusion. But these are just more demonstrations of anti realism in evolutionary thought. Evolutionary theory constructs mechanisms and explanations that do not correspond to the real world. So this is another problem Swamidass will need to overcome.

But that’s not all.

In recent decades the genomes of humans and chimps have been determined, and they make no sense on evolution. One of the main problems is that the genes of the two species are almost identical. They are only about 1-2% different and, if you’re an evolutionist, this means you have to believe that the evolution of humans from a small, primitive, ape-like creature was caused by only a tiny modification of the genome.

This goes against everything we have learned about genetics. You can insert far greater genetic changes with far less change arising as a consequence. It makes little sense that tiny genetic changes could cause such enormous design changes to occur. This is yet another problem for Swamidass to overcome.

But that’s not all.

Not only is evolution limited to tiny genetic modifications to create the human, but the majority of those modifications would have had to be of little or no consequence. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

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

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.” This is no way to evolve the most complex designs in the world and it is yet another problem for Swamidass to overcome.

But that’s not all.

The supposed divergence rate between chimps and humans also has an unexplainable variation towards the ends of most chromosomes. This is another problem that seems to make no sense on evolution, which Swamidass must explain.

But that’s not all.

This supposed divergence rate between chimps and humans also has an unexplainable variation that correlates with chromosomal banding. Again, this makes no sense on evolution. Why should the chimp-human divergence vary with the banding pattern? Evolutionists have only just-so stories to imagine why this would have happened, and it is another problem for Swamidass to address.

But that’s not all.

This supposed divergence rate between chimps and humans is not consistent with the supposed divergence rate between the mouse and rat. The mouse-rat divergence is about an order of magnitude greater than the chimp-human divergence. And yet the mouse and rat are much more similar than the chimp and human. It makes no sense on evolution. In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:

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

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

Another approach is to ignore the morphological similarities and reason from the number of generations available to produce the genomic differences between the mouse and rat. The mouse-rat divergence date is estimated by evolutionists to be older than the chimp-human divergence date. Furthermore, the lifespan and generation time for mice and rats are much shorter than for chimps and humans. From this perspective, and given these two effects, one would conclude that the mouse-rat genetic divergence should be much greater—at least two orders of magnitude greater—than the chimp-human genetic divergence. But it isn’t. It is only about one order of magnitude greater.

So either way the mouse-rat comparison does not help to explain things and is another problem for Swamidass to explain.

Swamidass arguments and evidences

The science makes no sense on evolution. If we begin by assuming chimps and humans share a common ancestor, we end up with all kinds of contradictions and failures. So what exactly are Swamidass’ arguments and evidences? How is it that he is so certain? What is it in the data that he finds to be so stunning? And most importantly, how does he resolve the above problems?

Well, he doesn’t.

Astonishingly, Swamidass doesn’t even mention the above problems. It is as though they don’t exist. After some stories and high claims of certainty, here is what Swamidass says:

As predicted by common ancestry, human and chimpanzee genomes are extremely similar (greater than 98% similarity in coding regions), much more similar than we would expect without common descent. Remarkably, just as predicted by the fossil record, humans are about 10 times more genetically similar to chimpanzees than mice are to rats.

First, the high chimp-human genomic similarity was not predicted by common ancestry. No such prediction was made and no such prediction is required by common ancestry. Common ancestry would be just fine with very different levels of similarity than 98-99%. In fact, this high similarity makes no sense on evolution, for several of the reasons given above.

Swamidass’ claim that this evidence is a stunning confirmation of common ancestry is utterly at odds with the science. It is in stark contrast to the scientific facts.

Second, Swamidass’ claim that mouse-rat divergence, compared with the chimp-human divergence, is “just as predicted by the fossil record” is also blatantly false. While evolutionists can always combine various explanatory mechanisms to rationalize just about any comparison, that does not make for stunning evidence that is “just as predicted.”

Finally, the real strength of Swamidass’ argument lies in its metaphysics. The professor states that the chimp-human genome comparison is “much more similar than we would expect without common descent.”

Without common descent?

The evolutionist has just made an unbeatable (and unfalsifiable) argument.

This is not science. Swamidass’ claim about what is and isn’t likely “without common descent” is not open to scientific scrutiny.

Scientists, qua scientists, do not have knowledge of all possible explanations for the origin of life. This is why scientists, qua scientists, make statements about theories, not about the complement of a theory. A scientist cannot know that something is unlikely “without” his theory. That implies knowledge of all other possible theories. And that knowledge does not come from science.

This is the strength of Swamidass’ argument. Notice that with this metaphysical knowledge, all of the scientific problems melt away. No wonder he does not address them. They are inconsequential. At worst, they are simply interesting puzzles. The truth of the matter is already known.

If Swamidass is correct then, yes, of course, the genomic data must be strong evidence for common ancestry. But it all hinges on his metaphysics. This is not about science. It never was.

[Ed; Removed sentence about the orangutan, 1-Mb segments section, and the gene functionality section. Please see the followup article here.]

RNA-Directed DNA Methylation: The Evolution of a Complex Epigenetic Pathway in Flowering Plants

Nada

The problem with epigenetic mechanisms is that they respond to future, unforeseen, environmental challenges. They don’t work in the present, and so even if random mutations somehow created such mechanisms, they would not be selected for. In other words, epigenetic mechanisms contradict evolutionary theory—there is no fitness improvement at the time of origin by random mutations, so there is no selection. Nor do evolutionists have an explanation for this—they don’t even try. Consider a paper discussing a particular epigenetic mechanism subtitled: “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.”

The paper discusses a complicated cellular process in which different segments of DNA are copied (creating RNA transcripts). The RNAs work together to methylate the DNA at a particular location. The methylation “mark” helps to regulate gene expression. But how did this epigenetic mechanism evolve?

This epigenetic mechanism involves a small army of molecular machines. For instance, the different RNAs are transcribed, from the DNA, by different copying machines. These copying machines consist of a dozen protein subunits. The paper states that two of the copying machines—which are central to the epigenetic mechanism—each evolved from a third copying machine. Why?

The idea of the two copying machines evolving from the third copying machine is problematic because there are significant differences between them. The paper gives no justification for such an unlikely event. It gives no justification because there is none, save for the presupposition that evolution is true. Under evolutionary theory it must have occurred.

In other words, there is no empirical evidence that the two copying machines evolved from the third copying machine and there are enormous problems with the idea. But it is taken as a given because evolution is assumed to begin with.

The point here is that in attempting to explain the evolution of a complex epigenetic pathway the paper presupposed evolution a priori.

Similarly, the paper states that the two copying machines “are evolving rapidly.” Again, where did this come from? Does the science actually show this to be true? Does the science even merely provide any evidence at all for this astonishing claim?

Again, no and no.

Nowhere does the science demonstrate or prove that the two copying machines “are evolving rapidly.” In fact, the science doesn’t even provide any evidence at all for this.

Nada.

What the science shows is that the proteins in the two copying machines have significant differences compared to the corresponding proteins in the third copying machine. The two copying machines are more different from the third copying machine, than would normally be expected if they had evolved from that third copying machine.

But since evolution is assumed to be true to begin with, then those two copying machines must be “evolving rapidly.”

Again, the claim is driven by the belief that evolution is true. There is no empirical evidence that the two copying machines are evolving rapidly, let alone that they even evolved at all.

This is all dogma. There is no science here.

The paper then spends considerable effort attempting to reckon with the various problems that arise when their evolutionary history is assumed. There are duplication events and introns are mysteriously inserted. There are fusion events to explain unexpected differences, and other cases are simply unknown. There must have been a complex series of evolutionary events the reasons for which “remain obscure,” and the evolutionary origin of one gene is “a mystery.”

It is a long sequence of just-so stories. A long sequence of special events just happened to happen, which luckily produced this new epigenetic mechanism.

And then, after all of this, it would not be selected for. All of these events, and the resulting epigenetic mechanism would not improve the evolutionary fitness.

This evolutionary tale is not supported by the empirical evidence. Instead, it is supported by the prior assumption that evolution occurred.

Andrew Xiao Confirms Adenine Methylation in Mammals—Thinks it Evolved

This Isn’t Working

Evolutionists are going to need a bigger rug as Yale professor Andrew Xiao now has a new pile of stuff he is absurdly trying to ascribe to evolution. Xiao’s team has confirmed that in mammals the fundamental epigenetic signal—the methyl group—is sometimes attached to a second type of DNA base. DNA is made up of four types of bases (cytosine [C], guanine [G], adenine [A] and thymine [T]) and, as in the lower species, methyl groups are sometimes attached to adenine in mammals as well.

Such epigenetic signals help to cause directed adaptation in organisms—the ability to rapidly respond to new environmental challenges. And this new finding means that not just with cytosine, but with adenine as well, random mutations must have created the proteins (i) to attach the methyl groups and (ii) to remove them.

Both types of proteins are needed to make the epigenetic response work. With either protein alone, you just have chaos.

You also need the network of signals and regulation to set these proteins in action at the proper times, and only at the proper times. And of course these epigenetic signals must somehow influence the transcription process.

This isn’t going to happen with random mutations. And, no, natural selection doesn’t help.

But this is only the beginning.

In the lower species, attaching the methyl group to adenine caused gene activation. But in the mammals studied, the new research found that adenine methylation caused gene inactivation. In other words, the exact same methylation signal attached to the same nitrogen atom in the same base, somehow reversed polarity.

That makes no sense. Any change in polarity in the circuitry logic would throw the system into chaos. Imagine your thermostat now works in reverse. When you adjust the temperature lower, the heater rather than the air conditioner, turns on. You wanted it to be cooler, but instead it got even hotter.

Such a change in polarity in the circuitry would have to take place simultaneously, at several functions throughout the logic. This isn’t going to happen with random mutations. And, no, natural selection doesn’t help.

This is all a bad joke. The science makes no sense on evolution, and like the drunk at the party, evolutionists are the only ones who don’t get it.