A Pond-Dwelling, Single-Celled Organism Does Amazing Genetic Engineering

One of Nature’s Attempts to Become More Complex

A new paper was published last week on a remarkable single-celled organism, Oxytricha trifallax, that has two nucleus’ and 16,000 chromosomes (recall that humans have 46). The organism uses one nucleus to store its active DNA and the other nucleus to store an archive of the genome. Amazingly, Oxytricha trifallax, disassembles the archived copy into a quarter-million pieces and then rapidly reassembles them into a new and improved version. This reassembly occurs at mating time as the organism and its mate exchange about half their genome.

Creating and maintaining a backup copy of the genome, disassembling that copy, integrating disassembled material from an external source, reassembling the whole thing to produce improved, rejuvenated chromosomes—it all just smacks of blind mutations.

Incredibly evolutionist Laura Landweber explains that Oxytricha trifallax is “one of nature’s early attempts to become more complex despite staying small … People might think that pond-dwelling organisms would be simple, but this shows how complex life can be.”

One of nature’s early attempts to become more complex? This is a typical example of the underlying Aristotelian thought that pervades evolution. Evolutionists have no idea how Oxytricha trifallax amazing capabilities could have evolved by random variation such as mutations. So they describe it in teleological language. This isn’t science.

Of course the idea that Oxytricha trifallax evolved doesn’t come from the science. It comes from a dogmatic commitment to evolution.

Religion drives science, and it matters.

When I Pointed Out the De Novo Gene Evidence an Evolutionist Came Unglued

Primitive Thinking

It is interesting that evolutionists, who believe they came from primitive apes, display a certain primitive thought in their communications. The latest example is an evolutionist who criticized a book skeptical of evolution. The book made the point that fundamentally new genes are unlikely to have evolved by the usual random change and natural selection mechanisms. The book elaborated on this problem at length. But the evolutionist retorted that this was all wrong:

[The book] claims that the origin of new genes is a mystery, when in fact it is basically a solved problem (as long as you aren’t talking about the origin of the very first genes at the origin of life—and allegedly this book is supposed to be about the Cambrian Explosion, not the origin of life).

In other words, aside from the origin of life, the origin of fundamentally new genes is not a mystery and is basically has been solved by evolutionists.

That is, of course, false. When I pointed out the evidence the evolutionist harshly criticized me.

Look up jingwei and sdic and the literature on their origin. Look up Long et al. 2003. Why can’t you even get these totally obvious basic points right?

The problem is jingwei and Sdic are not fundamentally new genes, but rather have significant similarities to parts of other genes. And the paper he cited did little to resolve this question of how fundamentally new genes arose. In fact, about the only thing the paper did say about the evolution of such genes is that it is rare. That view has since been discarded as too many of these fundamentally new genes have been discovered.

So the evolutionist cited two irrelevant genes and a paper that gave an outdated view, and accused me of missing “totally obvious basic points.”

When I pointed all this out, the evolutionist tried to walk back his points. He claimed that I was the one who brought up fundamentally new genes, and that he merely was referring to genes that are mostly rearrangements of other genes. “Shame!” he vindictively concluded.

And there we have it. At this point the evolutionist is in checkmate. For he has just forfeited his claim that the book is all wrong, that the evolution of new genes is a solved problem, and by extension that evolution is a fact. He cannot now say, “Oh, but I was also referring to fundamentally new genes also.”

He has made it clear that the book’s criticism is on solid ground. For as I pointed out (here and here), the evolutionary reasoning that such genes evolved by the usual random mutations and selection is circular. And the explanations for how this could have happened is little more than hand waving. Even evolutionists agreed it was impossible until, that is, the existence of such genes could not be denied. At that point evolutionists had to come up with some sort of explanation. The result is a speculative idea that relies on serendipity and ignores known, enormous problems.

A theory cannot fail to explain a plethora of fundamental observations and be a fact. Not a scientific fact, at least.

So will the evolutionist admit to any of these things? Will he agree that evolution is not a fact? Of course not. I’ll take the shame and the blame, and all the harsh criticism, if we can just agree on the overwhelming scientific evidence which checkmates evolution. Evolution is not a fact, and it never was.

Here is the Latest Example of Evolution Undermining Law

A Falsification of Evolution Becomes a Legal Premise

Evolution is not merely a scientific mistake. It is not a theory gone wrong, started by a guy in 1859. Evolutionary thinking was alive and well when Charles Darwin codified it in the emerging life sciences, for it had been developed and promoted by theologians and philosophers since the seventeenth century. If you understand that history, then today’s world makes much more sense. It is often said that evolution is the most influential scientific theory, but that is because evolution isn’t just a scientific theory, it is a broader world view. So with the dominance of evolution comes a wide array of influences, in government and in society, and across the political spectrum. Another example of this came last week when the United States Court of Appeals for the Seventh Circuit ruled that laws in Indiana and Wisconsin, defining marriage to be between a man and a woman, are unconstitutional.

While it is no secret that evolutionary premises now inform opinions across the political spectrum, this decision (written by a Reagan appointee) made those premises explicit as it cites evolutionary research and is based on the assumption that evolution is true. Its point is that homosexuality is a result of evolution so therefore gay marriage should be a legal right.

Should we point out that evolution is scientifically flawed? Or should we point out that homosexuality, the usual mental gymnastics of evolutionists notwithstanding, makes no sense under evolution? Remember that part about reproductive success?

It is all reminiscent of Judge John Jones—exalted as one of Time magazine’s 100 Most Influential People of the Year—hilariously revealing that he actually wanted to see Inherit the Wind a second time in preparation for the 2005 Dover case, over which he presided, because, after all, the film puts the origins debate into its proper “historical context.”

Proper historical context? You’ve got to be kidding.

What a classic mistrial. Jones had been so indoctrinated by the Warfare Thesis that he actually believed the evolutionary propaganda to be historically accurate. If the perfect crime is the one that is never discovered, the perfect propaganda is the one that is never understood. Jones later reminisced about the trial, unbelievably explaining that “I understood the general theme. I’d seen Inherit the Wind.”  Jones was not educated, he was brainwashed.

And unfortunately Jones is not simply a lone nut. Legal expert Andrew Cohen not only gave high praise to Inherit the Wind, but absurdly called it “one of the great trial movies of all time.” The movie is a fictional construct, based on the fictional Warfare Thesis erected by evolutionists, and long since discredited by historians. Are they showing it in law schools these days?

So the Seventh Circuit’s explicit premise of evolution is not surprising. It is simply a confirmation that dangerous ignorance pervades the highest levels of power.

Evolutionists are Doubling Down on De Novo Gene Evolution

They Win Again

How can a new protein-coding gene emerge from a random stretch of DNA? According to evolutionists this occurs via the usual random mutations and natural selection. In fact, as I explained last time, evolutionists are saying this is “basically a solved problem.” But such de novo gene evolution is not anywhere close to a solution. Even evolutionists, only a few years ago, agreed this was a heroic idea and that such genes could not have evolved, at least in the usual way. In typical fashion they pushed the problem into the recesses of deep time where anything can happen by mysterious mechanisms that no longer are present and so cannot be critiqued. That narrative serviced evolutionary thought for many years until the evidence for unique, so-called “orphan,” genes became undeniable.

And why were orphan genes a problem? If any design, such as orphan genes, exists in a species but not its allied species then according to evolutionary thinking, said design must not have been present in the common ancestor of those species. It must have evolved after the split from the common ancestor. And that means such a heroic evolutionary event cannot be pushed into deep time. And that’s a problem.

At first evolutionists rejected such an idea. They said such orphan genes would no longer be orphans once we decode the genomes of more species. But with more genomes came more orphans. Orphan genes did not diminish, they escalated, much to the chagrin of evolutionists.

So next evolutionists admitted that there were some novel, orphan genes, but they were exceedingly rare. An evolutionary novelty. And of course novelties are not fundamental to a theory, and so don’t need to be explained.

But the orphan genes just kept on coming. And coming. Finally evolutionists had to admit that there were a whole bunch of orphan genes, and so a whole bunch of genes, in various creatures, must have evolved relatively recently.

And as only evolutionsts can do, after losing every battle, they once again won the war. They turned defeat into victory by explaining that they now have evidence that genes are routinely evolving. The de novo mechanism went from rags to riches. It now was the predominant mode of gene evolution—it happens all the time, and there is no mystery.

And what exactly was that evidence that resolved the mystery? How can evolutionists now be so confident of what, only a few short years ago, they insisted was not possible? Well, err, the orphans are the evidence. Orphans exist in only a single species, so therefore the orphans must have evolved recently.

There, I said it.

And immediately this new truth was broadcast to the people. The New York Times assured its readers that evolutionists have discovered a “step-by-step process” for fast, efficient, modern gene evolution.

So it wasn’t too surprising when an evolutionist claimed recently that the origin of new genes, save for the very first genes way back in deep time, is “basically a solved problem.” That is, after all, the party line.

But when I pointed out the circular reasoning, the failed expectations, and the lack of any real solution beyond hand-waving, the evolutionist doubled down. He cited an 11 year old irrelevant paper (which repeats the now discounted refrain that “the true de novo origination of new genes from previously non-coding sequences is rare”). He also cited two proteins, neither of which are even examples of de novo gene evolution.

And so there we have it. Another evolutionary victory snatched from the jaws of defeat.

Is the Origin of New Genes “Basically a Solved Problem”?

De Novo Genes a Done Deal

It is no surprise that proteins—the essential machines of life—are not likely to have evolved. At least, that is, if you believe in science. Even according to evolutionists and the most optimistic assumptions possible, the evolution of proteins is so unlikely it is beyond practical consideration. While this conclusion is intuitive and hardly surprising, there are several reasons for it. One of the reasons is that the scenarios evolutionists typically envision involve the pre existence of proteins. For instance, proteins are needed to create proteins, at least in today’s biological world. Indeed, proteins are also required for life as we know it. So the first proteins would have had to evolved in a very different kind of biological world. Another reason why protein evolution is difficult is that the fitness landscape in protein sequence space is mostly flat and rugged. A few random mutations will quickly degrade protein function and most of the hyper-dimensional sequence space has little or no function and is far from a useful protein. It is extremely difficult for a random sequence to migrate via mutations close enough to a useful protein for natural selection to take over. In fact this challenge makes the protein evolution difficult regardless of whether proteins already exist. But in spite of this problem, evolutionists believe that protein evolution is not a significant problem. Recently an evolutionist commented that it is “basically a solved problem.”

It wasn’t too many years ago that evolutionists ruled out such protein evolution. Because the problem is so difficult, they believed proteins somehow evolved very early in evolutionary history, and have merely undergone various modifications ever since. As one recent paper explains:

In the pre-genomics era it was widely assumed that much of present-day genetic diversity could be traced by common ancestry to a molecular big bang, where all genes evolved at once.

Likewise another recent paper states:

The emergence of new genes has long been thought to be almost exclusively driven by duplication or recombination of existing gene fragments. The possibility of de novo evolution from intergenic non-coding sequences seemed remote.

But that has all changed now. Not because evolutionists have figured out how new proteins can evolve de novo, but because, if evolution is true, new proteins must have evolved de novo. For in this post-genomic era, we now know that the genomes of species are chocked full of unique, one-time, protein-coding genes. They are not found in allied species, which under evolutionary theory means those genes must have evolved relatively recently.

But how?

If you read the headlines, you would have the impression that the problem is well in hand. For instance, super-star science writer Carl Zimmer wrote in the New York Times earlier this year that “researchers have documented the step-by-step process by which a new gene can come into existence.”

Case closed right?

Well not quite. In fact, not even close. What Zimmer tells his readers is a “step-by-step process” is what scientists affectionately refer to as a cartoon. In fact, here it is:

Was it not a bit serendipitous that DNA segments could so easily become transcribed?

And once transcribed and translated, the resulting protein would most likely be worthless junk. It would be somewhere in the middle of that rugged protein sequence hyperspace, light years away from a design that would improve fitness.

Yet the protein would continue to be synthesized by the patient organism, waiting forever as mutations randomly sample the rugged hyperspace. If that was the case then such experiments would rapidly accumulate, and the organism would be producing a plethora of junk proteins.

For this evolutionists envision that the rapid rise of these experimental protein-coding genes is offset by their destruction:

This fast rate of gene emergence raises the question why the genomes do not fill up with such genes over time. In spite of huge variation in total genome size, genomes do not show a proportionally large variation in terms of protein-coding repertoires. Hence, the emergence rate of new genes must in some way be balanced with a corresponding loss rate.

So evolutionists must say that mutations halt the progress, for example, by creating stop codons somewhere in the middle of the gene.

But if that was the case, then the incredible problem of searching through the sequence space just became that much more impossible. Not only must we search through an astronomically huge, flat, rugged fitness landscape that makes finding a needle in a haystack seem trivial, but now the searches are routinely interrupted and must start all over again from scratch. It is an evolutionary treadmill where mutations are working furiously and getting nowhere as they are continually creating and destroying genes.

This evolutionary narrative is certainly not “basically a solved problem.” In fact, what evolutionists have are high claims of the spontaneous evolution of incredibly complex structures, not because of the evidence, but in spite of the evidence.

So what gives evolutionist’s their confidence? It is not that they understand how such genes could have evolved, but that the genes are observed over and over. And since evolution must be true, then those solo genes must evolved:

Several studies have by now also shown that de novo emerged transcripts and proteins can assume a function within the organism. All of this provided solid evidence that de novo gene birth was indeed possible.

And what exactly do these studies show? Did they really show that “de novo emerged transcripts and proteins can assume a function within the organism”?

Not exactly.

One study found a gene in a yeast species, but the corresponding genome location in allied species came up blank. Again, it is the belief that evolution must be true that does the heavy lifting. A gene is found in a species, it is not found in allied species, those species must share a common ancestor, that common ancestor must have existed relatively recently because the species are similar, therefore the gene must have evolved recently.

It all hinges on evolution being true.

The same logic applies in the other studies, such as the one which found a gene in the mouse genome that is missing in other mammals.

Two more studies found more of these de novo genes in the fly genome, and upon testing discovered that such genes are often surprisingly essential. That doesn’t help. Now, the genes must not only have somehow evolved rapidly, they must have rapidly become essential. It was another surprise for evolutionists. Other studies have found genes in only some individuals, within a population.

Does any of this mean that the de novo genes evolved from random mutations as the evolutionists claim? Of course not.

This de novo gene story parallels the twentieth century evolutionary insistence that species adapt by random biological variation, not geared to help with the current environmental challenges. Those random variations are then subject to natural selection, and the resulting adaptation is the first step toward the large-scale change evolution requires to create the species.

Only recently have evolutionists begun to reckon with the failure of that narrative. I don’t know how genes arose, but once again evolutionists have made unscientific and unsubstantiated claims, and set themselves up for another failure. Only a few years ago they agreed that such evolution of new genes would be impossible. Now they have been forced to adopt it because the evidence unambiguously reveals solo genes, and evolutionists dogmatically insist that everything must have spontaneously evolved. So it is yet another false prediction followed by yet another epicycle, making the theory far more complicated and unlikely.

Here is How the Cytoskeleton Evolved

Not Easy to Explain

Though illustrations of the cell often depict it as a bag full of various organelles and folded membranes, this fundamental unit of life is actually organized upon a highly-structured three-dimensional truss structure known as the cytoskeleton. Until the early 1990s the cytoskeleton had been observed only in the more complex eukaryotic cells. But a series of detailed studies emerged indicating that the other two domains of life (bacteria and archaea) also have cytoskeletons. The wikipedia entry gives a good introduction to this subject:

The cytoskeleton is a network of fibers composed of proteins contained within a cell's cytoplasm. Although the name implies the cytoskeleton to be stable, it is a dynamic structure, parts of which are constantly destroyed, renewed or newly constructed.

In most cells of all domains of life (archaea, bacteria, eukaryotes) a cytoskeleton is found (notably in all eukaryotic cells which includes human, animal and plant cells). The cytoskeletal systems of different organisms are composed by similar proteins. However, structure, function and dynamic behaviour of the cytoskeleton can be very different, depending on organism and cell type. Similarly, within the same cell type the structure, dynamic behaviour, and function of the cytoskeleton can change through association with other proteins and the previous history of the network.

The cytoskeleton of eukaryotes (including human and all animals cells) has three major components: microfilaments composed of the protein actin and microtubules composed of the protein tubulin are present in all eukaryotic cells. By contrast intermediate filaments, which have more that 60 different building block proteins have so far only been found in animal cells (apart from one non-eukaryotic bacterial intermediate filament crescentin). The complexity of the eukaryotic cytoskeleton emerges from the interaction with hundreds of associated proteins like molecular motors, crosslinkers, capping proteins and nucleation promoting factors.

There is a multitude of functions the cytoskeleton can perform: It gives the cell shape and mechanical resistance to deformation; through association with extracellular connective tissue and other cells it stabilizes entire tissues; it can actively contract, thereby deforming the cell and the cell's environment and allowing cells to migrate; it is involved in many cell signaling pathways; it is involved in the uptake of extracellular material (endocytosis); it segregates chromosomes during cellular division; it is involved in cytokinesis - the division of a mother cell into two daughter cells; it provides a scaffold to organize the contents of the cell in space and for intracellular transport (for example, the movement of vesicles and organelles within the cell); it can be a template for the construction of a cell wall. Furthermore, it forms specialized structures such as flagella, cilia, lamellipodia and podosomes.

A large scale example of an action performed by the cytoskeleton is muscle contraction. During contraction of a muscle, within each muscle cell, myosin molecular motors collectively excert forces on parallel actin filaments. This action contracts the muscle cell, and through the synchronous process in many muscle cells, the entire muscle.

Evolutionary theory predicts there to be an evolutionary progression of cytoskeleton designs, as this key aspect of the cell design evolved. But this is not what the science reveals.

For example, in eukaryotes, the proteins actin and tubulin are the building blocks for the microfilament and microtubule structures, respectively. In bacteria and archaea these roles are performed by proteins such as MreB and FtsZ, respectively. But these cousin proteins do not reveals signs of an evolutionary progression. The actin and tubulin proteins show very few changes between different species. In fact they are among the most highly conserved proteins in the eukaryotes.

Even between species as different as yeast and rabbits there is only about a 12% difference in the respective actin proteins. Therefore there is no sign of how a gradual progression of protein evolution could have arrived at the actin and tubulin building block proteins. Importantly, this includes the MreB and FtsZ proteins. The sequence relationships between actin and MreB, and between tubulin and FtsZ, are essentially what we find between any two randomly selected proteins. With evolution we must believe that molecular evolution traversed an enormous gap without leaving a trace of sequence evidence.

This finding is not restricted to the molecular sequence data. The function and distribution of the bacterial components vary dramatically from what we find in the eukaryotes. As one review paper admitted,

it has become clear that there is no simple relationship between the cytoskeletons of prokaryotes and eukaryotes. Moreover, there is considerable diversity in both composition and function between cytoskeletons in different lines of prokaryotes and eukaryotes.

In fact the bacterial designs are highly divergent amongst themselves. Molecular sequences, proteins used, lateral interactions within the filament, polarity (left-handed versus right-handed filaments), and so forth, are all inconsistent across the bacteria. It is not a story of an evolutionary progression.

Another surprise for evolutionists is much of the eukaryotic cytoskeletal functionality must trace back to the first eukaryotic cell—the so-called LECA or Last Eukaryotic Common Ancestor. It is yet another case of complexity pushed farther and farther back in history, to the era of early evolution where the supposed evolution of such complexity is hidden in evolutionary gaps. Here is a particularly candid admission from our review paper:

One of the most surprising results of our increasing ability to probe the characteristics of the LECA has been how much of the biological complexity in extant cells can be traced back to this ancestral cell. The LECA possessed much of the complexity now seen in the replisome, the spliceosome, and the endocytic system, as well as the machineries necessary for meiosis and phagotrophy. Moreover, comparative analysis of the genome of the free-living excavate Naegleria gruberi identified ∼4,000 protein groups that probably were present in the LECA.

This “complexity early” model of eukaryotic evolution is mirrored in the cytoskeleton (Fig. 2 D). Somewhere in the evolutionary space between prokaryotes and the LECA, single proto-tubulin and proto-actin molecules diversified into multiple specialized forms. Three classes of motors arose independently, and evolved to include at least nine classes of dynein, eleven classes of kinesin, and three classes of myosin. As well as these, the axoneme formed, with 100–200 associated proteins, many of which have no prokaryotic orthologues. Between the prokaryotes and the LECA, a revolution occurred in cytoskeletal biology.

Such complexity cannot have appeared fully formed, but arose by stepwise elaborations of cell structure (and genetic repertoire). However, the large number of simpler intermediate forms that must have existed appear to have left no descendants. This is perhaps because a great many of these changes occurred in a relatively short time, with one innovation creating a favorable landscape for the evolution of the next. Alternatively, all descendants of these intermediate forms have been simply out-competed by the arrival of the LECA, with its mitochondrial endosymbiont, endomembrane system, and sophisticated cytoskeleton. What is clear is that since this complex LECA, the diversification into many eukaryotic lineages has often been accompanied not by the addition of further classes, but by loss of ancestral ones. Some of these losses are associated with loss of specific structures or functions (such as axonemal motility), but there appears to be a remarkable flexibility in the precise repertoire of many of these ancient families that is required for eukaryotic cell function.

From a scientific perspective, it would be difficult to imagine a more absurd narrative. Evolutionary explanations, such as this one, are the height of creative story-telling, contorting the theory to try and fit awkward facts.

h/t: La Victoria

Death as the Engine of Progress

Ideas Have Consequences

Watch this short video to see how ideas have consequences.

At some future period, not very distant as measured by centuries, the civilized races of man will almost certainly exterminate and replace throughout the world the savage races.—Charles Darwin, The Descent of Man

the war of annihilation … is a natural law, without which the organic world … could not continue to exist at all.—Gustav Jaeger, 1870

just as in nature the struggle for existence is the moving principle of evolution and perfection … so also in world history the destruction of the weaker nations through the stronger is a postulate of progress.—Friedrich Hellwald, 1875

according to Darwin’s theory wars have always been of the greatest importance for the general progress of the human species … the physically weaker, the less intelligent, the morally lower … must give place to the stronger.—Heinrich Ziegler, 1893

Those people who are, from the outset, failures, oppressed, broken— they are the ones, the weakest, who most undermine life among human beings, who in the most perilous way poison and question our trust in life, in humanity, in ourselves.—Friedrich Nietzsche, On the Genealogy of Morals

The law of selection exists in the world, and the stronger and healthier has received from nature the right to live … Woe to anyone who is weak, who does not stand his ground! He may not expect any help from anyone.—Adolf Hitler

Müller Cells are Wavelength-Dependent Wave-Guides

Enhancing the Cone Photoreceptor Sensitivity

The best arguments for evolution have always been from dysteleology. This world, as evolutionists explain, just does not appear to have been designed. Consider our retina for example. Isn’t it all backwards, with the photocells—which detect the incoming light—pointed toward the rear and behind several layers of cell types and neural processes. Does this make any sense? Surely such a claptrap would offend any “tidy-minded engineer,” as Richard Dawkins put it. But such arguments have never worked and the history of evolutionary thought is full of their failures. Aside from the fact they are metaphysical and not open to scientific testing, they inevitably are simply false. The “bad retina design” argument, as discussed here, here, here, here and here for example, has repeatedly been rebuked. As we learn more we find the retina has all kinds of subtle and clever designs. And now new research out of Israel continues to confirm this trend. Unbelievably, the scientists have demonstrated that the retina’s Müller cells are wavelength-dependent wave-guides that focus the longer-wavelength green-red light onto the cone photoreceptors and pass the shorter-wavelength blue-purple light through to the rod photoreceptors.

It just so happens that is a great idea because while the cone photoreceptors are fast acting and provide color vision, they are less sensitive and need all the help they can get. The rod photoreceptors, on the other hand, are mainly sensitive to the shorter-wavelength blue-purple light, so they don’t miss too much the filtering out of the green-red light. As one science writer concluded:

Having the photoreceptors at the back of the retina is not a design constraint, it is a design feature. The idea that the vertebrate eye, like a traditional front-illuminated camera, might have been improved somehow if it had only been able to orient its wiring behind the photoreceptor layer, like a cephalopod, is folly.

It just isn’t very smart to criticize a design when you’ve never built one yourself and, much less, don’t even know how it works. It’s even worse to then use that ill-conceived criticism as justification for the claim that the design arose spontaneously. From a scientific perspective that claim was always weak. Now it is simply ridiculous. The retina’s incredible design reveals the details of what always was intuitively obvious. As Paul explained, God has made foolish the wisdom of this world.

Evolutionist: Dinosaurs “Were Experimenting” With Flight

Just-So Stories With Final Causes: Aristotle Meets Kipling

Did dinosaurs really shrink so fast on their way to producing birds? That is what happened according to a new study out this week. As the LA Times explains, “Paleontologists have long known that birds evolved from dinosaurs known as theropods,” and now they have confirmed that over a 50 million year period that evolutionary pathway proceeded at several times the normal pace. But as usual the evolutionist’s certainty is underwritten by a mix of speculation and Aristotelianism.

How exactly has this new study confirmed that dinosaurs evolved birds at a fast pace, and how exactly is it that “paleontologists have long known that birds evolved from dinosaurs known as theropods”? In fact there was no such confirmation and there is no such knowledge, not in any scientific sense.

When we say that scientists “know” something, we do not mean that they personally believe it (which paleontologists do), we mean that they have compelling, overwhelming evidence for it (which paleontologists do not). In the scientific sense, which of course is the sense in which evolutionists portray themselves and the sense intended by the Times article, paleontologists have no such knowledge.

That is not in question. How can I know this? Because I’ve read what they have to say. I know their arguments. Unless they’ve been cleverly hiding their proofs, there is no question that they do not “know” dinosaurs evolved into birds—at a fast pace or otherwise.

In fact what evolutionists have most of to offer is speculation, sometimes referred to as “just-so” stories after Kipling’s classic by the same name. For example, evolutionists speculate that as the dinosaurs became smaller (for some reason) their embryonic development phase shortened. And this abbreviated development period meant (for some reason) that the miniaturized dinosaurs retained into adulthood their juvenile features, “some of which were uncannily bird-like.”

And why would dinosaurs become smaller in the first place? Well maybe they were adapting to living in trees where massive size, after all, puts one at a decided disadvantage. Instead, they would need to be small and agile. And maybe nocturnal as well, so evolving feathers to stay warm would help. Longer forelimbs would also help swing from tree to tree, and perhaps those longer forelimbs evolved into wings.

What evolutionists lack in evidential support they make up for with imagination. And evolutionists frame their just-so stories in Aristotelian, final causes, terminology. For example, there was a “push” toward smaller size, and the smaller sizes in dinosaurs helped to “trigger” a host of different traits. A wing-like surface area would have developed “to help glide” from tree to tree. After all, dinosaurs “were experimenting” with flight in various modes and finally “made the crucial leap” to powered flight, and so birds “were born.”

Dinosaurs were experimenting with flight? This isn’t science, this is absurdity.

Gigantic School of Rays

Evolution at Work

Evolutionists are certain these rays arose spontaneously even though they can’t explain how that could have happened.

Birds With Ornamental Eyespots Have Unlikely Neighbors

More Independent Evolution

When a peacock spreads out its train the feathers form a huge display. Near the end of each feather is a colorful, circular object that looks something like an eye and the feathers are positioned just right so that the eyes, or ocelli, are beautifully arrayed across the entire display. The iridescence of the eyes comes not from the material itself, which isn’t colorful, but from its finely-tuned nanostructure which reflects the light to produce the different colors. Such eye-spot feathers are found in three different bird genera and according to a new evolutionary analysis of their genetics, they would likely share a common ancestor as has always been expected by evolutionists. There’s only one problem. The analysis also finds that other bird genera that are without these ornamental eyespots, are also closely related to these genera that do have eye-spot feathers.

If these other genera are so closely related, then why do they not also have ocelli? With evolution we must say that they had the eye-spot feathers but later lost them for some reason, over the course of evolution. Or that the eye-spot feathers evolved independently in the different genera that have them. Either way these are just-so stories, manufactured to fit the theory. As the new study concludes:

The close relationship between taxa with and without ocelli suggests multiple gains or losses. Independent gains, possibly reflecting a pre-existing bias for eye-like structures among females and/or the existence of a simple mutational pathway for the origin of ocelli, appears to be the most likely explanation

This is yet another evidence, in a long, long list, which demonstrates that evolution is not a simple, parsimonious explanation that, in a stroke, easily explains a set of disparate and otherwise unlikely or confusing observations.

Rather, evolution is a complex theory with a never-ending list of epicycles that are needed to explain a wide variety of evidences that are inconsistent with the basic theory. This makes evolution a tautology.

Here Are the Three Important Take-Aways From That New Spider Study

Nothing is Going Right

A new study out of Harvard continues to find problems with the spider evolution story. This time it is a massive genetic study demonstrating that spiders that create orb webs do not fall into the expected evolutionary pattern. As usual, the problem cannot simply be explained away as a consequence of methodological problems and evolutionists are left with convergence or extinction as their only explanations. Either orb weaving evolved multiple times, or it evolved once, proliferated, and then a bunch of species became extinct. Ever since Darwin this denouement has repeated itself over and over—evolutionists apply their theory to a particular problem, their predictions turn out false, and they respond by accommodating the new findings. Skeptics say the theory is failing and evolutionists say this is just good science at work. Did you expect every prediction to be perfect? Inevitably the debate devolves into one over falsification and unfortunately misses what is really important.

There literally are thousands of stories like this spider study. Evolutionary expectations fail, evolutionists adjust and move on, explaining that there’s nothing there that falsified evolution, it was merely a particular prediction that was falsified.

But that doesn’t mean that such failures do not pose serious problems for the theory of evolution. Evolutionists go easy on their theory. They set the bar high and enjoy the ability of their theory to avoid falsification.

To be fair though, one should not expect the practitioners and promoters of a theory to be serious skeptics. Evolutionists sometimes say they would love to falsify their theory, as that would make them famous. But in science there are enormous conformance pressures, ranging from social to monetary. And this is even more so with evolution. If you genuinely question evolution (not just question a sub hypothesis) then you become an anathema. You will be called a creationist. You will be blackballed and rather than becoming famous, you become infamous.

So what is the problem with evolution’s failed predictions, such as this latest study of orb weaving spiders? Actually there are three problems. It is true that the predicted failure, alone, does not falsify evolutionary theory. That’s a rather silly notion given how evolution was never confirmed in the first place, and how flexible is the theory. Evolutionists cannot even explain, in any scientific sense, the evolution of a single protein.

Evolution is metaphysically motivated and has always failed on the science. So the problem is not that new prediction failures falsify the theory. The first problem with such failures is their quantity. There are thousands of such failures. Evolution is consistently coming up short. Its predictions are always wrong and evolutionists are always surprised. To say this steady stream of failure is just a sign of good science is an incredible euphemism.

The second problem with such failures is that they cause the theory to lose parsimony. With each failed prediction, the theory becomes far more complicated as patches and epicycles are added. And this brings us to the third problem, which is related to the second problem.

These failed predictions cause evolution to lose its smoking gun. The strong scientific argument for evolution was that in a stroke it resolves myriad puzzles in the life sciences. There is a consilience across a wide spectrum of disparate disciplines and data, and previously unlikely or bizarre findings are suddenly and simply explained by Darwin’s elegant theory.

This is all a myth as there never was any such genuine consilience. But if one selectively examines the evidence, one can construct such a story. And it is a powerful story. Why do so many species have the pentadactyl structure? It doesn’t seem to make sense, but with common descent it suddenly falls into place. Across those many species, the pentadactyl structure falls neatly into evolution’s common descent pattern. It is all so obvious.

Take this example along with so many others, and you have a consilience. These curious evidences are the smoking gun that compels us to accept evolution. There’s only one problem. There is no such consilience. This latest spider study is just one more example of how the evidence does not fall neatly into the evolutionary pattern—it contradicts that simple, elegant pattern.

Even the venerable pentadactyl structure failed. As Stephen J. Gould put it, “The conclusion seems inescapable, and an old ‘certainty’ must be starkly reversed.”

So it is not that evolutionists cannot explain away all these failures. Of course they can. Evolution is an over-arching, vague, notion that can accommodate myriad findings with all manner of creative explanations. The problem is there is no reason to think, from a scientific perspective, that evolution is a good theory. It cannot explain how the species arose, and the patterns that the species form don’t fit evolution’s expected pattern. There is no smoking gun.

Consider how one report explains the new spider study findings:

For decades, the story of spider evolution went like this: As insects became more and more diverse, with some species taking to the skies, spiders evolved new hunting strategies, including the ability to weave orb-shaped webs to trap their prey. From that single origin, the story goes, orb-weaver spiders diverged along different evolutionary paths, leading to today, where several species weave similar -- though not identical -- webs. It's a good story, but there's just one problem -- Harvard scientists now know it's not true. The largest-ever phylogenetic study of spiders, conducted by postdoctoral student Rosa Fernández, Gonzalo Giribet, Alexander Agassiz Professor of Zoology, and Gustavo Hormiga, a professor at George Washington University, shows that, contrary to long-held popular opinion, the two groups of spiders that weave orb-shaped webs do not share a single origin.

As the study explains, the findings demand “a major reevaluation of our current understanding of the spider evolutionary chronicle.”

A Key Evidence for Evolution Involving Mobile Genetic Elements Continues to Crumble

More Junk DNA That Isn’t Really Junk After All

It is difficult to keep track of all the studies indicating that junk DNA isn’t really junk DNA after all. I have no idea how much actual junk there is in our genomes, but evolution has a long history of failed claims of disutility, inefficiency and junk in nature’s designs. That is why I think Dan Graur took the wrong side of history in his “either the genome is mostly junk or evolution is false” proposition.

A study published last week found strong signs of function in mobile repetitive DNA elements. Mobile genetic elements have been heavily recruited by evolutionists in recent years as powerful, undeniable proofs of common ancestry. An underlying assumption in those proofs, aside from the usual non scientific metaphysics, is that such mobile elements insert themselves into the genome at random. But this study suggests they are at least sometimes nonrandom and functional. As one report explains:

“We’ve come to understand that not all repeat sequences are junk DNA,” said Pawel Michalak, an associate professor at the Virginia Bioinformatics Institute.  “These repetitive sequences are increasingly being recognized as agents of adaptive change. We discovered a larger than expected amount of genetic variation in these repeating sequences between the fly populations and saw that the variation resulted in potentially functional differences in important biological processes, such as stress resistance and mating.”

[…]

The biological roles of these place-jumping, repetitive elements are mysterious.

They are largely viewed as “genomic parasites,” but in this study, researchers found the mobile DNA can provide genetic novelties recruited as certain population-unique, functional enrichments that are nonrandom and purposeful.

“The first shocker was the sheer volume of genetic variation due to the dynamics of mobile elements, including coding and regulatory genomic regions, and the second was amount of population-specific insertions of transposable DNA elements,” Michalak said. “Roughly 50 percent of the insertions were population unique.”

The fact is, as this study further suggests, we don’t really understand genetics well enough to support the kind of hard claims evolutionists make about the evidence.

Here’s That Protein-Protein Interaction Problem

Evolutionists Don’t Know What They’re Doing

In Chapter 7 of The Edge of Evolution, Michael Behe explained why protein-protein interactions are a problem for evolution. Here is a summary of the problem. First, protein-protein interactions are important. Proteins often work in teams where half a dozen or more proteins may be interacting with each other to form a molecular machine. Protein-protein interaction is ubiquitous throughout life—so ubiquitous that we now have a name for the collective set of such interactions: the interactome. You can’t do much without protein-protein interactions. It is not as though protein-protein interactions are a convenient extra that makes cells a bit more efficient or bequeaths a few nice-to-have functions. Protein-protein interactions are fundamental to life, and are fundamental at all levels. Evolution must have been creating protein-protein interactions throughout evolutionary history as new species and capabilities arose.

And yet it is difficult to get two proteins to interact in a meaningful way. Such interactions must not be too strong or too weak. Imagine that you had two proteins that you needed to bind meaningfully to each other. If you randomly selected the amino acids at the binding patch on the surface of one of the two proteins, then meaningful binding would be unlikely. In fact, you would have to repeat the experiment millions of times before you could expect to get a good result.

But evolution does not have such resources. It cannot conduct millions of evolutionary experiments in order to luckily find amino acid sequences on protein surfaces that are required for important biological functions. And even if it could, that would only be the first step, because molecular machines are often comprised of multiple proteins, interacting with each other at multiple sites. So evolution would have to luckily find several sequences, in multiple proteins, and get them to arise in similar time frames, so the molecular machine would function.

But that is not all, for molecular machines often work in conjunction with other molecular machines. Having a molecular machine without its neighbors would often not help much.

And yet even with all this there remain more problems. For instance, most proteins are not highly modifiable. You can’t just randomly go about swapping in different amino acids. Protein function typically degrades rapidly with amino acid substitutions. So it is challenging for very much interaction site experimentation to take place in the first place. And of course another problem is that it is astronomically difficult for evolution to evolve a single protein to begin with, let alone meaningful interaction sites.

Simply put, from a scientific perspective protein-protein interaction is another problem for evolution.

A Triplex RNA Structure For Real Time Frame Shifting

More Biological Fine Tuning

Protein-coding genes provide a sequence of nucleotides that is read three nucleotides at a time. Each triplet is translated into a particular type of amino acid. So a sequence of 300 nucleotides codes for 100 amino acids, which are attached to each other to make a protein. But what if you started not with the first nucleotide in the sequence, but with the second one? You would have a different sequence of nucleotide triplets, and so a different sequence of amino acids. This is also true if you started with the third nucleotide. In fact you could switch over to the opposing DNA strand (the other half of the double helix) and again you would have the choice between three different “frames,” resulting in three different sequences of amino acids. So in all you can choose between six different reading frames. So any given gene has the theoretical possibility of containing different genetic messages, in the different reading frames. And indeed, years ago it was discovered that genes are overlapping—portions of their nucleotide sequence exist on the same segment of DNA, just in a different reading frame. But an even more bizarre theoretical possibility is that the reading frame could shift while the sequence of nucleotides is being read. In that case you are mixing and matching partial sequences from different reading frames. Now, a new study has investigated this capability and discovered a fascinating mechanism that apparently enables the real-time frame shifting.

Nucleotide sequences are translated into amino acid sequences at the cell’s ribosome structures and the new study found that this translation process can be programmed to skip a nucleotide, and so switch to another reading frame, attaching two short snippets of nucleotide segments, known as microRNAs, to the main nucleotide sequence at certain locations. The study suggests that a pseudoknot, or triplex, RNA structure is formed causing the skip to occur. Of course the right nucleotide sequence is required, and the right microRNA sequences are required. It was not easy to solve this complicated puzzle, as one researcher explained:

These are really complex RNA structures. It takes a lot of computer memory to search for them in human cells. It wasn’t until the past decade that computers were fast and powerful enough to find these signals.

It is yet another “novel mode” of realtime biological response resulting in “fine-tuned” cell performance. It all just smacks of random mutations.